The phrenic afferents activated neurons in Lamina III and IV of areas 3a and 3b. 
In Lamina III, where low threshold afferents terminate, EGFP-labelled neurons were never depolarised but either hyperpolarised (25%) or not affected (75%) by noradrenaline.
Most Lamina III/IV NK1r cells at both levels projected to LPb, but few were labelled from PAG.
Immunohistochemical comparison of the L1-L6 spinal cord segments showed an increased area of CGRP immunoreactivity in the dorsal horn (Lamina III/IV) of treadmill-trained SCI compared with intact and sedentary SCI animals.
A previously unknown excitatory input to the superficial dorsal horn from Lamina III-IV was identified in a subset of the vertical cell population.
All NK1r-positive Lamina III/IV neurons had numerous GluR2-immunoreactive puncta in their dendritic plasma membranes, and virtually all (97%) of the puncta tested were labelled (usually strongly) with the GluR4 antibody. These results show that synaptic AMPArs on the dendrites of the Lamina III/IV NK1r projection neurons contain GluR2, GluR3 and GluR4, but not GluR1 subunits..
Most lamina I and Lamina III/IV NK1r-immunoreactive spinothalamic neurons in cervical and lumbar segments could be labeled from injections centered on PoT. We found that 85% of the Lamina III/IV NK1r-immunoreactive neurons in C6 and 17% of those in L5 belong to the spinothalamic tract, and these apparently project exclusively to the caudal thalamus, including PoT.
Furthermore, exquisitely sensitive down hair follicle afferents projected throughout the inner half of the SG (i.e., Lamina III) and sent dense clusters of terminals well into the outer SG (IIo), where they intermingled with those of unmyelinated nociceptors.
In laminae I-II, approximately 65% were GluR1-positive and approximately 60% were GluR3-positive, while in Lamina III the corresponding values were 34% (GluR1) and 80% (GluR3). Puncta stained with antibody against the C-terminus of GluR4 (which only detects the long form of this subunit) made up 23% of the AMPAr-containing puncta in lamina I, approximately 8% of those in lamina II and 46% of those in Lamina III.
Thus transmission reliability at synapses between Lamina III/IV interneurons overall is low, and efficacy of these connections is related to firing properties of the presynaptic cells.
Second, we anatomically identified in the MDH Lamina III a subpopulation of NK1R-expressing local interneurons that relay nociceptive information from the MDH to downstream Sp5O neurons. We conclude that, in contrast to central sensitization that is controlled by a spino-bulbo-spinal loop, Sp5O WDR neuron windup is regulated through a local circuit activated by MDH Lamina III NK1Rs..
We found that virtually all of the Lamina III/IV NK1r-immunoreactive neurons contained pERK after each of these stimuli and that in the great majority of cases there was internalisation of the NK1r on the dorsal dendrites of these cells. In addition, we also saw neurons in Lamina III that were pERK-positive but lacked the NK1r, and these were particularly evident in animals that had had the pinch stimulus. CONCLUSION: Our results demonstrate that Lamina III/IV NK1r-immunoreactive neurons show receptor internalisation and ERK phosphorylation after mechanical, thermal or chemical noxious stimuli..
Within Lamina III-IV of the lumbar spinal cord, there was an increase in OX42 positive microglia.
More than 90% of the dually labeled neurons were distributed in lamina I (marginal zone), less than 10% of them were located in lamina II (substantia gelatinosa), and only a few (about 1%) were found in Lamina III (magnocellular zone).
Selective elimination of NK1R+ neurons in lamina I and Lamina III/IV of the dorsal horn also suppresses development of hyperalgesia and allodynia. Therefore, we tested whether Ca2+-permeable AMPA receptors are located on lamina I and Lamina III/IV NK1R+ neurons postsynaptic to primary afferent fibres, using inward rectification and polyamine toxins for receptor identification. We examined three different populations of dorsal horn neurons; lamina I NK1R+ neurons, including projection neurons, and non-NK1R+ (NK1R-) neurons including interneurons, and Lamina III/IV NK1R+ neurons, believed to contribute to the low-threshold mechanosensory pathway. Lamina III/IV NK1R+ neurons and lamina I NK1R- neurons have a significantly higher proportion of postsynaptic Ca2+-permeable AMPA receptors than lamina I NK1R+ neurons.
Post-synaptic neuronal activities in Lamina III-IV were suppressed earlier than those in lamina I-II.
Correlations between the thickness of laminae II-III and columnar spacing in Lamina III within individual cytoarchitectonic areas in both hemispheres of each donor were calculated.
At all levels of the spinal cord dorsal horn, HCN1 immunoreactivity (HCN1-IR) was predominantly absent from laminae I and II, while a dense band of punctate labeling was visible in Lamina III.
Lamina I NK1R+ neurons were shown to receive high-threshold (Adelta/C fiber) monosynaptic input, whereas Lamina III NK1R+ neurons received low-threshold (Abeta fiber) monosynaptic input. In lamina I NK1R- and Lamina III NK1R+ neurons, disinhibition enhanced control-evoked responses, and this was also NMDA receptor dependent.
At least seven distinct Y1 receptor-positive populations could tentatively be recognized: Type 1) abundant small, fusiform Y1 receptor-positive neurons in laminae I-II, producing a profuse neuropil; Type 2) Y1 receptor-positive projection neurons in lamina I; Type 3) small Y1 receptor-positive neurons in Lamina III, similar to Type 1 neurons, but less densely packed; Type 4) a number of large, multipolar Y1 receptor-positive neurons in the border area between laminae III-IV, with dendrites projecting toward laminae I-II; Type 5) a considerable number of large, multipolar Y1 receptor-positive neurons in laminae V-VI; Type 6) many large Y1 receptor-positive neurons around the central canal (area X); and Type 7) a small number of large Y1 receptor-positive neurons in the medial aspect of the ventral horns (lamina VIII).
We found that preprotachykinin B-immunoreactive neurons were present throughout laminae I-III, constituting 10-11% of the neuronal population in laminae I-II, and 4% of that in Lamina III. They formed a prominent band in the ventral half of lamina II (where they made up 16% of the population) and the dorsalmost part of Lamina III.
To learn whether central projections were altered after inflammation, CGRP immunoreactivity in the protein kinase Cgamma-IR Lamina III was quantified and found to increase.
The simulated terminals were connected nonselectively to nearby dendrites of 135,000 simulated Lamina III-IV cells whose dendritic surface area distributions were based on intracellularly stained cells.
Isolation rearing or methamphetamine treatment alone reduced the projections from lamina V/VI to the frontal and from Lamina III to the insular cortex, and from both laminae to the parietal cortex.
Moreover, dense reaction product was found in the most medial aspect of lamina II, especially lamina II inner part, and less in Lamina III and IV of levels L3-L5.
A study of Lamina III in the left hemisphere of human brains revealed a wider separation between cell columns and more non-neuronal (empty) space within cell columns compared to the right hemisphere.
Approximately one-half of the Abeta-fiber terminations in Lamina III contain N-cadherin; none contain E-cadherin.
Aside from somatic motor neurons and autonomic preganglionic neurons choline acetyltransferase-immunoreactivity was found throughout the spinal cord in Lamina III of the superficial dorsal horn and near the central canal.
Immunolabeling was particularly dense in lamina IX and in the dorsal horn Lamina III.
We report significant increases at C8 and L5, in CGRP-IR in Lamina III compared to control tissue (P < 0.05).
Capsaicin induced an increase in the frequency of miniature excitatory postsynaptic currents in 73% of lamina I and 43% of Lamina III/IV neurons expressing NK1-receptor indicating that these neurons receive direct input from capsaicin and heat sensitive nociceptors..
We found a lower density of Lamina III N200-positive neurons in major depressive disorder than in schizophrenia or bipolar disorder.
Afferent boutons in Lamina III were often surrounded by several presynaptic axons and postsynaptic dendrites (thus forming type II glomeruli), while boutons in laminae IV-V had only simple, nonglomerular interactions.
Numerous alpha2C-AR axons were apposed to cell bodies and proximal dendrites of cells in lamina I and also to distal dendrites that originate from labeled cell bodies in Lamina III/IV.
The GCM C afferents projected rostrocaudally for two or three segments and ran at the surface of the dorsal funiculus, giving off collaterals into laminae I and II and sometimes into parts of Lamina III.
The potency of capsaicin to produce internalization was progressively lower in Lamina III (EC(50)=1.9 microM) and lamina IV (EC(50)=14.5 microM), suggesting that neurokinins released in laminae I-II become diluted as they diffuse to the inner dorsal horn.
Vacuolation in area V1 was most severe in Lamina III and the glial cell reaction in lamina V or VI.
At P20, prenatal cocaine exposure resulted in a significant increase in alpha1 subunit mRNA in ACC Lamina III and a significant reduction in the amounts of the beta2 subunit mRNA in ACC lamina II.
(2) A second population of choleratoxin-labelled vibrissal afferents was also observed, terminating only in Lamina III of the caudal subnucleus. (3) After peripheral nerve transection, NPY-immunoreactive supraorbital vibrissal primary afferent fibres appeared in their appropriate barrelettes in the principal sensory nucleus and the caudal part of the interpolar subnucleus, while in the caudal part of the caudal subnucleus NPY-immunoreactive vibrissal primary afferent terminals were found exclusively in the inner part of lamina II, extending over the outer part of Lamina III.
GABA and glycine-like immunoreactivity in axons and dendrites in synaptic contact with the afferent terminals was demonstrated by using a postembedding immunogold method, and serial section reconstruction was used to show the distribution and nature of these interactions in Lamina III of the dorsal horn.
Both cingulate areas demonstrated a significant loss in Lamina III in AD, while only the posterior cingulate manifested a loss in lamina V.
Most of the PKCgamma-, CB-, CR- and PV-immunoreactive neurons were observed in lamina II; some were also encountered in lamina I and Lamina III of the medullary dorsal horn. Neurons co-expressing CB/PKCgamma, CR/PKCgamma and PV/PKCgamma were also mainly found in lamina II, while in lamina I and Lamina III, only a few neurons co-expressing CB/PKCgamma, CR/PKCgamma and PV/PKCgamma were encountered.
Collaterals invaded the entire gray matter from lamina IX up to Lamina III; the fibers and terminals were most numerous in laminae VII and VIII.
It has been shown that the Lamina III/IV NK1 receptor-immunoreactive projection neurones are densely and selectively innervated by substance P-containing primary afferent neurones, and there is evidence that these afferents also target lamina I projection neurones with the receptor. The Lamina III/IV neurones also receive numerous synapses from axons of local inhibitory interneurones which contain GABA and neuropeptide Y, and again this input shows some specificity since post-synaptic dorsal column neurones which also have cell bodies in laminae III and IV receive few contacts from neuropeptide Y-containing axons.
Over 90% of FG-labeled neurons in the marginal layer (lamina I) and a few FG-labeled neurons in the superficial part of the magnocellular layer (Lamina III) showed PKCgamma-LI.
Retrograde tracing experiments demonstrated that both presylvian and cruciate corticostriatal projections originated from neurons in Lamina III and the upper aspects of lamina V.
In the lumbar dorsal horn, mGluR2/3-like immunoreactivity is localized preferentially in Lamina III with lighter staining in laminae III and IV. The dense mGluR2/3-like immunoreactivity in Lamina III is consistent with the localization of these receptors in I-B4-labeled dorsal root ganglion cells. Since these receptors are concentrated in Lamina III and also largely co-localized with I-B4, they may have considerable influence on nociceptive processing by what are considered to be non-peptidergic primary afferent neurons..
We have examined the labeling pattern in the spinal dorsal horn by an intra-sciatic nerve injection of cholera toxin B subunit conjugated horseradish peroxidase (HRP) after transection of the posterior cutaneous nerve and inferior gluteal nerve, and found that the cholera toxin B subunit conjugated HRP labeling in lamina I was expanding into lamina II and there was a shrinking gap between lamina I and Lamina III.
The alpha-synuclein probe showed intense labeling of pyramidal cells in Lamina III and V in both patients and controls.
In rats perfused with 0.5% paraformaldehyde, LM showed a more punctate staining, mainly in the ventral part of Lamina III and Lamina III, than in material fixed with 4% paraformaldehyde. The lectin from Bandeiraea simplicifolia (IB4) is selectively taken up by unmyelinated primary afferent fibers that terminate in the outer part of lamina II (IIo) and dorsal part of Lamina III, whereas the B subunit of the cholera toxin (CTB) is selectively taken up by a broader class of primary afferents which, in superficial DH, terminate mainly in laminae I, ventral part of IIi, and III.
Using stereological estimates of neuron numbers from electron microscopic sections, we found that stimulation of A-fibers in an intact sciatic nerve at 10 Hz, 20 Hz, and 50 Hz in 10-minute intervals at a stimulus strength that activates both Abeta and Adelta fibers resulted in the loss of 25% of neurons in Lamina III, the major site of termination of large Abeta fibers, but not in lamina I, where Adelta fibers terminate. Furthermore, sciatic nerve lesions did not result in detectable neuron loss, but activation of A fibers in a previously sectioned sciatic nerve did cause substantial cell death not only in Lamina III but also in laminae I and II.
Synaptic volume density (Nv) was quantified in Lamina III and V of the superior-middle frontal cortex employing the physical disector. The stereological assessment demonstrated maintenance of Nv in both Lamina III and V of the frontal cortex.
Seven days after unilateral rhizotomy, there was a marked reduction of CGRP-IR fibres in the ipsilateral superfical layers and distinctly CGRP-IR neurons could be detected in the ipsilateral Lamina III. CGRP mRNA-positive neurons were observed in Lamina III in both the ipsilateral and contralateral dorsal horn.
Four weeks following diabetes induction, staining of axon terminals of nonpeptidergic unmyelinated neurons labeled with the isolectin IB4 or enzyme activity for thiamine monophosphatase (TMP) was reduced in Lamina III of the lumbar dorsal horn, particularly in the medial region which receives distal sciatic afferents. GDNF treatment had no effect on CGRP-ir projections but restored TMP labeling in Lamina III.
Neurokinin B-like immunoreactivity occurred in all superficial laminae, with the highest density in inner lamina II and the lowest in Lamina III. Some of these dendritic profiles were part of synaptic glomeruli in inner lamina II and Lamina III.
Furthermore, the density of the SP receptor immunoreactivities was considerably decreased in the nerve cells of Lamina III.
Neural ensemble activity in the thalamorecipient zone (lower Lamina III) and supragranular cortical laminae (upper Lamina III and lamina II) was measured using multiunit activity and current source density techniques and the degree of phase-locking to the f0 was quantified by spectral analysis.
In control animals, PKC betaII immunoreactivity extended from lamina I into Lamina III, while PKC gamma immunoreactivity was concentrated within laminae II and III.
All anti-mGluR1a antibodies strongly and specifically immunolabeled dendritic and somatic membranes of neurons in the deep dorsal horn (Lamina III-V) and the ventral horn (lamina VI-IX).
In the hedgehog, the greatest (P<0.001) GABA-dependent reduction of zolpidem inhibition constants was mostly registered in alpha1- and/or alpha5-enriched areas, such as the frontoparietal cortex Lamina III (235%), ventrolateral thalamic nucleus (128%), and substantia nigra pars reticulata (110%) of the male.
Serial sections from the principal nucleus (Vp), dorsomedial parts of the oral and interpolar nuclei (Vdm), and Lamina III/IV of caudal nucleus (Vc) were immunostained for Glu and GABA by using a postembedding immunogold technique. The frequency of synapses onto somata or primary dendrites per Glu-IR PAT was higher in the Vdm than in either the Vp or Vc Lamina III/IV. The frequency of contacts of the p-endings per Glu-IR PAT was higher in the Vp than in the Vdm and Vc Lamina III/IV.
In vitro whole cell patch-clamp recording techniques were utilized to study silent pure-N-methyl-D-aspartate (NMDA) receptor-mediated synaptic responses in lamina II (substantia gelatinosa, SG) and Lamina III of the spinal dorsal horn. In contrast, in slices from naive adult rats, no silent pure-NMDA EPSCs were recorded in SG neurons following focal intraspinal stimulation (n = 27), and only one pure-NMDA EPSC was observed in Lamina III (n = 23).
FP recordings from dorsal horns of normal spinal cord slices revealed long-latency synaptic responses in lamina II and short-latency responses in Lamina III. The majority of monosynaptic EPSPs recorded with intracellular microelectrodes from lamina II neurons in control slices were elicited by high-threshold nerve stimulation, whereas the majority of monosynaptic EPSPs recorded in Lamina III were elicited by low-threshold nerve stimulation. The majority of low-threshold EPSPs in lamina II neurons after axotomy displayed properties similar to low-threshold EPSPs in Lamina III of control slices. These results indicate that reoccupation of lamina II synapses by sprouting Abeta fibers normally terminating in Lamina III occurs after sciatic nerve neuroma formation.
Animals that had allodynia also demonstrated a significant increase in the level of c-fos labelling in Lamina III, IV and V of the dorsal horn without stimulation.
In Lamina III the labelled perikarya were evenly distributed, while those in lamina IV accumulated mainly in the lateral part.
Strongly stained mGluR2/3 was seen in the inner layer of lamina II and the dorsal part of Lamina III. Similar staining for mGluR2/3 was also seen in Lamina III-VI and in lamina X, but mGluR2/3 immunoreactivities were few in lamina VII-IX.
Immunoreactive neurons were concentrated in ventral lamina II, but were also present in Lamina III. Cells with the neurokinin 1 receptor are found in lamina I and Lamina III, and PKCgamma was present in 22% and 37% of these populations, respectively.
We previously identified a strong monosynaptic link between substance P-containing primary afferents and cells in Lamina III or IV with the neurokinin 1 (NK1) receptor. In this study, we used confocal microscopy to examine the input to Lamina III/IV NK1 receptor-immunoreactive neurons from NPY-containing axons. In addition, the NK1 receptor-immunoreactive Lamina III/IV cells received few contacts from nitric oxide synthase-containing axons (which belong to a different population of GABAergic dorsal horn neurons).
Moreover, electrical stimulation sufficient to excite C fibers evoked SPR internalization in 22% of SPR+ Lamina III neurons after nerve transection and in 32-36% of SPR+ neurons in Lamina III and IV after inflammation.
When assessed 1 hr after sodium selenite, stain was distributed throughout the neuropil of the spinal cord, especially in Lamina III and the area surrounding the central canal.
Myelinated afferent terminals labelled transganglionically with cholera-toxin beta-subunit gain a small advantage in collaterally sprouting into the adjacent denervated neuropil in Lamina III after prior peripheral nerve lesion.
In the spinal cord, a marked increase in CTB labelling was seen in laminae I, II, and the dorsal part of Lamina III.
High concentrations of Glu-R1 distinguished laminae II: substantia gelatinosa and the outer region of Lamina III.
By combining reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry for NO-producing neurons with immunogold labeling for substance P, CGRP, and glutamate, we show that (1) NO-producing neurons in Lamina III are islet cells; (2) these neurons rarely form synapses onto peptide-immunoreactive profiles; and (3) NADPH diaphorase-positive dendrites are often in close spatial relationship with peptide-containing terminals and are observed at the periphery of type II glomeruli showing glutamate-immunoreactive central endings. These results provide compelling evidence that glutamate released at type II glomeruli triggers the production of NO in islet cells within Lamina III after NMDA receptor activation.
Cholinergic neurones in Lamina III (which are also GABAergic) invariably showed each type of GluR-immunoreactivity.
Immunoreactivity for mGluR1 alpha was detected in laminae I-III of the dorsal horn, whilst mGluR2/3 immunoreactivity was detected primarily in Lamina III.
Primary afferents of the sciatic nerve have their cell bodies located predominantly in the L4 and L5 dorsal root ganglia (DRGs), and the A-fibres of each DRG have central termination fields that show an extensive rostrocaudal overlap in Lamina III in the L4 and L5 spinal segments. In this study, we have found that C-fibres from either DRG have central terminal fields that overlap much less in lamina II than A-fibres in Lamina III.
A model of Lamina III-IV dorsal horn cell receptive fields (RFs) has been developed to visualize the spatial patterns of cells activated by light touch stimuli.
Following this study, the responses of single Lamina III-V dorsal horn neurons to an innocuous A beta fibre brush stimulus and a noxious C fibre (mustard oil) stimulus were extracellularly recorded and the effect of ionophoretically applied drugs was examined.
These Ret-expressing small neurons are selectively labeled by the lectin IB4 and project to Lamina III of the dorsal horn.
The presumed nociceptive neuronal profiles in close apposition to axon terminals with 5-HT-LI were mainly those of laminae I and II neurons as well as dendrites of Lamina III neurons.
The density of contacts from substance P-immunoreactive varicosities onto these cells was significantly higher than that seen on cholinergic neurons in Lamina III (which do not possess the receptor).
Medial cutaneous afferents terminate predominantly in Lamina III, but a few terminate in the medial region of the intermediate zone. In particular, interneurons in lamina II are born after those in Lamina III, paralleling the early and late termination of cutaneous afferents in these laminae.
MOR1 immunoreactivity was seen on many small neurons in lamina II and a few in the dorsal part of Lamina III. Although immunostaining was mainly restricted to the cell bodies and dendrites of these neurons, in some cases it was possible to see their axons, and a few of these entered Lamina III.
mu-Receptors are located in Lamina III followed by I and II in cingulate, frontal, insular and parietal cortices and lamina IV in temporal and occiptotemporal cortices.
In addition, we observed TUNEL of Lamina III neurons in a subset of older subjects who had normal cognition but abundant neocortical senile plaques.
Two non-pyramidal noxious-tap neurons were located in lamina V and 1 pyramidal noxious-tap neuron was located in lamina VI, and 2 pyramidal NS neurons were in Lamina III.
By P11, a few additional, faintly labeled, Zif268-positive neurons appeared in Lamina III Around P16, however, many immunoreactive neurons were found in laminae I-III and a few in laminae IV-VII.
In all species, the linear arrangements of perikarya in Lamina III, and to a lesser extent, in lamina V, closely resemble that of the early fetal template, whereas perikaryal arrangements in layers II and IV diverge from the template formation.
beta 2/beta 3-subunit immunoreactivity was the most intense in inner lamina II, Lamina III, and lamina X, and it was the least intense in lamina IX.
These neurons were distributed mainly in lamina I, and additionally in Lamina III..
GABA-IR elements were also observed in the Lamina III.
In contrast, the central projections of TrkA-negative neurons, as visualized by BSI-B4 staining, were particularly dense in Lamina III.
A moderate density (1.8-3.0 fmol/mg tissue) of specific binding was observed in Lamina III, whereas in other areas, i.e.
The strongest c-FOS expression was observed within the inner layer of lamina II near its border with Lamina III.
Most of the cells observed in Lamina III were small and had relatively restricted dendritic trees which could often not be followed into lamina II, however some larger cells in laminae III and IV had dendrites which extended through lamina II and into lamina I.
Seven interneurons responding to innocuous mechanical stimuli were intracellularly recorded in Lamina III/IV of an isolated preparation of hamster spinal cord with partially intact innervation from an excised patch of hairy skin. We conclude that Lamina III/IV interneurons make axodendritic synapses predominantly with distal dendrites.
In neocortical areas Lamina III pyramidal neurons were more heavily labelled than those in lamina V. 5-HT2A receptor mRNA was present in all neocortical areas examined, where it was located in pyramidal neurons, of lamina V more than in those of Lamina III, as well as in putative interneurons, especially within lamina IVc of the striate cortex.
All of the 68 galanin-immunoreactive neurons tested were GABA-immunoreactive, while only one of them (in Lamina III) was glycine-immunoreactive.
In Alzheimer's disease brains, more than 90% of pyramidal neurons in lamina V and 70% in Lamina III displayed 2- to 5-fold elevated levels of cathepsin D (Cat D) mRNA by in situ hybridization compared with neurologically normal controls.
In the ipsilateral Lamina III, the number of neuropeptide Y-positive nerve terminals markedly increased after axotomy, with a moderate increase in lamina IV.
An increased number of galanin-positive nerve terminals was observed in Lamina III of the ipsilateral dorsal horn after axotomy.
In all three areas examined (laminae I and II, Lamina III and lamina IX) the majority of profiles which were presynaptic at gephyrin-immunoreactive synapses were enriched with glycine-like immunoreactivity. It was estimated that at least 83% of profiles presynaptic to gephyrin-immunoreactive synapses in the superficial dorsal horn (laminae I and II) were glycine-immunoreactive, while for Lamina III and the ventral horn (lamina IX) the proportions were at least 91% and 98% respectively. Many of the boutons which were presynaptic at axoaxonic synapses in the ventral part of lamina II and in Lamina III were glycine- and GABA-immunoreactive and in many cases the postsynaptic element was the central axon of a type II synaptic glomerulus.
PVi clearly delineated the primary auditory cortex (AI), which was characterized by two PV+ bands: dense terminal-like labeling within Lamina III/IV and PV+ somata in lamina VIa. PV+ nonpyramidal cells in lamina IV and Lamina III were predominantly large basket-type cells with bitufted dendritic domains and tangentially oriented local axonal plexuses. The terminal-like label within Lamina III/IV derived in part from the basket-cell axons, which formed pericellular arrays around unstained somata.
Mechanical stimulation produced delayed activation in laminae III-IV, V and VII at 30 min, 60 min and 2 h, respectively, and thermal stimulation in Lamina III at 50 min.
At 68 days of gestation (term = 146 days), the earliest fetal tissue examined, there was no evidence of binding sites in lamina I or the outer regions of lamina II (lamina IIo), although there was a sparse distribution of binding sites in the inner region of lamina II (Lamina III).
Thalamic afferents originating in the ventral division of the medial geniculate body (vMGB) terminate in patches within Lamina III/IV of the primary auditory cortex in adult rabbits.
Three area 3a TPNs were identified in lamina II, eight in Lamina III, seven in lamina V, and one in lamina VI. Five 3b TPNs were identified in lamina II, 19 in Lamina III, 7 in lamina IV, 7 in lamina V, and 1 in lamina VI. Thalamic and tooth pulp latencies of Lamina III and IV TPNs were shorter than those of lamina II and V TPNs. Lamina III TPNs were classified according to their morphological characteristics as pyramidal or nonpyramidal stellate TPNs. Pyramidal Lamina III TPNs had typical pyramidal somata, like those of lamina V pyramidal cells. Lamina III area 3b TPNs had morphological properties similar to those in area 3a.(ABSTRACT TRUNCATED AT 400 WORDS).
Most frequently, neuropeptide Y-positive boutons formed axodendritic and axosomatic synaptic junctions (range = 64% of synapses in laminae V/VI to 83% in Lamina III).
Walking on the rotating rod induced a large increase in the number of Fos-like immunoreactive neurons in regions of the cervical and lumbar spinal cord gray matter that contain neurons that respond to non-noxious stimuli: the inner part of the substantia gelatinosa (Lamina III), the nucleus proprius and the medial parts of laminae V and VI.
Previous studies have shown that the B subunit of the lectin Griffonia simplicifolia (GSA I-B4) binds selectively to a subset of small neurons in the trigeminal ganglion and to a subset of C fibers preferentially distributed to inner lamina II and outer Lamina III of nucleus caudalis in the brainstem trigeminal complex in the rat.
Double-labeled neurons were few in Lamina III after thermal stimulation and entirely lacking in Lamina III after the two kinds of stimulation.
The statistical data showed no change in synaptic density between control and Alzheimer subjects, in either Lamina III or V of the cortex.
Single injections of either tracer into the vMGB labeled multiple "patches" of afferent axons in Lamina III/IV of the ipsilateral auditory cortex.
In the dorsal horn these groups were (1) large neurons in the lateral dorsal horn (laminae I and IV), (2) small neurons in the lateral dorsal horn (lamina II), and (3) small neurons in the medial dorsal horn (Lamina III).
Neuronal somatostatin-binding sites are visualized on neurons in Lamina III and, in particular, in lamina V/VI of the primary somatosensory cortex and in the magnocellular nucleus of the telencephalic cholinergic system.
Four months after injection of the pronase, the area of label determined by measurement of the width of the saphenous territory in Lamina III was expanded by 24% on the pronase side.
Huge numbers of strongly labelled cells formed a dense collection in lamina II and superficial parts of Lamina III. Many neurons in lamina II and superficial parts of Lamina III expressed GluR1 moderately.
The simple and complex arbors, which are both bouton-containing, were distributed mainly in laminae III-V, although some complex arbors projected dorsally into Lamina III.
Ultrastructural examination of the tissue revealed a highly significant AD-related decline in synaptic numbers in Lamina III and V in both the superior and the middle temporal gyrus.
One hundred six somatostatin-immunoreactive neurones located in lamina II and the dorsal half of Lamina III were tested with antiserum or monoclonal antibody to GABA and none of these cells showed GABA-like immunoreactivity. However, 8 out of 13 somatostatin-immunoreactive neurones located deeper in the dorsal horn (ventral Lamina III and lamina IV) showed glycine-like immunoreactivity, and 6 of these were also GABA-immunoreactive.
However, a transient TRH-like immunoreactivity was detected in Lamina III of the dorsal horn between post-natal days 14 and 30: at ultrastructural level, immunoreactive varicosities were seen to establish axodendritic synapses.
Sparse labeling was present in trigeminal nucleus caudalis (Lamina III-V) and trigeminal nucleus interpolaris; few or no labeled cells were detected in other parts of the trigeminal nuclear complex, thalamus, cerebral cortex, cerebellar cortex or trigeminal ganglion.
These observations indicate that the medial part of the LCN receives input from lamina I neurons, and probably from Lamina III-V neurons as well, at cervical and lumbar spinal levels.
Our interpretation is that there may be an extension of fine primary afferent fibers into Lamina III and possibly lamina IV following peripheral axotomy.
The dorsal horn (DH) of chickens exhibits a novel pattern of cytoarchitectonic lamination among vertebrates, whereby Lamina III lies medial, rather than ventral, to lamina II. Indeed, cutaneous nerves labeled with horseradish peroxidase (HRP) form two separate projections across the mediolateral axis of the superficial DH; each projection is somatotopically organized, such that two non-overlapping somatotopic maps are formed: the medial map within Lamina III and the lateral map within lamina II.
In order to determine whether different morphological types of neurone in Lamina III of rat spinal dorsal horn contain different neurotransmitters, a combined Golgi and immunocytochemical study was performed. These cells had dendrites which were oriented along the rostrocaudal axis and occupied Lamina III, with some extension into lamina IV and the ventral half of lamina II. These results indicate that there is a relationship between morphology and function for neurones in Lamina III.
In the cerebral cortex, mercury was present in neurons populating Lamina III in the isocortex.
By means of a computerized method, quantitative data characterizing the human Lamina III pyramidal neuron at the end of gestation are provided..
In Golgi-Cox impregnated parietal cortex (regio postcentralis) of two children (20 months of age or 6 years of age) with Down's syndrome the pyramidal neurons of Lamina III and V were investigated qualitatively and quantitatively. The comparison of quantitative parameters suggests the pyramidal cells of the older child show more degenerative changes, concerning especially Lamina III pyramids but in lamina V pyramids as well.
Moderately to strongly stained neurons were found in the dorsal horn, in particular in Lamina III, as well as around the central canal.
56:43-62, '73) that Lamina III lies medial, rather than ventral, to lamina II in the chicken dorsal horn.
Furthermore, on the experimental side, the distribution of both SBA and RL-29 reactivity was increased, extending into Lamina III.
Moreover, Lamina III neurons in the monkey are more complex than monkey lamina V neurons.
Then, after 4 months, we observed a regrowth of serotonergic axons giving rise to an immunoreactive pattern close to that of intact animals, except in Lamina III which was spanned by growing fibres.
Additionally, cells in Lamina III at the cervical and lumbar enlargements contain preproCCK mRNA, suggesting that cells expressing CCK may be important in the processing of sensory information from the appendages..
The five types of labelled terminal arbors occurring in Lamina III (Cruz et al., '87: J. These features, together with the location in dorsal Lamina III, suggest their belonging to the fluoride resistant acid phosphatase (FRAP)-reactive population. The occurrence of the swarm, undulating, and lateral plexuses in ventral Lamina III, which seems to lack FRAP or peptidergic terminals, suggests an origin from other, still unidentified neurochemical populations of fine primary afferents..
This was followed by staining in neurons of Lamina III in the isocortex and ultimately all layers were stained after 28 days of treatment.
Pre-embedding immunohistochemistry with monoclonal antibody to choline acetyltransferase was combined with post-embedding immunohistochemistry with antisera to GABA and glycine in order to study the pattern of coexistence of GABA, glycine and acetylcholine in neurons in Lamina III of rat spinal dorsal horn. Of 50 neurons which were choline acetyltransferase immunoreactive, 47 showed GABA-like immunoreactivity and none were immunoreactive with antiserum to glycine, despite the fact that glycine is thought to be present in the majority of GABAergic neurons in Lamina III. This suggests that while acetylcholine and glycine can both coexist with GABA in Lamina III neurons, they are present in different populations of GABAergic cells.
The projections to lamina IV were organized in a similar manner as in Lamina III, even though the projections showed a higher degree of overlap than in Lamina III.
Most of the PV-positive cells were found in the inner layer of lamina II, Lamina III, internal basilar nucleus, central gray region, and at the dorsomedial and ventromedial aspects of the lateral motor column in the ventral horn.
Immunoreactivity was present in cell bodies in Lamina III, and in dendrites and axons of all three laminae. Immunoreactive axonal varicosities were often presynaptic to the central varicosities of type II synaptic glomeruli in lamina II and Lamina III, less often presynaptic to the central elements of type I glomeruli in lamina II, and often presynaptic to dendrites in both type I and type II glomeruli.
Ultrastructural studies of biopsied cortical tissue from the right frontal lobe of 8 patients with mild to moderate Alzheimer's disease (AD) revealed that the number of synapses in Lamina III of Brodmann's area 9 was significantly decreased when compared with the number in age-matched control brains (n = 9; postmortem time, less than 13 hours).
Because the final common pathway for neurotransmission involves synaptic integrity, we quantitatively assessed synaptic number and synapse size in Lamina III and V of human frontal cortex (Brodmann area 9) in patients with AD and age-matched controls. We found a significant decrease in synaptic number per unit volume in both lamina, more marked in Lamina III (-42%) than V (-29%). This appeared to be a compensatory response, rather than a selective loss of small synapses, since the total amount of synaptic contact area per unit volume did not decline in lamina V (despite a 29% loss of synapses); in Lamina III it was reduced 11% despite a 42% loss of synapses.
Within the area striata the Lamina III-pyramid neurons are more invariable than the lamina V-pyramid neurons.
the "flame-shaped arbors" of hair follicle afferents in Lamina III of the dorsal horn, or the projection of nociceptive afferents onto lamina I.
Immunoreactive axons, dendrites and cell bodies were observed in all three laminae, but were most common in Lamina III.
The glial fibrillary acidic protein stain displayed extensive laminar gliosis mainly of the layers I, IIa, IV and VI; layers III and V, largely occupied by the AT, remained conspicuously spared from gliosis (especially the Lamina III).
Sparse labeling was noted in Lamina III and in the nucleus proprius (laminae III and IV), generally considered to be nonnociceptive areas of the cord.
Positive somata had long rostrocaudally oriented dendrites confined to narrow sagittally arranged sheets within this band and axons that entered lamina II or the superficial portions of Lamina III.
In order to determine how information conveyed by fine primary afferent fibres might reach the deeper laminae of the spinal dorsal horn, 5 Golgi-stained neurones with somata in Lamina III or IV and dendrites that entered lamina II were examined by electron microscopy. In addition, all 3 cells were postsynaptic to degenerating axons within Lamina III.
The cholinoceptive properties of dorsal horn neurons (Lamina III-V) were investigated by means of intracellular recordings from the rat isolated spinal cord slice preparation.
Dense patches of anterograde labeling were located within the centers of the layer IV barrels and extended superficially through Lamina III; the septa between barrels contained considerably less reaction product.
Substance P injections into the magnocellular layers (Lamina III-IV) or deep magnocellular layers (lamina V-VI) had no significant effects.
In Lamina III the enzyme was associated with small and medium-sized cells.
Within lamina II the receptors were especially concentrated in the deeper inner segment (IIi) where they formed a dense band lying immediately dorsal to Lamina III. The density of receptors in this inner region of lamina II (23.5 fmol/mg) was almost double that in the outer segment of lamina II (12.2 fmol/mg), which showed the next highest density of receptors, and more than three times that in the adjacent lamina I (6.9 fmol/mg) and Lamina III (7.1 fmol/mg).
With the exception of one high-threshold mechanosensitive unit none of the stained fibres possessed terminal arborization and boutons in Lamina III.
UEA-I binding displayed a similar distribution pattern in both Vc and Vi, but extended into Lamina III and the superficial part of Lamina III in Vc.
The cells of origin of both the ipsilateral and contralateral corticostriate projections lie mainly in lamina V (especially lamina Va) with very small numbers in Lamina III of the neocortex and mesocortex, and in the deep laminae of the allocortex.
The present study provides detailed anatomical evidence that the strongly texture-sensitive complex neurones of the cat's striate cortex constitute a discrete subset of all complex neurones, and lie in two bands, deep in Lamina III and in lamina V.
We have studied the postnatal development of Lamina III/IV spine-free nonpyramidal neurons in the auditory cortex of the New Zealand white rabbit.
Lamina III pyramidal neurons had extensive short and long axon collaterals which contributed synaptic boutons to all laminae of the cortex. Stimulation of the ventrolateral nucleus of the thalamus resulted in epsps in pyramidal neurons of Lamina III, V, and VI at latencies between 1.0 and 5.0 msec..
Throughout brain development, NK-1 receptor sites are present in low densities with some enrichment seen in Lamina III while NK-3 binding sites are concentrated in layers IV and V.
Almost all neurones that were penetrated satisfactorily and labelled successfully were found to be pyramidal neurones located in Lamina III or lamina V. Pyramidal neurones located in Lamina III and lamina V (including PTNs) were excited at short latency by stimulation of the premotor cortex (1.1-4.0 ms) and somatosensory cortex (1.1-6.5 ms). There were no statistical differences in the distributions of latencies of corticocortical EPSPs between those evoked in Lamina III neurones and those recorded in lamina V neurones, or between corticocortical EPSPs evoked from the premotor cortex in comparison with those from the somatosensory cortex.
Numerous lateral and oblique dendrites branched from the apical dendrites in lamina V and near its border with Lamina III: short basal dendrites arborized in the vicinity of the soma in lamina V. Four pyramidal neurones in Lamina III were stained well. The number and arborization of intracortical collaterals from the axon of Lamina III cells varied widely; from three to twelve collaterals arose from the axon. The biggest arbor of collateral branches involved all the cortical laminae and was about 3 mm wide mediolaterally, while the smallest arbor was restricted mainly to Lamina III in the vicinity of the soma.
Injections into the magnocellular layers (Lamina III-IV) had no significant effect on secretion of catecholamines.
Using the Golgi silver impregnation technique the present study examines the morphology and development of presumptive local circuit neurons in Lamina III of the rat lumbar spinal cord. These neurons generate local axonal plexuses which remain within the gray matter and dendritic trees which arborize in Lamina III and the inner zone of lamina II.
Type I collaterals divide into well defined medial and lateral collateral branches which arborize mainly in Lamina III with a few branches to lamina IV.
The dendritic systems of Lamina III/IV spine-free nonpyramidal cells in the auditory cortex contralateral to the deafened ear were digitized from 340-micron-thick coronal sections with the aid of a computer microscope.
The dendritic system of Lamina III/IV pyramidal neurons contralateral to the deafened ear was digitized from frontal sections using a computer microscope system.
In pyramidal neurons of Lamina III or V of the anterior cingulate cortex several neuronal parameters were estimated in a single dendritic field (EDF) indicative for the development of the dendritic tree and spine distribution of these neurons. Likewise, in the Lamina III pyramidal neurons of experimental animals, the apical dendritic tree was shortened by 25-30%, the basal dendritic tree by 10% at the end of the undernutrition period. The differences in the recovery pattern of both neuron types are explained by the hypothesis that the Lamina III pyramidal neurons are phylogenetically younger and, therefore, have a considerably longer postnatal differentiation phase.
To get some morphological data, we investigated Golgi impregnated pyramidal neurons in Lamina III of regio precentralis agranularis of the major cortex from adult rats.
One neuron with its soma located in Lamina III received additional contacts from central elements of glomerular complexes.
The density of glycine-labeled neurons in lamina IV, however, was significantly less than the number observed in Lamina III even though Lamina III was farther away from the injection site which was at the boundary between laminae V-VI.
Terminal fields in caudal pars caudalis and in the spinal cord dorsal horn were concentrated largely in the outer half of lamina II, with lesser accumulations in lamina I, the deeper half of lamina II, and in Lamina III.
Besides the flame-shaped arbors located in deep Lamina III as an extension of the arbors of Lamina III, which were derived from 1.7-micron thick stem fibers (probably A alpha beta fibers), six types of terminal arbors, all rostrocaudally oriented, arising from fine stem fibers and having preferential locations, were disclosed. Fibers ending in terminal bouquets and issuing from 1-micron thick stem fibers (C or A delta) occupied the dorsal part of middle and medial Lamina III, while the intermediate part contained clusters (swarms) of ultrafine boutons arising from extremely fine fibers. The whole medial Lamina III also contained fine undulating fibers arising from 0.3 micron-thick stem fibers (C fibers) with large boutons near their ends.
While there are similarities between the morphology of the central terminals of cutaneous low-threshold mechanoreceptors in the rat and those previously described in the cat (for example, the longitudinally continuous arrangement of the mediolaterally restricted flame-shaped HFA arborizations and the discontinuous RA arborizations arising from a dorsally located axon), there are also some major differences: the large number of HFA arbors extending to Lamina III and to lamina IV rather than being restricted to Lamina III, the deeper location of the RA arbors (in laminae IV and V rather than Lamina III),(ABSTRACT TRUNCATED AT 400 WORDS).
In the present intracellular staining study of this class of neuron we retrieved one cell with its soma in lamina I which arborized in laminae I through III and another cell with a soma in Lamina III and a dendritic arbor which extended from lamina I through V.
The highest density of opiate receptors was localized within the inner segment of lamina II where the receptors formed a very dense band lying immediately dorsal to Lamina III. The density of receptors in this inner region of lamina II (33 +/- 2 fmol/mg) was more than two-and-one-half times greater than that in the remaining upper laminae which showed moderate receptor densities: lamina I (12 +/- 4 fmol/mg) and outer lamina II (13 +/- 3 fmol/mg) both showed similar receptor densities which were higher than those in Lamina III (10 +/- 3 fmol/mg) The tract of Lissauer (11 +/- 2 fmol/mg) also showed a moderate density of opiate receptors which was intermediate between the densities in laminae I/IIo and the density of Lamina III.
In particular, a conspicuous band-shaped region of axon terminals was observed in laminae II and III, while the cell bodies were most frequent in Lamina III.
The axons of many of these cells either remained in Lamina II or passed ventrally into Lamina III.
Lamina III nearly doubled in thickness while lamina IIo decreased markedly. The FRAP-band was large on days P2 and P5 virtually covering Lamina III, then shrank to a thinner strip in its dorsal part. It is suggested that Lamina III growth is due to the massive arrival of FRAP-reactive thin primary axons followed by large afferents from deep layers occurring during the postnatal period, and the subsequent establishment of synaptic connections with the developing dendritic trees of dorsal horn cells..
There were no traces of serotonin fibers in Lamina III in the stages examined up to posthatching day 5.
Prominent immunocytochemical staining for TRH in the dorsal horn was seen in varicose fibers mainly in lamina II and superficial Lamina III of the dorsal horn of the spinal cord of control rats.
Reactive CI-terminals are heterogeneously distributed across the dorsoventral thickness of lamina II, with maximal frequency in the zone heavily stained for FRAP in light micrographs, which roughly corresponds to the dorsalmost portion of Lamina III.
This longitudinally oriented column of terminal and en passant boutons angled from lamina V rostrally to Lamina III caudally.
Within this lamina the receptors were concentrated mainly in its deeper, inner portion which lies immediately adjacent to Lamina III, with some overlap dorsally into the outer segment of lamina II and ventrally into the adjacent region of Lamina III.
The dendritic arbor is moderately extended dorsoventrally in type IIA cells and reaches Lamina III in the larger type IIB cells.
In comparison to the normal control group, the cases with Alzheimer's disease and senile dementia show a significant decrease in the gray level index of Lamina III..
Cholinergic fibers were most prominent in Lamina III of the dorsal horn and originated from cholinergic neurons within the spinal cord.
Based on the staining pattern with an antiserum to the octapeptide-metenkephalin-arg-gly-leu, we suggest that the dense enkephalin terminal immunoreactivity in the inner part of the substantia gelatinosa derives from cells in Lamina III.
The collaterals of large, myelinated primary afferents formed terminal arbors in the outer part of the spinal trigeminal nucleus when they were rostral to or near the obex (rostral-type collaterals), in lamina V when in the rostral part of Vc (caudalis-type collaterals), and in Lamina III/IV when in the caudal part of Vc (spinal dorsal horn-type collaterals). The collaterals of D-hair afferents showed the same types of collaterals as were seen in the large, myelinated primary afferents, except that terminal arbors of the spinal dorsal horn-type collaterals were distributed in lamina IIb in addition to Lamina III/IV.
The majority of normal CAT activity resided in lamina I, II, and upper Lamina III; CAT loss in AD resulted in large losses from all depths, most notably the upper cortical layers.
Golgi-impregnated neurons in Lamina III of the cat spinal cord were examined using light microscopy and combined light and electron microscopy.
In the rostral part of the subnucleus caudalis (Vc) they were confined to lamina V (caudalis type collaterals) and in the caudal part of Vc and in cervical segments they were confined to Lamina III/IV (spinal-dorsal-horn-type collaterals). The terminal arbors of the rostral type of collaterals formed an interrupted, rostrocaudally oriented column like those seen in the lumbar dorsal horn, but the column shifted down to lamina V near the obex, and more caudally, gradually shifted upward to Lamina III.
The next VEP component, a surface negative potential at 95 msec, is coincident with current sources and sinks in Lamina III, and is consistent with stellate cell input to supragranular elements.
In addition, it was found that Lamina III consists of two adjacent bands (IIIa and IIIb) of contralateral retinal input, separated by a terminal-free zone 20-40 micron wide. Neurons in each lamina of the nucleus have dendritic arbors which ramify extensively within adjacent laminae, except cells in Lamina IIIb, which have relatively few dendrites that cross into the cell-free zone and lamina IV..
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