High levels of netrin-4 mRNA was found in the pyramidal cell layer of the cerebral cortex, prepiriform cortex, amygdaloid nuclei, pyramidal layer of hippocampus, Purkinje's cells, medial cerebellar nucleus and interposed cerebellar nucleus, medial nucleus of the trapezoid body and mitral cell layer of the olfactory bulb. 
Target areas are the anterior olfactory nucleus, the entire prepiriform cortex, ventral tenia tecta, periamygdaloid cortex and the rostral part of the entorhinal cortex. Further anterograde labelling was found in the endopiriform nucleus deep under the prepiriform cortex and within an anterolateral strip of the olfactory tubercle.
In the forebrain GRP-immunoreactive (GRP-ir) cells were found in the hyperstriatum accessorium, medial and lateral parts of the neostriatum, corticoidea dorsolateralis and temporoparieto-occipitalis areas, hippocampus, pre- and parahippocampal areas and prepiriform cortex.
RESULTS: The surface of the TMR is subdivided into several areas: anteriorly, the lateral olfactory gyrus is covered by prepiriform cortex; dorsomedially, the semilunar gyrus and uncus hippocampi consist, respectively, of cortical amygdaloid nucleus and hippocampal cytoarchitectonic fields; and ventrolaterally, the anterior part of the parahippocampal gyrus is covered by periamygdaloid cortex, entorhinal, and transentorhinal areas and its posterior part is covered by Fields TH and TF per Von Economo and subicular complex.
Hippocampal pyramidal cells in CA1, CA3 and subiculum showed bilateral damage greater on the side of stimulation, and prepiriform cortex sustained bilateral symmetrical lesions.
These variables were measured before and after a bilateral injection of L-threonine (2 nmol into each side) into the prepiriform cortex (PPC).
An area of the deep prepiriform cortex is a controlling site for limbic seizures. Focal pharmacologic blockade of NMDA receptors in the deep prepiriform cortex protects against hippocampal cell injury during limbic seizures induced by intravenous kainate and during the excitotoxicity of global ischemia. In the current study, the deep prepiriform cortex was lesioned bilaterally by microinjection of kainate, 3 days before 10 min of global ischemia induced by four-vessel occlusion. During seizures induced from the deep prepiriform cortex, the immediate early gene cox-2 is expressed in the hippocampus. These results indicate that deep prepiriform cortex can be a modulatory site for ischemic hippocampal injury..
The medium-sized non-pyramidal parvalbumin neurons were found in layers II-IV and VI of the neocortex and in stratum multiforme of the prepiriform cortex.
Amino acid concentrations in plasma, prepiriform cortex and anterior cingulate cortex were not significantly different among treatments. Norepinephrine concentration in the prepiriform cortex was not affected by dietary treatment.
The present study investigates the role of pharmacologic blockade of NMDA (N-methyl-D-aspartate) and non-NMDA receptors at deep prepiriform cortex (area tempestas, AT) in neuronal injury during prolonged seizures in rat.
Deep prepiriform cortex has an important role in modulating neurotransmission during limbic seizures. We used pharmacologic blockade of non-N-methyl-D-aspartate (NMDA) receptors to study excitatory circuitry from the deep prepiriform cortex to the hippocampus during global ischemia in rat. NBQX, a potent non-NMDA glutamate receptor antagonist, was microinjected stereotactically into the deep prepiriform cortex before global ischemia for 10 min. Thus, excitatory amino acid-mediated circuitry emanating from deep prepiriform cortex modulates ischemic neuronal injury in the hippocampus..
Deep prepiriform cortex modulates excitatory activity in the limbic system during seizures. The non-NMDA antagonist NBQX was microinjected bilaterally into deep prepiriform cortex prior to 10 min of global ischemia. NBQX significantly decreased the number of HSP positive cells in both CA1 and CA3 hippocampal subsectors, suggesting the possibility that pathways from deep prepiriform cortex to hippocampus modulate excitotoxicity in target neurons during ischemia..
The human olfactory pathways are well defined up to the level of the prepiriform cortex but the neocortical projections and their functional organization are still largely unknown.
the prepiriform cortex and the hippocampus, are separated from each other by a six-layered neocortex.
Using the same methods strong labelling was also typical of the neuropil in the retrosplenial cortex, of layer Ia in the prepiriform cortex and the hippocampal CA3 field.
Pulsed trains of suprathreshold electric current, were administered bilaterally to either of four rostral forebrain sites: orbital cortex, medial precentral cortex, deep prepiriform cortex, or rostral caudate-putamen (n = 8 per site).
As seizure propagation within limbic structures is mediated in part by a small area of deep prepiriform cortex (area tempestas), we investigated the role of area tempestas in modulating hippocampal injury induced by systemic kainate administration.
The functional relationship between the area tempestas (AT), an epileptogenic site within the deep prepiriform cortex, and the regions in the posterior piriform cortex which are innervated by AT, were studied in the rat.
With the aid of retrograde tracers, we studied the thalamic projections of primary olfactory (olfactory tubercle and prepiriform cortex) and transitional orbital (areas PAII, Pro, 13) and medial (areas 25, 24, 32) areas, and of eulaminate (areas 11, 12, 9) cortices for comparison.
Focal injection of the adenosine A2A receptor agonist CGS21680 (2-[ p-(2-carboxyethyl)phenylethylamino]-5'-N-ethyl-carboxamidoaden osine) in the rat prepiriform cortex produced a reduction in the severity of bicuculline methiodide-induced motor seizures. Pharmacological characterization of the anticonvulsant response in the prepiriform cortex revealed a significant correlation between the potency of adenosine analogs as anticonvulsants and their respective affinities for adenosine A1 receptors in vitro. These results indicate that the low affinity of CGS21680 for adenosine A1 receptors is sufficient to account for the anticonvulsant activity of this compound in the rat prepiriform cortex..
Sodium lactate (pH 7.0) infused over the area tempestas, an epileptogenic site in the prepiriform cortex, protected rats from limbic motor seizures induced by infusion of a GABA receptor antagonist in area tempestas.
Labeled neurons in primary olfactory areas (prepiriform cortex, anterior olfactory nucleus and olfactory tubercle) were directed mainly to a posterior orbitofrontal region and to a lesser extent the neighboring caudal part of area 13.
Unilateral focal injection of 1,3-di(2-tolyl)guanidine (DTG) caused a dose-dependent and potent (ED50 = 5.25 nmol, 95% confidence limits 1.1 to 25.0 nmol) suppression of generalized motor seizures induced by (-)-bicuculline methiodide in the rat prepiriform cortex.
A1 adenosine receptors in the rat prepiriform cortex play an important role in the inhibition of bicuculline methiodide-induced convulsions. All compounds evaluated were unilaterally microinjected into the rat prepiriform cortex. Together the proconvulsant effect of an adenosine receptor antagonist and the convulsant action of an ecto-5'-nucleotidase inhibitor further support the role of endogenous adenosine as a tonically active antiepileptogenic substance in the rat prepiriform cortex..
Fluoxetine was administered intraperitoneally (i.p.) 1 h before seizures were induced by focal intracerebral application of the GABAA receptor antagonist, bicuculline methiodide (118 pmol) unilaterally into a discrete epileptogenic site in the deep prepiriform cortex ("area tempestas," AT) of rats.
Limbic motor seizures were induced by the unilateral focal application of bicuculline methiodide into area tempestas (AT), an epileptogenic site in the deep prepiriform cortex.
Microinjection of N-methyl-D-aspartate (NMDA; 1 and 2.5 nmol) or kainate (KA; 50 pmol) into the deep prepiriform cortex elicited behavioral signs of seizure activity. No epileptiform activity was observed after deep prepiriform cortex microinjection of either L-arginine (L-Arg, 5 and 10 nmol) or its D-enantiomer, D-arginine (D-Arg, 2.5-10 nmol). Motor and electrocortical seizures were observed after microinjection of the NO donor sodium nitroprusside (SNP; 5 to 20 nmol) into the deep prepiriform cortex. Furthermore, prior infusion of a subconvulsant dose of SNP into the deep prepiriform cortex significantly potentiated the seizure activity elicited by either NMDA (1 and 2.5 nmol) or KA (50 pmol). These results support the proposal that NO is formed from L-Arg upon excitatory amino acid receptor activation within the deep prepiriform cortex, thereby contributing to the genesis of seizure activity..
Using in situ hybridization, we previously investigated (17) the regional pattern of c-fos mRNA increases in the brain following convulsive seizures elicited from a highly circumscribed epileptogenic site located in the deep prepiriform cortex.
Using in situ hybridization histochemistry for the detection of c-fos mRNA, we examined the pathways activated by seizures evoked by a focal application of bicuculline into a highly discrete epileptogenic site in the deep prepiriform cortex, the area tempestas (AT).
The role of excitatory amino acid receptors in the genesis of motor and electrocortical seizures, elicited by administration of the polyamine putrescine into the deep prepiriform cortex, has been evaluated in rats. Motor and electrocortical seizures occurred in rats receiving unilateral local injections into the deep prepiriform cortex, of putrescine (10 or 20 nmol). The selective N-methyl-D-aspartate receptor antagonist, 2-amino-7-phosphonoheptanoate (AP7), injected previously (15 min) into the deep prepiriform cortex, prevented the development of seizures induced by putrescine, injected at the same site. In addition, dizocilpine (MK-801), a non-selective NMDA antagonist or ifenprodil, a specific inhibitor of the polyamine site at the NMDA receptor, when injected into the deep prepiriform cortex, 15 min prior to putrescine, significantly protected against seizures elicited by this polyamine. A subconvulsant dose of putrescine (5 nmol) potentiated the convulsant effects of NMDA, when injected into the deep prepiriform cortex. These data indicate a potential role of polyamines in the genesis of seizures, elicited from the deep prepiriform cortex. They further suggest that activation of the polyamine site, located at excitatory amino acid NMDA receptors, within the deep prepiriform cortex, may contribute to the genesis of seizure activity in this area..
An experimental animal model of complex partial seizures which become secondarily generalized is produced by microinfusion of the GABA antagonist bicuculline (BIC) into the deep prepiriform cortex (DPC) of rats.
Bilateral focal injections of the serotonin uptake inhibitor, fluoxetine (1.75-7.0 nmol) into substantia nigra (SN) protected against convulsive seizures evoked by the focal injection of bicuculline methiodide into area tempestas, an epileptogenic site within the deep prepiriform cortex.
We describe a novel model of status epilepticus produced by the focal application of bicuculline methiodide into the deep prepiriform cortex of rats pretreated with lithium chloride.
Seizures were induced by microinjecting bicuculline unilaterally into an epileptogenic site within the deep prepiriform cortex, area tempestas (AT).
We have investigated the ability of an array of putative noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists to suppress convulsions induced by a unilateral, focal injection of (-)-bicuculline methiodide (118 pmol) into the rat prepiriform cortex. The anticonvulsant potency of these compounds, (+)-5-methyl-10,11- dihydro-5H-dibenzo[ a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801) greater than dextrorphan greater than or equal to 1-(1-phenylcyclohexyl)piperidine hydrochloride (PCP) greater than dextromethorphan greater than (+)-pentazocine, upon microinjection into the prepiriform cortex, was highly correlated (r = 0.971; P less than 0.01) with their respective affinities for the [ 3H]dextrorphan-labelled NMDA receptors in rat forebrain membranes.
A small area of deep prepiriform cortex is uniquely susceptible to convulsant and anticonvulsant drugs in the rat.
The peripheral LHRH-immunoreactive (ir) cells and fibers (nervus terminalis) are dispersed along the basal surface of the forebrain from the olfactory bulbs to the prepiriform cortex and the interpeduncular fossa.
The present study further examined PPI hydrolysis induced by trans-ACPD, a selective agonist of the metabotropic EAA receptor, as well as by IBO in brain slices of rats kindled from the deep prepiriform cortex (DPC).
Prior kindling did not alter [ 35S]TBPS or [ 3H]flunitrazepam binding in the central nucleus or cortex of the inferior colliculus, the medial geniculate, or the deep prepiriform cortex.
Forebrain cortical regions that receive afferents from the olfactory bulb, such as the anterior olfactory nucleus, olfactory tubercle, prepiriform cortex, entorhinal cortex, and amygdala, exhibited distinct immunoreactivity, while olfactory bulb was almost devoid of staining.
Computer maps revealed high values in the outer and inner layers of the cortex, some hippocampal and olfactory bulb layers, prepiriform cortex, dorsal part of the caudate-putamen, globus pallidus, lateral septum, reticular thalamic nucleus, lateral habenular nucleus, circumventricular organs, nuclei of the medial hypothalamus, substantia nigra, interpeduncular nucleus, and mamillary body.
In addition, convulsive seizures evoked by the focal injection of bicuculline methiodide (40 ng) in an epileptogenic site within the deep prepiriform cortex (area tempestas) were not potentiated by intranigral isoniazid.
Samples were obtained by microdialysis perfusion of freely moving animals receiving deep prepiriform cortex (DPC) electrical stimulation.
A locus in the deep cell layer (layer III) of the rostral portion of the posterior piriform cortex (PPC) is described, which is considerably more sensitive to electrical stimulation than adjacent areas of the PPC, including the deep prepiriform cortex or the amygdala.
electrographic spikes recorded from the deep prepiriform cortex coincided with myoclonic jerks, while both brain areas exhibited an increase in afterdischarge frequency at the onset of forelimb tonic extension. However, when functional interactions were assessed, the tonic-clonic behaviors produced by kindling stimulation of the inferior collicular cortex were prevented by microinjections of procaine into the deep prepiriform cortex.
Bicuculline methiodide (BMI), a gamma-aminobutyrate (GABA) antagonist, is a powerful convulsant agent when injected into the cerebral ventricles, amygdala, hippocampus, thalamus, neocortex, and deep prepiriform cortex in rats.
The role of nitric oxide (NO) in the genesis of motor and electrocortical seizures elicited by administration of excitatory amino acid agonists into the deep prepiriform cortex (DPC) has been evaluated. These data confirm the role of excitatory amino acid transmission in the genesis of seizures elicited from the deep prepiriform cortex.
Moreover, area 13 of the orbitofrontal cortex, the frontal and temporal subdivisions of the prepiriform cortex, and the cortical and deep nuclei of the amygdala also contribute fibers to the anterior commissure.
An epileptogenic region of the deep prepiriform cortex, area tempestas (AT), triggers convulsive seizures in response to the focal application of GABA antagonists, muscarinic agonists and excitatory amino acid agonists.
Kainic acid (KA), microinjected unilaterally into the rat prepiriform cortex (PC), produces generalized motor seizures in a dose-dependent manner.
The gamma-aminobutyric acid (GABA) antagonist, bicuculline, induces generalized motor seizures when injected into a discrete site ('area tempestas') in the deep prepiriform cortex at concentrations considerably lower than those that induce convulsions from closely adjacent areas or other forebrain sites such as amygdala and hippocampus. This argues against the suggestion that the deep prepiriform cortex plays a crucial role in the generation of seizures following systemic administration of GABA antagonists..
The protective effects of a series of stable adenosine analogs against generalized seizures initiated by focal injection of bicuculline methiodide into the rat prepiriform cortex (PPC) were studied by microinjection of these compounds into this brain area.
Electrodes were placed on frontal and occipital cortices, into the hippocampus and into a region of the prepiriform cortex, area tempestas (AT).
The functional relationship between the substantia nigra (SN) and the area tempestas (AT), an epileptogenic site in the deep prepiriform cortex, was investigated.
The EC spontaneous field potentials (EEGs) were related to those recorded simultaneously from the more rostrally lying olfactory bulb (OB) and prepiriform cortex (PPC), using coherence functions.
Several critical brain regions have been identified in which application of gamma-aminobutyric acid (GABA) potentiating agents in small quantities can suppress or prevent generalized and kindled amygdala seizures, i.e., substantia nigra and deep prepiriform cortex.
The amygdala and prepiriform cortex have been implicated in monitoring amino acid (AA) balance, and hence food intake in rats.
The deep prepiriform cortex of the rat is an important site for both initiation and arrest of generalized seizures induced by systemic convulsants.
The effects of a unilateral thermocoagulating lesion of the deep prepiriform cortex on the development of amygdala kindling were studied in adult rats. The results suggest that the deep prepiriform cortex may not be important in the development of amygdala kindling..
Comparatively ventral deposits gave rise to prominent labeling of the hippocampal subiculum, various parahippocampal areas, and prepiriform cortex. On the basis of afferent connections, it is possible to divide the cat's medial prefrontal cortex into an infralimbic component, MPFil, marked by strong afferents from prepiriform cortex and the cortical amygdala, and a dorsal component, MPFd, without afferents from these structures.
The basic characteristics of the electroencephalograms (EEGs) of the entorhinal cortex (EC) were compared to those of the olfactory bulb (OB) and prepiriform cortex (PPC) in the awake cat, using methods that take into account linear (coherence functions) and non-linear relationships (mutual information).
Infusion of 2-amino-7-phosphonoheptanoate into the prepiriform cortex resulted in a small but significant reduction in seizure severity. These results suggest that inhibition of excitatory transmission within the substantia nigra and the reticular formation effectively blocks the output pathway for the audiogenic seizures, whereas the role of the prepiriform cortex in this process is relatively minor..
The ventral part of the claustrum has reciprocal connections predominantly with the entorhinal cortex, and possibly with the anterior olfactory nucleus and the prepiriform cortex.
The prepiriform cortex (PPCx) shows high sensitivity to the epileptogenic action of chemo-convulsants and to the protective action of the NMDA receptor antagonist, 2-amino-7-phosphono-heptanoate (APH) against pilocarpine-induced (motor) limbic seizures in rats.
Histopathologic examination of the prepiriform cortex (PPC) in four documented cases of dementia of the Alzheimer type revealed increased numbers of neurofibrillary tangles and neuritic plaques.
The deep prepiriform cortex (DPC) has been recently suggested to be a crucial epileptogenic site in the rat brain. We investigated the susceptibility of the DPC to the development of electrical kindling as compared to that of the superficial prepiriform cortex (SPC) and amygdala as well as the transfer interactions between the two prepiriform sites and amygdala. Adult rats with electrodes implanted in the right prepiriform cortex (DPC or SPC) and left amygdala were divided into a DPC-amygdala and SPC-amygdala group while a third group consisted of rats with electrodes implanted in the ipsilateral DPC and amygdala. These results indicate that the prepiriform cortex can be readily kindled but not faster than the amygdala and that there are unequal kindling transfer interactions between prepiriform cortex and amygdala..
Microinjection of gamma-vinyl GABA (GVG), a GABA elevating agent, into a discrete region of the deep prepiriform cortex elevated local GABA levels nearly 4-fold and exerted an anticonvulsant action against seizures induced by intravenous injection of the GABA antagonist, bicuculline, but was ineffective against seizures induced by maximal electroshock. This, together with a previous finding that blockade of GABA transmission in the deep prepiriform cortex induces convulsions, suggests that this area may be crucial, if not primarily responsible, for the genesis of clonic seizures resulting from a deficit in GABA function..
Within the cortical projections a medial-to-lateral topography could be observed such that the entorhinal cortex projects predominantly to the allocortical and periallocortical limbic areas, including parts of the subicular complex, the ventral retrosplenial and the infralimbic cortices, and olfactory related areas--i.e., the olfactory bulb, the anterior olfactory nucleus, the prepiriform cortex, and the ventral tenia tecta.
Focal injection into the prepiriform cortex (PC) of an N-methyl-D-aspartate receptor antagonist, 2-amino-7-phosphonoheptanoic acid (APH), 1-10 pmol, potently protects against these seizures and their pathological consequences.
Previous studies in our laboratory have shown that bilateral motor seizures can be elicited from a discrete site within the deep prepiriform cortex (DPC) after a single, unilateral microinjection of picomole amounts of bicuculline, carbachol or kainic acid.
Microinjection of 2-amino-phosphonoheptanoic acid (2APH, 1 nmol), and antagonist for n-methyl-d-aspartate-sensitive receptors, into the deep prepiriform cortex (DPC) of the rat, prevented seizures induced by the intravenous administration of bicuculline.
The olfactory peduncle, the prepiriform cortex, the cortico-amygdaloid transition area, the entorhinal cortex, the subiculum (ventral, posteroventral, and posterodorsal sectors), the caudomedial band of the hippocampal formation and the postsubiculum are the allocortical sources of afferents to the PFC.
The staining characteristics of the two methods were compared by examining two allocortical regions, prepiriform cortex and entorhinal cortex, in the brain of the European hedgehog. In the 3 layers of prepiriform cortex and the 6 layers of entorhinal cortex the methods revealed sublayers, which allows a precise delimitation of areas 28M, 28L, a short transition zone, and the prepiriform cortex.
These are structures of the palaeocortex (the prepiriform cortex and the diagonal area) and those of the hypothalamus (the supraoptic, arcuate, ventromedial, mammillary nuclei, anterior and posterior fields).
In a discrete area in the vicinity of prepiriform cortex, a single, unilateral injection of bicuculline (49 pmol) produced generalized clonic seizures documented behaviorally and electroencephalographically.
For the prepiriform cortex claustral efferents could be established unequivocally only with the horseradish peroxidase technique.
Field potentials and unit activity elicited by electrical stimulation of the olfactory bulb (OB) and anterior and posterior prepiriform cortex (PPCa and PPCp) were measured extracellularly in the entorhinal cortex (EC) of the cat.
The spatial organization and laminar distribution of projections from the olfactory bulb and the anterior (PPCa) and posterior (PPCp) divisions of the prepiriform cortex to the entorhinal cortex were studied with anterograde (3H-leucine) and retrograde (WGA-HRP) tracing techniques. The lateral and medial entorhinal areas are also reached by fibers from the prepiriform cortex.
The cortex dorsal and posterior to the insular cortex we consider auditory cortex, as it receives afferents from the principal part of the medial geniculate nucleus, and the cortex ventral to the insular cortex (below the fundus of the rhinal sulcus) we consider to constitute the prepiriform cortex, which is athalamic.
Neurotensin-like immunoreactive fibers located in these areas decreased remarkably in numbers on the operated side after the destruction of the ventral part of the endopiriform nucleus and the adjacent prepiriform cortex where numerous cells with neurotensin-like immunoreactivity were detected. This strongly suggests that such cells located in the endopiriform nucleus and the adjacent prepiriform cortex send a neurotensin-like projection ipsilaterally to the anterior olfactory nucleus and to the nucleus of the diagonal band of Broca..
Tritiated amino acid (TAA) injections in some of the cortical regions which contained retrogradely labeled neurons confirmed projections to the insula from prefrontal granular cortex, orbital frontal cortex, prepiriform cortex, temporal pole, rhinal cortex, cingulate gyrus, frontal operculum, and parietal cortex.
In the insula as well as in lateral orbital and temporopolar areas, the agranular sector is directly contiguous with prepiriform cortex.
The results of the present study indicate that the main and accessory olfactory bulbs, the anterior olfactory nucleus, the prepiriform cortex and discrete regions of the medial frontal lobe, the insular and temporal cortices, as well as the perirhinal and entorhinal cortices and the ventral subiculum project to the amygdaloid complex. Of the allocortical regions the prepiriform cortex distributes its fibers to the lateral, basolateral, and cortical nuclei, whereas the ventral subiculum projects to the medial division of the lateral central nucleus and the cortical nuclei.
Scarce projections from the subicular cortex terminate in the dorsal prefrontal, temporal, parietal and prepiriform cortex.
Recent evidence suggests that the main olfactory bulb projects caudally beyond the prepiriform cortex and the cortical amygdaloid nuclei to the region of the piriform lobe called the parahippocampal area.
LHRH-cell bodies are found in the ventral hypothalamus that includes its preoptic, anterior and central parts, in the septum, the olfactory tubercle, the main and accessory olfactory bulb, and the prepiriform cortex.
(3) EPSPs were recorded in the GCL neurons by stimulation of the deep-lying structure of the prepiriform cortex as well as by stimulation of the AC.
The olfactory bulb and prepiriform cortex project to layers IA and IB, respectively, of all three subdivisions, but the lateral amygdaloid nucleus has a restricted projection to layer III of the ventral subdivision only.
Projections are described from the basolateral, lateral and anterior cortical nuclei of the amygdaloid complex, and from the prepiriform cortex, to several discrete areas of the cerebral cortex in the rat and cat and to the mediodorsal thalamic nucleus in the rat. The anterior cortical amygdaloid nucleus and the prepiriform cortex both project to the infralimbic area and the ventral agranular insular area, and the anterior cortical nucleus also projects to the posterior agranular area and the perirhinal area. The endopiriform nucleus, deep to the prepiriform cortex, projects to the central segment of the mediodorsal nucleus; this may constitute the major olfactory input into the mediodorsal nucleus, since little or no projection could be demonstrated from the prepiriform cortex itself.
Of special interest were the distinct networks of varying densities in the amygdaloid cortex, the entorhinal cortex, the prepiriform cortex, the anterior cingulate cortex and the (pre-)frontal cortex.
2 Concentrations of pentobarbitone, ether, methoxyflurance, trichloroethylene and alphaxalone that are known to depress synaptic transmission in the prepiriform cortex also depressed the sensitivity of prepiriform neurones to L-glutamate.
LOT collateral branches bound for the prepiriform cortex veer laterally off the main trajectory of the tract at an angle of 50 degrees or less.
Slices from guinea pig brain containing the lateral olfactory tract (LOT) and the prepiriform cortex were studied in vitro.
In the youngest pups, long-lasting degeneration argyrophilia (LLDA) is found in two regions of prepiriform cortex: at the level of the rostral tubercle and rostral amygdala.
This was also shown by the decrease in the evoked activity of units in the prepiriform cortex.
The evoked potentials recorded from the surface of the prepiriform cortex comprised a negative wave (N-wave) of about 10-15 msec duration upon which a variable number of short duration positive notches were superimposed.
In all brains, the preoptic area, prepiriform cortex, olfactory tubercle, and septum had particularly high, long-lasting uptake of both hormones..
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