Pre- and postsynaptic proteins of Brodmann's area 9 from patients with Alzheimer's disease (AD) and age-matched controls were quantified by immunohistochemical methods and Western blots. 
A mass spectrometry based high throughput approach was employed to profile white and gray matter lipid levels in the prefrontal cortex (Brodmann area 9) of 45 subjects including 15 schizophrenia and 15 bipolar disorder patients as well as 15 controls samples.
Protein and mRNA expression of BDNF and of TrkB receptors were determined in the prefrontal cortex (PFC), Brodmann's area 9 (BA 9), and hippocampus obtained from 29 teenage suicide victims and 25 matched normal control subjects.
While multiple areas of frontal cortex co-activated with amygdala sub-regions, a specific region of dorsomedial prefrontal cortex (dmPFC, Brodmann's area 9/32) was the only area co-activated with both PAG and Hy.
Group analysis found that various brain areas of patients with congenital scoliosis showed glucose hypometabolisms in the left prefrontal cortex (Brodmann area 10), right orbitofrontal cortex (Brodmann area 11), left dorsolateral prefrontal cortex (Brodmann area 9), left anterior cingulate gyrus (Brodmann area 24) and pulvinar of the left thalamus.
We found the two receptors colocalized and quantified the overlap of their distribution in spines and axon terminals of prefrontal cortical area 9 in the Macaca mulatta monkey. These results indicate that dopamine activation of the two D1R subtypes does not modulate disparate populations of synapses onto dendritic spines in prefrontal cortical area 9; rather, dopamine can activate D1 and D5 receptors on the same spines, plus an additional group of spines that contains only D1.
In the present study we used immunohistochemistry against two specific neuronal markers (NeuN and MAP2) in order to establish the presence of these cell types in Brodmann area 9 (BA 9) of the human prefrontal cortex.
Converging data from the 2 methods demonstrate that the left posterior LPFC is critical for the higher levels of cognitive control and is organized into functionally different subregions (Brodman's area 9/46, 6/8/9, and 44/45).
Alterations in MAP2 staining in area 9 and 32 of schizophrenic prefrontal cortex. We found a significant reduction in the density of immunopositive pyramidal cells in area 9 (11%) layer III, (20%) layer V, area 32 (16%) layer III and (17%) layer V with no difference in immunopositive interneurons.
Comparing this condition with a passage-reading condition without prediction, we found out that the left anterior prefrontal cortex (aPFC) in Brodmann area 9/10 and the left anterior ventral inferior frontal gyrus (vIFG) in Brodmann area 47 elicited increased hemodynamic responses.
We examined the postmortem prefrontal cortical region (Brodmann's area 9) of patients with SCZ and BPD, and of age-matched control subjects, excluding suicide cases.
To address these issues, we used discrete microdissections of postmortem dorsolateral prefrontal cortex (DLPFC) (area 9) and an oligonucleotide (60mer) microarray hybridization procedure that increases sensitivity without RNA amplification.
area 9 of the dorsolateral prefrontal cortex is involved in inductive reasoning and specific components of working memory processes, while area 32 of the medial prefrontal cortex has been implicated in theory of mind.
Furthermore, RGS2 immunoreactivity significantly increased in the amygdala and the prefrontal cortex (Brodmann area 9 (BA9)) of the postmortem brain of the suicide subjects.
The work presented here demonstrates the first normative proteomic comparison of the soluble fractions of adjacent grey and white matter of a single brain area with a specific cytoarchitecture, Brodmann area 9 (BA9; part of the dorsolateral prefrontal region).
METHOD: We estimated the number of oligodendroglial satellites of pyramidal neurons and the size of pyramidal neurons in layer III (Brodmann's area 9) in Nissl stained sections in SCH, BPD, MDD and normal controls.
We quantified VGLUT1 and VGLUT2 in the prefrontal dorsolateral cortex (Brodmann area 9) of controls and AD patients using specific antiserums.
The network that was specifically activated by the nonliteral condition involved the left temporal cortex, the left superior medial frontal gyrus (Brodmann area 9), and the left inferior frontal gyrus (IFG).
For comparison, we also investigated the maturation of prefrontal area 9, which has few or no connections with visual areas.
Error detection invoked by failed inhibition activated dorsal anterior cingulate cortex (dACC) and right middle frontal Brodmann's area 9.
prefrontal cortex (Brodmann's area 9) levels of the methyl donor S-adenosyl methionine were increased by about two-fold in schizophrenia and bipolar disorder patients, but not in unipolar depressed patients compared with nonpsychiatric subjects from the Stanley Foundation Neuropathology Consortium (Bethesda, Maryland, USA). In schizophrenia and bipolar disorder patients, the increase of S-adenosyl methionine is associated with an overexpression of DNA methyltransferase-1 mRNA in Brodmann's area 9 GABAergic neurons.
Samples of post-mortem brain tissue from Brodmann area 9 were obtained from prefrontal cortex from subjects with schizophrenia, bipolar affective disorder, major depression, and from controls.
Patients exposed to HSV1 had decreased gray matter in Brodmann area 9 (dorsolateral prefrontal cortex) and 32 (anterior cingulate cortex) compared with patients without serological evidence of exposure to HSV1.
Changes in Brodmann area 9 were relatively consistently identified in resting, cognitive activation and treatment studies included in the meta-analysis.
In family-positive but not family-negative subjects, striatal D(2) receptors were associated with metabolism in anterior cingulate (Brodmann area 24/25) and orbitofrontal (Brodmann area 11) and prefrontal (Brodmann area 9/10) cortices, and with personality scores of positive emotionality.
There was a significant decrease in the binding of [ 3H]SB 269970 to the serotonin7 receptor in Brodmann's area 9 from subjects with schizophrenia compared to controls (Mean+/-S.E.M.: 8.3+/-0.76 vs. There were no significant differences in [ 3H]sumatriptan binding to the serotonin1D or serotonin1F receptor in Brodmann's area 9 from subjects with schizophrenia. These data would be consistent with the hypothesis that decreased levels of serotonin7 receptors in Brodmann's area 9 may be involved in the pathological processes of schizophrenia and that levels of cortical serotonin7 and 1D receptors can be affected by antipsychotic drug treatment..
Fibers from area 9/46d course via SLF I to the superior parietal lobule and medial parieto-occipital region, via SLF II to the IPL. Fibers from area 9/46v travel via SLF III to the rostral IPL and the frontoparietal opercular region and via the CING F to the cingulate gyrus..
We compared GS with GFAP immunoautoradiography in dorsolateral (area 9) and orbitofrontal (area 11/47) cortex. Optical density measures from film autoradiographs revealed an increase in GFAP immunoreactivity in area 9 in schizophrenia and a decrease in area 11/47 in both schizophrenia and bipolar disorder. The increase in GFAP in area 9 significantly correlated with lifetime antipsychotic drug treatment, whereas the reduction in area 11/47 occurred despite this effect.
Alterations in MAP2 staining in area 9 and 32 of schizophrenic prefrontal cortex. Neurogranin immunostaining was dramatically reduced in both layers III (72%) and V (50%) in area 9.
OBJECTIVE: In order to identify whether the mechanisms associated with neurotransmitter release are involved in the pathologies of bipolar disorder and schizophrenia, levels of presynaptic [ synaptosomal-associated protein-25 (SNAP-25), syntaxin, synaptophysin, vesicle-associated membrane protein, dynamin I] and structural (neuronal cell adhesion molecule and alpha-synuclein) neuronal markers were measured in Brodmann's area 9 obtained postmortem from eight subjects with bipolar I disorder (BPDI), 20 with schizophrenia and 20 controls.
The theta power in area 9 (the medial prefrontal cortex) and area 32 (the rostral ACC) was gradually increased from a few seconds before the movement and reached a peak immediately after the movement.
Four brain regions were analyzed: caudate nucleus, cerebellum, prefrontal association cortex [ Brodmann's area 9 (BA9)] and motor cortex [ Brodmann's area 4 (BA4)].
BACKGROUND: Although the somal volume of Nissl-stained deep layer 3 pyramidal cells is reduced in prefrontal cortex area 9 of subjects with schizophrenia, the subset of large pyramidal cells immunoreactive (IR) for nonphosphorylated neurofilament protein (NNFP) is not. METHODS: We labeled Necab-1-IR pyramidal neurons using immunoperoxidase techniques and estimated the mean somal volume in deep layer 3 of area 9 in 13 matched pairs of control and schizophrenic subjects.
The rostromedial prefrontal (area 9) and frontopolar (area 10) regions have very few extrastriate projections.
In order to determine whether the mRNA expression levels of Cdc42, Rac1, RhoA, Duo or drebrin are altered in schizophrenia, tissue sections containing DLPFC area 9 from 15 matched pairs of subjects with schizophrenia and control subjects were processed for in situ hybridization.
METHOD: Neuronal density, size and shape were estimated in the prefrontal cortex (Brodmann area 9) of the left and right hemispheres of brains taken post-mortem from 10 people with schizophrenia and 10 without mental illness (6 men, 4 women in both groups).
Compared with control subjects, BP-I subjects exhibited blunted regional cerebral blood flow (rCBF) increases in the left dorsolateral prefrontal cortex (Brodmann's area 9/46) during encoding.
Poor outcome among patients with schizophrenia was associated with weaker correlations between left frontal area 9 and both medial and lateral temporal cortices, as compared to normal subjects or good-outcome patients.
Morphometric changes in the general population of Nissl-stained neurons in area 9 of the dorsolateral prefrontal cortex have been reported in major depressive disorder (MDD) and schizophrenia. To test whether deep layer III pyramidal neurons are differentially affected in MDD or schizophrenia, an antibody was used that labels both phosphorylated and non-phosphorylated forms of the 200 kD neurofilament protein (NF200) in pyramidal cells of layer III in area 9. The packing density and somal size of NF200-immunoreactive (IR) pyramidal neurons were measured in area 9 in 13 subjects with nonpsychotic MDD, 11 subjects with schizophrenia and 13 psychiatrically normal controls. These results indicate that this neuronal subpopulation does not contribute to the smaller average size of neuronal somata in layer III of prefrontal cortical area 9 in schizophrenia or MDD.
To assess this possibility further, we investigated capillary length densities in prefrontal cortex area 9 and anterior cingulate cortex area 24 in postmortem brains from 13 schizophrenics and 13 age- and sex-matched controls. Mean cortical thickness was significantly reduced in area 24, but not in area 9, in schizophrenics. There were no differences in mean capillary length densities in either area 9 or 24 between the two groups.
Neurophysiological and functional brain imaging studies suggest the importance of dorsolateral area 9/46 for modality-independent working memory. Here, we describe the dramatic derangement of pragmatic memory after circumscribed lesion of the right area 9/46. This case exemplifies that an isolated lesion of the right area 9/46 may induce severe failure to schedule actions and memory retrieval, a disorder leading to severely disorganised behaviour and disability..
Within the P1 time frame, sleep loss led to greater activation in the right Brodmann's area 9/10.
Trials with greater context processing demands corresponded to activity in the middle frontal gyrus (Brodmann's area 9) in the comparison subjects and in the patients with nonschizophrenia psychosis, but not in the schizophrenia patients.
BACKGROUND: Deoxyribonucleic acid microarray analyses of dorsolateral prefrontal cortex (DLPFC) area 9 from 10 matched pairs of schizophrenic and control subjects revealed a consistent and significant decrease (p = .001; mean log2 signal difference = -.58) in transcript expression for a gene clone KIAA0417.
Polymorphisms of the gene encoding the regulator of G-protein signaling subtype 4 (RGS4) may confer risk for schizophrenia.(1) DNA microarray studies of postmortem brain samples have shown RGS4 underexpression in the dorsolateral prefrontal cortex (DLPFC, area 9), motor and visual cortices in schizophrenia patients relative to control subjects.(2) Underexpression of RGS4 in DLPFC is pathophysiologically significant because DLPFC pathology in schizophrenia has been supported by neurocognitive,(3,4) structural(5) and functional(6,7) imaging, postmortem,(8) cellular(9,10) and molecular(11) pathological studies.
This study aimed to investigate the binding affinity of [ 3H]GABA and [ 3H]beta-alanine to GABA transporters GAT-1 and GAT-3 in the human dorsolateral prefrontal cortex (Brodmanns' area 9) in schizophrenia.
Samples from caudate, putamen, ventral striatum, and prefrontal cortex (Brodmann's area 9, BA9) were analyzed by semiquantitative immunoblotting for relative densities of dopamine receptors (D1, D2), transporter (DAT), monoamine terminals (vesicular monoamine transporter type 2), vesicular docking and release proteins (VAMP-2, synaptotagmin, SNAP-25, syntaxin, synaptophysin), and receptors inhibiting dopamine release (alpha 2-adrenergic receptors, alpha-2A).
Using optical dissector methodology, we have now conducted a morphometric study of numerical density (Nv) of oligodendroglial cells in layer VI and in adjacent white matter of Brodmann area 9 (BA 9) of the Stanley Foundation Neuropathology Consortium (SFNC).
In the dorsolateral prefrontal cortex Brodmann's area 9 (BA 9), MR mRNA was significantly lower (p<0.05) in all laminae (I-VI) in BP, and in laminae I, III, IV and VI in SZ than in the controls.
Using functional magnetic resonance imaging (fMRI), we found that relative to young adults, older adults showed reduced refresh-related activity in an area of dorsolateral prefrontal cortex (left middle frontal gyrus, Brodmann's area 9), but not in other refresh-related areas.
area 9 exhibited loss of projection neurons in layers III (16%), V (31%), and VI (37%); these same layers were also reduced in width (25%, 34%, and 46%, respectively). Glial density was increased in deeper layers, reaching significance in layer VI (68%) of area 9 and in layer V (75%) of area 46; glial number was not altered. Thus, area 46 exhibited marked cortical thinning without apparent neuronal degeneration, whereas in area 9 neuronal loss was pronounced, consistent with an advanced phase of cortical pathology.
The theta power in the prefrontal area 9 and the prelimbic area 32 was higher in the S1-S2 interval than in the pre-S1 period.
We then determined the density, size and shape of the three pyramidal neuron sub-populations in area 9 in patients with schizophrenia, bipolar disorder, or major depressive disorder, compared to controls (n=15 in each group).
METHODS: Boucher and Lewis's test of SSTM and MP was administered pre- and postsurgically to 8 patients of either sex, between 5 and 19 years of age, with tumors of the cerebellum, PF (area 9 medial) or the parieto-occipital region, and on one occasion to 8 corresponding controls.
METHODS: These studies were performed in prefrontal cortex in Brodmann area 9 and hippocampus obtained in 27 suicide subjects and 21 nonpsychiatric control subjects.
RESULTS: 5-HT(2A) receptor binding was significantly increased after estrogen replacement therapy in the right prefrontal cortex (right precentral gyrus [ Brodmann's area 9], inferior frontal gyrus [ Brodmann's area 47], medial frontal gyrus [ Brodmann's area 6, 10] and the anterior cingulate cortex [ Brodmann's area 32]).
Signal intensity for PV mRNA expression in PFC area 9 was significantly decreased in the subjects with schizophrenia, predominantly in layers III and IV.
A methodology has been optimised to measure the binding of [ 3H]RX 821002 to alpha(2)-adrenoreceptors in human postmortem CNS and has shown that these receptors are not altered in Brodmann's area 9 from subjects with schizophrenia.
We focused on prefrontal cortex area 9 in elderly control cases in comparison to cases with different degrees of cognitive dysfunction.
Brodmann area 9 of the prefrontal cortex, a part of the dorsal lateral prefrontal cortex (DLPFC), was less activated during performance of the WCST in poor trackers (relative to good trackers).
Consequently, in order to determine the cell class and laminar specificity of the dendritic targets of pyramidal neuron local axon collaterals in monkey PFC area 9, we conducted ultrastructural analyses of local axon terminals labeled with the anterograde tracer, biotinylated dextran amine, and dendrites immunoreactive (IR) for PV or CR.
Specimens of the prefrontal cortex (Brodmann's area 9) were collected from 19 suicide and non-suicide depressed subjects and 13 control subjects.
In the present study, we performed a stereologic analysis of the proportions of intracellular and extracellular (ghost) NFT, and unaffected neurons in the deep part of layer III (layer IIIc) and the superficial part of layer V (layer Va) of Brodmann's prefrontal cortex area 9.
Cell density was reexamined in dorsolateral prefrontal area 9 as an internal control. In contrast, neuronal density in area 9 exhibited a 12% increase in the schizophrenic cohort, replicating previous findings. In addition, there was a significant effect of disease on laminar neuronal density in area 9, with neuronal density tending to be higher (7%-29%) in all layers.
We found increased activity in the bilateral prefrontal cortex (area 9/46), bilateral intraparietal sulcus regions, right cerebellum, and bilateral early visual cortices during the tool combination task with the right hand, compared with the single tool task.
The decrease in density reached 22% (p < 0.01) in layer III of area 9 and 20% (p < 0.02) in the white matter of the superior frontal gyrus.
When we studied the cerebral uptake of acetylcarnitine by using [ 2-(11)C]acetyl-L-carnitine in 8 patients with CFS and in 8 normal age- and sex-matched controls, a significant decrease was found in several regions of the brains of the patient group, namely, in the prefrontal (Brodmann's area 9/46d) and temporal (BA21 and 41) cortices, anterior cingulate (BA24 and 33), and cerebellum.
The main effects in healthy subjects, an rCBF increase in subgenual cingulate Brodmann's area 25 and a decrease in right prefrontal cortex Brodmann's area 9, were not present in the depressed groups.
The calcium-binding proteins parvalbumin, calbindin, and calretinin can be used as markers for specific subpopulations of cortical GABAergic interneurons.METHODS: Following our previous observation of a reduction in the density of parvalbumin- but not calretinin-immunoreactive cells in the prefrontal cortex (Brodmann area 10) in schizophrenia, we have quantified the laminar density of neurons immunoreactive for the calcium-binding proteins parvalbumin, calbindin, and calretinin in a further prefrontal cortical region (Brodmann area 9) in patients with schizophrenia, bipolar disorder, major depression, and in matched control subjects (each group n = 15).RESULTS: Initial statistical analysis revealed reductions in the total cortical density of parvalbumin- and calbindin- but not calretinin-immunoreactive neurons in schizophrenia relative to control subjects.
We examined the glial-type specific pathology in SCHZ by analyzing the glial fibrillary acidic protein- (GFAP) immunoreactive astroglia in contrast to the Nissl-stained general pool of glial cells in dlPFC (area 9) from 9 subjects with SCHZ and 15 psychiatrically normal control subjects.
We used retrograde transneuronal transport of the McIntyre-B strain of herpes simplex virus type 1 to examine the extent and organization of basal-ganglia-thalamocortical projections to five regions of prefrontal cortex in the cebus monkey (Cebus apella): medial and lateral area 9 (9m and 9l), dorsal and ventral area 46 (46d and 46v) and lateral area 12 (12l).
This region occupies the dorsal part of the ventrolateral prefrontal convexity just below area 9/46v.
We analyzed the dendritic differentiation of layer IIIc pyramidal neurons of prefrontal cortex (prospective area 9) in the brains of a premature infant and a 2.5-month-old infant with Down syndrome and two age-matched control subjects during the peak period of dendritic growth and differentiation.
area 9 exhibited a 42% reduction in layer V and a 36% reduction in layer III.
Developmental changes of parvalbumin-immunoreactive puncta in area 9 were similar to those in area 46.
Compared to controls, bipolar patients had significantly lower levels of CaMKII alpha mRNA in laminae I-VI of Brodmann's area 9 and laminae I-III and VI of area 46. Unipolar patients also exhibited significantly lower levels of CaMKII alpha mRNA in laminae I-IV of area 9 than did controls.
To determine whether abnormal expression of genes encoding proteins involved in cellular metabolism contributes to this dysfunction, we used cDNA microarrays to perform gene expression profiling of all major metabolic pathways in postmortem samples of PFC area 9 from 10 subjects with schizophrenia and 10 matched control subjects.
In this investigation we have characterized neuronal and glia cytoarchitecture in prefrontal area 9 using spatial point pattern techniques and two-dimensional measures of cell size and density.
METHODS: The authors used a computerized imaging program to measure details of cell column morphologic features in area 9 of the prefrontal cortex and areas 21 and posterior 22 (Tpt) within the temporal lobe of nine brains of autistic patients and controls.
This was associated with recruitment of a network of cortical regions, including the right prefrontal cortex (Brodmann area 9).
The mid-dorsolateral prefrontal cortex (area 9/46) increased activity while subjects received either positive or negative feedback, that is at the point when the current information must be related to earlier events stored in working memory.
METHOD: The densities of parvalbumin-immunoreactive varicosities (putative axon terminals) were determined in the superficial and middle layers of prefrontal cortex area 9 from 20 matched pairs of subjects with schizophrenia and normal comparison subjects.
In 7 of 22 subjects, the Brodman area 9 of the DLPFC was targeted correctly in this manner.
RESULTS: Relative to those of comparison subjects, the mean levels of [ (3)H]pirenzepine binding were significantly lower in Brodmann's areas 9 and 46 of the schizophrenia patients not treated with benztropine mesylate (18% lower in Brodmann's area 9 and 21% lower in Brodmann's area 46) and in all four examined regions of the patients who had received benztropine (51%-64% lower).
METHODS: We used design-based stereology to estimate the somal volume of pyramidal neurons in deep layer 3 of PFC area 9 in 28 subjects with schizophrenia, each of whom was matched to 1 normal comparison subject for sex, age, and postmortem interval.
METHODS: Dorsolateral prefrontal area 9 was analyzed using a three-dimensional morphometric method in postmortem brains from 10 BPD patients and 11 matched nonpsychiatric control subjects. RESULTS: area 9 in BPD was characterized by reduced neuronal density in layer III (16%-22%) and reduced pyramidal cell density in layers III and V (17%-30%).
To determine whether changes in the cannabinoid system were present in the brains of subjects with schizophrenia, we used in situ radioligand binding and autoradiography to measure the binding of [ 3H]CP-55940 to the cannabinoid-1 receptor in the dorsolateral prefrontal cortex (Brodmann's area 9), caudate-putamen and areas of the temporal lobe from schizophrenic and control subjects, some of whom had ingested cannabis close to death.
In contrast, apoD levels were significantly increased (92--287%) in dorsolateral prefrontal cortex (Brodmann's area 9) of schizophrenic and bipolar subjects.
We first used conventional retrograde tracers to map the origin of thalamic projections to five prefrontal regions: medial area 9 (9m), lateral area 9 (9l), dorsal area 46 (46d), ventral area 46, and lateral area 12.
METHOD: Tissue sections containing prefrontal cortex area 9 from 10 matched pairs of schizophrenic and comparison subjects were processed for in situ hybridization histochemistry with (35)S-oligonucleotide probes for GAT-1 mRNA.
Approximately 50% of the within-stripe axon terminals in monkey PFC area 9 targeted dendritic spines.
In situ hybridization analysis showed that the expression of PSD95 was significantly decreased in Brodmann area 9 of the prefrontal cortex but not in the hippocampus.
In addition, the present study demonstrated that lesions limited to area 9, which constitutes the superior part of the mid-dorsolateral prefrontal region, give rise to a mild impairment in the monitoring of information, whereas lesions of the complete mid-dorsolateral prefrontal region yield a very severe impairment..
METHODS: To determine whether the decreased protein levels reflect diminished expression of the synaptophysin gene by prefrontal cortex neurons, we used in situ hybridization histochemistry to determine the cellular levels of synaptophysin messenger RNA in prefrontal cortex area 9 from 10 matched pairs of schizophrenic and normal control subjects.
Recent studies with nonhuman primates have shown that lesions of the mid-dorsolateral prefrontal cortex, which extends from the lip of the dorsal bank of the sulcus principalis to the midline (i.e., dorsal area 46 and 9/46 and area 9), give rise to severe and long-lasting impairments on self-ordered and externally ordered tasks designed to tax executive processing within working memory, rather than short-term memory per se. Lesions limited to area 9 give rise to a mild impairment on these tasks.
RESULTS: Lower distribution volumes were found in the prefrontal cortex (Brodmann's area 9) of PTSD patients than in comparison subjects.
However, the recognition task produced greater activation in right area 9 extending into the anterior cingulate.
During task preparation, the left dorsolateral prefrontal cortex (Brodmann's area 9) was more active for color naming than for word reading, consistent with a role in the implementation of control.
When the two tasks were compared directly, however, the first memory task, which had the higher monitoring requirement, yielded significantly greater signal intensity changes in area 9/46 of the right mid-dorsolateral frontal cortex.
The distribution of tachykinin NK(1) and NK(3) receptors in the prefrontal (Brodmann area 9) and visual cortex (Brodmann area 17) of formalin-fixed postmortem human brain tissue was studied by immunohistochemistry.
This study investigated whether chronic schizophrenia is associated with glial changes in 3 regions of the cerebral cortex: dorsolateral prefrontal cortex (Brodmann's area 9), the superior temporal gyrus (area 22), and the anterior cingulate gyrus (area 24). A 28% increase (p < 0.05) was found in area 9 in 8 schizophrenics (115 +/- 9 cells/mm2) compared with 10 controls (89 +/- 5 cells/mm2), when combining all cortical layers and both cerebral hemispheres.
Within each layer of PFC area 9, neurons expressing a detectable level of GAD67 mRNA were quantified for cell density and the relative level of mRNA expression per cell (grain density per neuron).
METHOD: The authors employed immunocytochemical methods and antibodies against tyrosine hydroxylase, the rate-limiting enzyme in dopamine biosynthesis, and the dopamine membrane transporter to examine dopamine axons in the dorsomedial prefrontal cortex (area 9) from 16 pairs of schizophrenic and matched control subjects. CONCLUSIONS: These findings reveal that schizophrenia is associated with an altered dopamine innervation of prefrontal cortex area 9 that is lamina- and neurotransmitter-specific and that does not appear to be a consequence of pharmacological treatment.
In the present study, we compared neuropeptide Y mRNA expression levels in the prefrontal cortex (Brodmann area 9 and 46) of subjects diagnosed with major depression, bipolar disorder and schizophrenia with those in normal controls without a psychiatric history.
Projections from medial temporal memory-related cortices subdivided medial cortices into different sectors, by targeting preferentially caudal medial areas (area 24, caudal 32 and 25), to a lesser extent rostral medial areas (rostral area 32, areas 14 and 10), and sparsely area 9. area 9 was distinguished by its strong connections with premotor cortices. Projections from unimodal sensory cortices reached preferentially specific medial cortices, including a projection from visual cortices to area 32/24, from somatosensory cortices to area 9, and from olfactory cortices to area 14.
In the prefrontal cortex (Brodmann area 9) of schizophrenics, many immunopositive cell bodies were exhibited irregular axis arrangement and fiber disarray.
These results support a functional segregation within the dorsolateral prefrontal cortex for WM: the dorsolateral prefrontal cortex (area 46/8A) is selectively involved in spatial WM, whereas the dorsomedial convexity (area 9/8B) is not critically engaged in either spatial or nonspatial working memory.
In the present study, PV-immunoreactive (IR) axon terminals in the superficial layers (layers 2-3a) of monkey PFC area 9 were found to form exclusively type II synapses onto the dendritic spines (44%), shafts (39%), or somata/axon initial segments (17%) of pyramidal neurons. Similar to the macaque monkey, in area 9 of the human PFC, PV-IR axon terminals forming type I synapses onto dendritic spines were found in the middle layers.
The present analysis showed that only a restricted portion of what had previously been labelled as area 46 in the monkey has the same characteristics as area 46 of the human brain; the remaining part of this monkey region has the characteristics of a portion of the middle frontal gyrus in the human brain that had previously been included as part of area 9. 46 and 9/46), which constitute the lower half of the mid-dorsolateral frontal cortex, have a well-developed granular layer IV, and can easily be distinguished from area 9, on the upper part of the mid-dorsolateral region, which does not have a well-developed granular layer IV. area 9 has the same basic pattern of connections as areas 46 and 9/46, but, unlike the latter areas, it does not receive input from the lateral parietal cortex. Caudal to area 9, on the dorsomedial portion of the frontal cortex, there is a distinct strip of cortex (area 8B) which, unlike area 9, receives significant input from the prestriate cortex and the medial parietal cortex.
CONCLUSIONS: Contrasts of both 1) negative and reference picture-caption pairs and 2) positive and negative picture-caption pairs activated networks involving similar areas in the medial frontal gyrus (Brodmann's area 9) and right anterior cingu-late gyrus (areas 24 and 32). The area 9 sites activated are strikingly similar to sites activated in related positron emission tomography experiments.
Specimens of the prefrontal cortex (Brodmann area 9) were collected from 51 suicide victims and 31 control subjects.
Sections through area 9 of five monkeys were labeled with immunoperoxidase for tyrosine hydroxylase (TH), to identify dopamine terminals, and with immunogold-silver for PV.
Normal levels of SNAP-25 are noted in schizophrenics in area 17, decreased levels in areas 10 and 20, and an elevated level in area 9.
The neuropathology of area 46 in schizophrenia is similar in direction and magnitude to that previously described in area 9 (Selemon et al.
Because understanding the functional role of these connections requires knowledge of their synaptic targets, we made injections of biotinylated dextran amine (BDA) into layer 3 of macaque prefrontal area 9 and examined the labeled intrinsic axon collaterals by electron microscopy.
Pleasant and unpleasant emotions were each distinguished from neutral emotion conditions by significantly increased cerebral blood flow in the vicinity of the medial prefrontal cortex (Brodmann's area 9), thalamus, hypothalamus and midbrain (P < 0.005).
The density of 5-HT1A receptors was increased in areas 24, 9a (caudal part of area 9), 44, and 6 in subjects with schizophrenia.
Decreases in rCBF were observed in several areas: the left ventro-orbital prefrontal cortex (PFv, area 47/12), the left lateral cerebellar hemisphere, and, in the right hemisphere, a dorsal and rostral aspect of PM (PMdr, area 6), dorsal PF (PFd, area 9), and the posterior parietal cortex (area 39/40).
RESULTS: Happiness, sadness, and disgust were each associated with increases in activity in the thalamus and medial prefrontal cortex (Brodmann's area 9).
Thus, whereas damage to the lateral prefrontal cortex (Brodmann's area 9) in monkeys causes a loss of inhibitory control in attentional selection, damage to the orbito-frontal cortex in monkeys causes a loss of inhibitory control in 'affective' processing, thereby impairing the ability to alter behaviour in response to fluctuations in the emotional significance of stimuli.
The total number of 3H-paroxetine transporter and nontransporter binding sites (Bmax), was lower in the suicide group compared to controls in both Brodmann area 9 (prefrontal cortex; p = 0.02) and in Brodmann area 38 (temporal cortex, p = 0.01). We conclude that the number of serotonin transporter sites is not altered in Brodmann area 9 in suicide, and that fewer 3H-paroxetine and 3H-imipramine binding sites found in this region of cerebral cortex of suicides may be explained by a reduction in the nontransporter binding sites..
As [ 3H]ketanserin binds to the serotonin2 receptor our data suggest that this receptor is not changed in the Brodmann's area 9 of the frontal cortex.
Sections through prefrontal area 9 of cynomolgus monkeys were processed by immunoperoxidase for tyrosine hydroxylase (TH) to label dopamine varicosities and by pre-embedding immunogold for CalR.
RESULTS: Increased neuronal density was found in prefrontal area 9 (17%) and occipital area 17 (10%) in the schizophrenic brains. In area 9, neuronal density was increased in layers III to VI; cell packing of pyramidal and nonpyramidal neurons was elevated. Cortical thickness in the schizophrenic brains was slightly but not significantly reduced in both areas, with a disproportionate reduction in layer V in area 9.
Performance during the 'theory of mind' condition evoked the activation of a distributed set of neural networks with prominent activation of the left medial frontal lobe (Brodmann area 9) and left temporal lobe (Brodmann areas 21, 39/19, 38).
To gain insight into the organization of these circuits, intracortical connections of major laminar and sublaminar divisions were retrogradely labeled in Walker's area 9 and 46 in rhesus monkeys by using cholera toxin (B-subunit) conjugated to colloidal gold.
In area 9, the densities of tyrosine hydroxylase-labeled axons and varicosities in the superficial and deep cortical layers remained relatively constant during postnatal development.
Based on this exercise, we developed a set of conservative Talairach coordinates to define area 9 and 46. area 9 is located on the dorsal, lateral, and dorsomedial surfaces of the frontal lobe extending along the middle third of the superior frontal gyrus and adjacent portions of the middle frontal gyrus in all cases examined. Area 46 lies on the dorsolateral convexity and is either partially or completely surrounded by area 9.
Light microscopic analysis confirmed that the cortical layers are more differentiated in area 46 than in area 9, particularly at the borders of layer IV. Layers III and V exhibit clearer sublamination in area 9, while layer IV is also somewhat wider in area 46 than in area 9 (9.3% vs 6.4% of cortical thickness); the overall thickness of the cortex is the same in both areas. Cytometric analysis revealed that layer IV neurons of area 46 are more densely packed than those in area 9 (55.38 +/- 7.26 vs 45.80 +/- 4.45 neurons/0.001 mm3), as are neurons in the supragranular layers II and III combined (53.51 +/ 6.33 vs 45.69 +/ 3.81 neurons/0.001 mm3). Finally, neurons in area 46 are more homogeneous in size than those in area 9. Differences in myeloarchitecture are also evident: each area contains numerous, well-stained radial striae and two pronounced bands of horizontal fibers, but in general, area 46 is less myelinated than area 9.
We examined the postnatal development of two markers of excitatory and inhibitory inputs to a subpopulation of layer III pyramidal neurons in area 9 and 46 of rhesus monkey prefrontal cortex.
While performing a symmetrically reinforced visual discrimination GO/NO-GO task, five monkeys were injected with a GABAA antagonist, bicuculline methiodide (BMI), into Brodmann's area 9, 8, 6, or 4. Errors in performance increased 10-60 min after injection into 10 of 33 sites in area 9, 9 of 25 sites in area 8, 20 of 34 sites in area 6, and 2 of 10 sites in area 4.
Local injection of the alpha 2-adrenergic antagonist yohimbine (10 micrograms in 2 microliters saline) into the dorsolateral prefrontal cortex (Walker's area 46 and area 9) impaired the performance of the delayed-response task, and it was without effect on the performance of the task if there was no delay between the cue and choice signals.
The programming of the synergies induced by internal signals or motivational states involves projections from the dentate nucleus to prefrontal area 9 as well as to the supplementary motor (SMA) and premotor (PM) areas.
When all AD cases are combined, the average level of GAP-43 message in area 9 of the AD frontal association cortex was not significantly different from the level in the comparably aged control cortex.
Immunohistochemical techniques were used to evaluate the laminar distribution of tyrosine hydroxylase (TH)-immunoreactive axons in area 9 of infant and adult rhesus monkey prefrontal cortex.
Quantitative studies of basilar dendrite patterns in the trunk and hand-finger receptive zones of areas 3 and 1, superior gyrus of the prefrontal cortex (area 9), and supramarginal gyrus (area 39) of the parietal lobe, in the left hemisphere of 10 subjects are reported.
For example, in the lightly innervated fundus of the principal sulcus (area 46), labeled fibers were primarily present in layer I and layers V-VI, whereas in area 9, the most densely innervated region, TH-labeled fibers were present in all cortical layers.
The distribution of dopamine D-1 receptors has been determined in human prefrontal cortex (Brodmann's area 9) by an in vitro light microscopic autoradiographic method.
However, recent anatomical studies have elucidated the circuit basis for motor regulatory functions of the principal sulcus (Brodmann's area 9; Walker's area 46).
Area 24 (anterior cingulate) had the greatest density of immunoreactive cell bodies (148 +/- 14/mm2), area 9 was of intermediate density (109 +/- 13/mm2), and area 46 was the least dense (83 +/- 12/mm2).
When intermediate and deeper layers of the colliculus were injected, labelled cells were found also in posterior parietal cortex (area 7) where they were concentrated mainly on the posterior bank of the intraparietal fissure, in inferotemporal cortex (areas 20 and 21), in auditory cortex (area 22), in the somatosensory representation SII (anterior bank of sylvian fissure, area 2), in upper insular cortex (area 14), in motor cortex (area 4), in premotor cortex (area 6), and in prefrontal cortex (area 9).
Neurons in area 9 responded primarily (37%) during the bar pressing phase and less during the visual discrimination phase.
For example, area 8 receives many fibers from both the rostral part of area 9 and a small area adjacent to the inferior branch of the arcuate sulcus. On the other hand, area 9 in the inferior prefrontal convexity receives fibers from localized parts of areas 8 and 9 in the dorsolateral convexity as well as from area 6. Thus, the caudal half of the STs area projects to area 8 and a small adjacent part of area 9.
Comparatively weak and widely spread ipsilateral projections are noted from prefrontal area 9.
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