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PubMed1993

Co-localization of two calcium binding proteins in GABA cells of rat piriform cortex.

In the rat piriform cortex, double-fluorescence immunocytochemistry was used to study the coexistence of two calcium binding proteins, parvalbumin and calbindinD28k, and GABA. Layer I cells were immunoreactive only for GABA. In layer II a small number of cells were immunoreactive for all three substances. A few other cells contained only parvalbumin and GABA immunoreactivity. In layer III a subpopulation of calbindinD28k immunoreactive cells (about 60%) were also immunoreactive for both parvalbumin and GABA. The remainder showed only calbindinD28k and GABA immunoreactivity. Many immunoreactive terminals, which surrounded non-immunoreactive cell somata to form basket endings in layers II and III, were immunoreactive for all three substances. Their major source may be the non-pyramidal neurons in layer III, which contained the three chemical substances.

Animals↗
PubMed1998

Cholinergic agonist carbachol enables associative long-term potentiation in piriform cortex slices.

Pyramidal cells in piriform (olfactory) cortex receive afferent input from the olfactory bulb as well as intrinsic association input from piriform cortex and other cortical areas. These two functionally distinct inputs terminate on adjacent apical dendritic segments of the pyramidal cells located in layer Ia and layer Ib of piriform cortex. Studies with bath-applied cholinergic agonists have shown suppression of the fast component of the inhibitory postsynaptic potentials (IPSPs) evoked by stimulation of the association fibers. It was previously demonstrated that an associative form of LTP can be induced by coactivation of the two fiber systems after blockade of the fast, gamma-aminobutyric acid-A-mediated IPSP. In this report, we demonstrate that an associative form of long-term potentiation can be induced by coactivation of afferent and intrinsic fibers in the presence of the cholinergic agonist carbachol.

Afferent Pathways↗
PubMed1997

Piriform cortex ablations block navigational map learning in homing pigeons.

Young homing pigeons were subjected to ablations of the piriform cortex or left intact and allowed to learn a navigational map. Three months later, control and piriform cortex lesioned pigeons were released from three unfamiliar locations. Control pigeons oriented homeward indicating successful navigational map learning. In contrast, piriform cortex ablated pigeons consistently oriented east, took more time to return home and were more likely to get lost. The results demonstrate that piriform cortex ablations in young homing pigeons disrupt navigational learning. The data support the conclusion that participation of the piriform cortex is necessary for navigational map learning, and its role in navigational learning cannot be substituted for by other telencephalic olfactory processing regions. Further, the results show that the role of olfactory cues in building up the navigational map cannot be replaced by other non olfactory environmental stimuli.

Animals↗
PubMed1987

Distribution and ultrastructure of neurons in opossum piriform cortex displaying immunoreactivity to GABA and GAD and high-affinity tritiated GABA uptake.

GABAergic neurons have been identified in the piriform cortex of the opossum at light and electron microscopic levels by immunocytochemical localization of GABA and the GABA-synthesizing enzyme glutamic acid decarboxylase and by autoradiographic visualization of high-affinity 3H-GABA uptake. Four major neuron populations have been distinguished on the basis of soma size, shape, and segregation at specific depths and locations: large horizontal cells in layer Ia of the anterior piriform cortex, small globular cells with thin dendrites concentrated in layers Ib and II of the posterior piriform cortex, and multipolar and fusiform cells concentrated in the deep part of layer III in anterior and posterior parts of the piriform cortex and the subjacent endopiriform nucleus. All four populations were well visualized with both antisera, but the large layer Ia horizontal cells displayed only very light 3H-GABA uptake, thus suggesting a lack of local axon collaterals or lack of high-affinity GABA uptake sites. The large, ultrastructurally distinctive somata of layer Ia horizontal cells receive a very small number of symmetrical synapses; the thin, axonlike dendrites of small globular cells are exclusively postsynaptic and receive large numbers of both symmetrical and asymmetrical synapses, in contrast to somata which receive a small number of both types; and the deep multipolar and fusiform cells receive a highly variable number of symmetrical and asymmetrical synapses on somata and proximal dendrites. Labeled puncta of axon terminal dimensions were found in large numbers in the neuropil surrounding pyramidal cell somata in layer II and in the endopiriform nucleus. Moderately large numbers of labeled puncta were found in layer I at the depth of pyramidal cell apical dendrites with greater numbers in layer Ia at the depth of distal apical segments than in layer Ib. High-affinity GABA uptake was demonstrated in the termination zone of the projection from the anterior olfactory nucleus to the anterior piriform cortex. Cell bodies of origin of this projection displayed heavy retrograde labeling with 3H-GABA. Matching neuropil and cellular labeling was demonstrated with the GABA-BSA antiserum but not with the GAD antiserum, thus suggesting that GABA is normally present in these cells but is taken up from the neuropil rather than synthesized. No comparable high-affinity GABA uptake was demonstrated in the association fiber systems that originate in the piriform cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2003

Lithium/pilocarpine status epilepticus-induced neuropathology of piriform cortex and adjoining structures in rats is age-dependent.

Distribution of LiCl/pilocarpine status epilepticus-induced neuronal damage was studied in the piriform cortex and in adjoining structures in 12-day-old, 25-day-old and adult rats. No distinct structural and neuronal alterations were detected in the basal telencephalon in 12-day-old rats surviving status epilepticus (SE) for one week or two months. In 25-day-old rats a decrease in Nissl staining was evident. There was also cell loss and gliosis in the caudal 2/3 of the piriform cortex, in the superficial amygdaloid nuclei, in the dorsal and ventral endopiriform nucleus and in the rostrolateral part of the entorhinal cortical area. In adult animals, the topography of neuropathological changes in the basal telencephalon was comparable to those in 25-day-old rats. The damage in the caudal 2/3 or caudal half of the piriform cortex in adult rats with survival times one week or two months was characterized by a marked loss of neurons and striking glial infiltration. The thickness of the piriform cortex and superficial amygdaloid nuclei was significantly reduced. In 25-day-old and in adult animals the sublayer IIb and layer III of the piriform cortex was more affected, while sublayer IIa was less damaged. Parvalbumin (PV) immunocytochemistry revealed a significant decrease in the number of PV-immunoreactive neurons in the rostral piriform cortex and in the dorsal claustrum in animals surviving for two months.

Aging↗
PubMed2003

Odor-evoked activity is spatially distributed in piriform cortex.

Much data on the olfactory bulb (OB) indicates that structural characteristics of odorant molecules are encoded as ordered, spatially consolidated sets of active cells. New results with "genetic tracing" (Zou et al. [2001] Nature 414:173-179) suggest that spatial order is also present in projections from the OB to the olfactory cortex. For the piriform cortex (PC), results with this technique indicate that afferents conveying input derived from single olfactory receptors (ORs) are distributed to well-defined patches in the anterior PC (APC) but that these patches are much larger than in the OB. We have used c-fos induction to examine how input patterning for single ORs is translated into patterns of odor-evoked cellular activity in the PC. The laminar distribution of labeled cells and dual-immunostaining for gamma-aminobutyric acid (GABA)ergic markers indicated that activity was detected largely in pyramidal cells. In odor-stimulated rats, labeled cells were present throughout the posterior PC (PPC) but were concentrated in prominent rostrocaudal bands in APC. Analysis of responses to different odorants and concentrations revealed that locations and shapes of bands conveyed no apparent information regarding odor quality, rather, they appeared to correspond to subregions of the APC distinguished by cytoarchitecture and connectivity. Small-scale variations in labeling density were observed within APC bands and throughout the PPC that could reflect the presence of a complex topographical order, but discrete patches at consistent locations as observed by genetic tracing were absent. This finding suggests that as a result of afferent overlap and intracortical processing, odor-quality information is represented by spatially distributed sets of cells. A distributed organization may be optimal for discriminating biologically relevant odorants that activate large numbers of ORs.

Animals↗
PubMed1997

Delayed development of spontaneous seizures and prolonged convulsive state in rats after massed stimulation of the anterior piriform cortex.

We studied the short- and long-term epileptogenic effects of massed stimulation (MS) of the piriform cortex. Sprague-Dawley rats with electrodes implanted bilaterally in the anterior piriform cortex and the dorsal and ventral hippocampi underwent MS: electrical stimulation of the left piriform cortex every 5 min for 6 h (afterdischarge threshold, 60 Hz, 1 ms, 1 s). Animals were retested (5 stimulations) 3-4 times later at different time points to check for the kindled state. Our data showed that MS resulted in delayed development of severe epilepsy. The interval between MS and the first appearance of convulsive response (2 weeks) was characterized by deep refractoriness to seizure (silent period). Unexpectedly, dramatic seizure activity occurred 4-7 weeks after MS. This was manifested by (1) generalized tonic-clonic convulsions with multiple failings, which were elicited repeatedly during retest; (2) frequent progression of elicited generalized convulsions into a prolonged (> 8 min) postictal convulsive state expressed mainly by continuous partial seizures and even new bouts of generalized seizures, and (3) development of mild spontaneous seizures. We found that epileptiform activity predominated in the ventral hippocampus. Mossy fiber sprouting was also most pronounced in this area. We propose that the MS resulted in formation of pathological circuits which involve both piriform cortex and ventral hippocampus and lead to severe epilepsy.

Aging↗
PubMed1989

Analysis of synaptic events in the opossum piriform cortex with improved current source-density techniques.

1. The piriform cortex of the opossum was studied by current source-density (CSD) analysis of field potentials to determine the laminar and temporal distribution of synaptic currents evoked by lateral olfactory tract (LOT) stimulation. 2. Extracellular conductivity was measured as a function of depth at high resolution and incorporated into CSD computations. Inclusion of the conductivity term resulted in relatively subtle changes in the shapes of CSD profiles. Resolution and accuracy of CSD computations was further improved by use of a new smoothing approach and averaging of multiple potential profiles obtained at the same site. 3. The CSD depth profile resulting from LOT stimulation revealed six major synaptic events that were consistently present at anterior, middle, and posterior sites: one during the first (A1) peak of the initial surface negative dichrotic field potential component, three during the second (B1) peak, one during the surface positive field potential component (period 2), and one during the second surface negative component (period 3). In addition, CSD profiles were computed for the population spike generated by synchronous discharge of action potentials. Depths of the net inward and outward membrane currents underlying these events were correlated with the cortical lamination as determined histologically by placement of small dye marks. 4. In agreement with previous reports it is concluded that the large inward membrane current in layer Ia during the A1 wave underlies a monosynaptic EPSP evoked in distal apical dendritic segments of pyramidal cells by afferent fibers. This EPSP displays a marked paired shock facilitation. 5. Based on anatomic and physiological considerations it is concluded that the three spatially and temporally distinct inward membrane currents (sinks) that were observed in layers III, superficial Ib, and mid- to deep-Ib during the B1 wave, underlie disynaptic EPSPs resulting from direct synaptic interactions between pyramidal cells. It is postulated that the layer III sink is generated in basal dendrites largely via local axon collaterals, the superficial layer Ib sink in intermediate apical dendritic segments by association fibers originating in the anterior piriform cortex, and the deep Ib sink in proximal apical segments by association fibers originating largely in the posterior piriform cortex. 6. The latencies of the layer Ia and superficial layer Ib sinks (presumed mono- and large disynaptic EPSPs, respectively) increased from anterior to posterior. Amplitude of the superficial Ib sink relative to the Ia sink increased from anterior to posterior.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Olfactory bulb repetitive stimulations reveal non-homogeneous distribution of the inhibitory processes in the rat piriform cortex.

Optical signals were recorded in the in vivo rat piriform cortex in response to a burst of seven electrical stimulations (100 ms interval) delivered in the olfactory bulb. Based on the recorded responses, three types of signal could be identified according to the relative amplitude of their monosynaptic and disynaptic components. The dysynaptic component had a larger (type 1) or an equal amplitude (type 2) compared with the monosynaptic one. Type 3 exhibited only the monosynaptic component. Type 1 represented 96% of the first response. The second response was characterized by an increase in type 3 signals (39%). The remaining type 1 signals were lower in amplitude when compared with the first response. The responses to the last five stimulations did not differ from one another but were different from the first two (type 1, 74%; type 2, 7.8%; type 3, 18.2% on average). The spatial distribution of these three types of signal was analysed by dividing the piriform cortex into several areas. These areas were not homogeneous in the percentage of each signal type: the percentage of type 3 signals was highest (approximately 30%) in the area near the lateral olfactory tract and < 10% in the most posterodorsal area. Thus the level of inhibition remained high in some piriform areas whereas it decreased rapidly in others, suggesting that the inhibitory processes were not homogeneously distributed in the whole piriform cortex. Functional implications are discussed.

Animals↗
PubMed1991

Kindling from stimulation of a highly sensitive locus in the posterior part of the piriform cortex. Comparison with amygdala kindling and effects of antiepileptic drugs.

The piriform cortex, especially its deep anterior part, has been recently suggested to be a crucial epileptogenic site in the rat brain. We investigated the susceptibility of different parts of the piriform cortex to the development of electrical kindling as compared to that of the basolateral amygdala. 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. The sensitive locus in the PPC can be readily kindled, and focal seizure thresholds in fully kindled rats are 60-90% lower than respective thresholds in rats kindled from other loci. Treatment of fully kindled rats with antiepileptic drugs diazepam, carbamazepine, phenobarbital, and valproate showed that anticonvulsant effects of these drugs in animals kindled from stimulation of the PPC were comparable to respective effects in animals kindled from stimulation of the basolateral amygdala, although the locus in the PPC tended to be more resistant. The data support the idea that the piriform area may contain the most sensitive neuronal tissue responsible for the generation of seizures during kindling. It remains to be determined if the described locus in the PPC is critical to the kindling process when kindling is induced from other structures within the olfactory-limbic system.

Amygdala↗
PubMed1997

Neuropeptide Y, somatostatin, and cholecystokinin of the anterior piriform cortex.

In addition to its role in olfaction and as a primary epileptogenic site, the anterior piriform cortex has been suggested to play a role in neuroperception of deficiencies or imbalances in physiologically essential amino acids. In recent studies, amino acid deficient diets were shown to induce expression of c-fos in the anterior piriform cortex within the rapid time frame associated with the normal anorectic response to such diets. It became important to examine the neurocytochemical architecture of this region for clues as to how and more precisely where dietary amino acid deficiency or imbalance might be monitored. The relationships of neuropeptide Y-, somatostatin-, and cholecystokinin-containing neurons were of particular interest because ongoing studies indicate that those peptides administered to the anterior piriform cortex alter intake of diets deficient in essential amino acids. The neuropeptides were endogenous to intrinsic neurons only; none resembled pyramidal projection neurons. Peptidergic neurons and fibers were concentrated most heavily in layer III of the paleocortex. The cytoarchitecture suggests that neuropeptide Y-, somatostatin-, and cholecystokin-containing neurons of the anterior piriform cortex may relate synaptically or multisynaptically to local circuit neurons during electrical activity, modulation of olfactory information, and neuroperception of essential amino acids.

Animals↗
PubMed1989

Changes in cholinergic but not in GABAergic markers in amygdala, piriform cortex, and nucleus basalis of the rat brain following systemic administration of kainic acid.

Three days after systemic administration of kainic acid (15 mg/kg, s.c.), selected cholinergic markers (choline acetyltransferase, acetylcholinesterase, muscarinic acetylcholine receptor, and high-affinity choline uptake) and GABAergic parameters [benzodiazepine and gamma-aminobutyric acid (GABA) receptors] were studied in the frontal and piriform cortex, dorsal hippocampus, amygdaloid complex, and nucleus basalis. Kainic acid treatment resulted in a significant reduction of choline acetyltransferase activity in the piriform cortex (by 20%), amygdala (by 19%), and nucleus basalis (by 31%) in comparison with vehicle-injected control rats. A lower activity of acetylcholinesterase was also determined in the piriform cortex following parenteral kainic acid administration. [3H]Quinuclidinyl benzilate binding to muscarinic acetylcholine receptors was significantly decreased in the piriform cortex (by 33%), amygdala (by 39%), and nucleus basalis (by 33%) in the group treated with kainic acid, whereas such binding in the hippocampus and frontal cortex was not affected by kainic acid. Sodium-dependent high-affinity choline uptake into cholinergic nerve terminals was decreased in the piriform cortex (by 25%) and amygdala (by 24%) after kainic acid treatment. In contrast, [3H]flunitrazepam binding to benzodiazepine receptors and [3H]muscimol binding to GABA receptors were not affected 3 days after parenteral kainic acid application in any of the brain regions studied. The data indicate that kainic acid-induced limbic seizures result in a loss of cholinergic cells in the nucleus basalis that is paralleled by degeneration of cholinergic fibers and cholinoceptive structures in the piriform cortex and amygdala, a finding emphasizing the important role of cholinergic mechanisms in generating and/or maintaining seizure activity.

Amygdala↗
PubMed1990

Serotonin (5-HT) induces IPSPs in pyramidal layer cells of rat piriform cortex: evidence for the involvement of a 5-HT2-activated interneuron.

In a slice preparation of rat piriform cortex, both intracellular and extracellular techniques were used to examine the pharmacological and electrophysiological actions of serotonin (5-HT). Bath application of 5-HT resulted in either depolarization (57%), hyperpolarization (34%) or no change (9%) in membrane potential of cells in the pyramidal cell layer (layer II) of piriform cortex. Additionally, when KCl-containing electrodes were used, 5-HT induced an increase in depolarizing synaptic potentials in 41% of these cells. It was concluded that these potentials were reverse inhibitory post-synaptic potentials (IPSPs) because they were blocked by bicuculline and tetrodotoxin. The induction of IPSPs by 5-HT was blocked by the 5-HT2-selective antagonist ritanserin. By recording extracellularly in the presence of 5-HT, a group of 5-HT-activated, putative interneurons was found at the border of layers II and III of piriform cortex, 5-HT but not norepinephrine activation was blocked by ritanserin. The actions of 5-HT were mimicked by the 5-HT2 agonist alpha-methyl-5-HT; the 5-HT2 partial agonist, 2,5-dimethoxy-4-methyl-amphetamine had a small agonist action of its own and blunted the effect of 5-HT. Activation of a larger group of putative interneurons by the more universal excitant N-methyl-D-aspartate showed that the 5-HT-activated interneurons represented 23% of the interneurons located on the border between layers II and III. We conclude that 5-HT induces IPSPs in layer II pyramidal cells by activating a subpopulation of interneurons at the border of layers II and III of piriform cortex.

Animals↗
PubMed1984

Analysis of association fiber system in piriform cortex with intracellular recording and staining techniques.

The piriform cortex of the opossum has been studied with intracellular recording and staining techniques. The experiments were designed to investigate the association fiber system, but the results have also revealed new properties of the afferent fiber system from the olfactory bulb and the inhibitory systems within the piriform cortex. Following shock stimulation of the lateral olfactory tract (LOT), the response of pyramidal cells consists of an initial excitatory postsynaptic potential (EPSP) followed by a long-lasting inhibitory postsynaptic potential (IPSP). The LOT-evoked EPSP consists of two components: an initial monosynaptic followed by a disynaptic component. The monosynaptic EPSP can be isolated by the use of conditioning LOT shocks to block the IPSP and disynaptic EPSP. The disynaptic EPSP can be demonstrated by cutting LOT fibers at the surface of the cortex to eliminate the monosynaptic EPSP and by the use of bicuculline to block the IPSP. The latency of the IPSP is sufficiently brief so that the disynaptic EPSP is blocked at presumed intrasomatic recording sites unless these experimental manipulations are carried out. In all histologically verified pyramidal cells in both layers II and III in which the appropriate tests were carried out, both mono- and disynaptic EPSP components were present. It was concluded on the basis of anatomical considerations, however, that a small number of pyramidal cells would be expected to receive only a disynaptic EPSP. Evidence that the LOT-evoked disynaptic EPSP is mediated, at least in part, by association axons was provided by direct stimulation of these fibers in layer III and by demonstrating that the EPSP is present distal to cuts that sever LOT axons. Direct stimulation of association axons in layer III evokes both a monosynaptic EPSP and a disynaptic IPSP in pyramidal cells at similar latencies. This IPSP is indistinguishable in properties from that evoked by LOT stimulation. Indirect evidence indicates that it is mediated via both feedforward and feedback mechanisms. In most neurons the association fiber-evoked EPSP is masked by the IPSP in response to single deep shocks but can be demonstrated by blocking the IPSP with a preceding LOT shock or by application of bicuculline. Intracellular injection of horseradish peroxidase (HRP) revealed that pyramidal cell axons give rise to an extensive system of local collaterals with a large number of synaptic terminal-like swellings in layer III. It is postulated that these collaterals synapse on both pyramidal and nonpyramidal cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Bursting-induced epileptiform EPSPs in slices of piriform cortex are generated by deep cells.

Previous study revealed that bursting activity generated by a variety of means in slices of piriform cortex induces persistent epileptiform EPSPs in superficial pyramidal cells by an NMDA-dependent process. The present study was undertaken to test the hypothesis that the observed epileptiform EPSPs in superficial pyramidal cells are driven by deep cells. This hypothesis was suggested by recent findings from in vitro studies of the properties of deep cells and in vivo studies indicating that the deep part of the piriform cortex or neighboring deep structures are involved in the generation of seizure activity in animal models of epilepsy. Results from simultaneous cell-pair recordings, examination of subdivided slices, and local application of excitatory and inhibitory agents provided strong evidence in support of this hypothesis. It was concluded that the endopiriform nucleus, a collection of cells immediately deep to the piriform cortex, plays a central role in generation, but that cells in the deep part of layer III and the claustrum may also contribute. Furthermore, it was found that generation of prolonged ictal-like activity only occurs in slices of piriform cortex in which the endopiriform nucleus is present. Implications of these findings for epileptogenesis are discussed.

Animals↗
PubMed2002

Learning and memory of cue-reward association meaning by modifications of synaptic efficacy in dentate gyrus and piriform cortex.

This article begins with a review of recent experiments investigating the synaptic efficacy changes occurring in rat dentate gyrus and piriform cortex during an associative olfactory task. In all these experiments, animals were trained to discriminate among an artificial cue, a patterned electrical stimulation distributed to the lateral olfactory tract associated with a water reward, and a natural odor associated with a flash of light. Monosynaptic field potential responses evoked by single electrical stimuli to the lateral olfactory tract were recorded in the ipsilateral piriform cortex before and just after each training session. Monosynaptic field and polysynaptic field potentials evoked by single electrical stimuli applied respectively to the lateral perforant pathway and lateral olfactory tract were also recorded in ipsilateral dentate gyrus. The results showed an increase in synaptic efficacy subsequent to the first training session in the dentate gyrus network when compared with piriform cortex at the later stage of the learning. The early increase of monosynaptic response in the dentate gyrus was observed immediately after the first learning session but disappeared 24 h later. Inversely, a synaptic depression developed across sessions, becoming significant at the onset of the last (fifth) session. The polysynaptic potential recorded in this structure increased substantially when rats began to discriminate the leaming cues, usually after the second or third learning session. Then, from the third to the fifth session, an LTP like-phenomenon appeared in piriform cortex when rats perfectly mastered the associations. Experiments using high-frequency stimulation to prevent changes in gyrus dentatus indicated that the onset of the observed depression was necessary for the learning of the olfactory associations. The fact that hippocampal and cortical neuronal networks exhibited different timing in synaptic efficacy changes could physiologically explain learning and memory processes.

Animals↗
PubMed2002

PSA-NCAM expression in the piriform cortex of the adult rat. Modulation by NMDA receptor antagonist administration.

Administration of NMDA receptor antagonists upregulates the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) in the adult hippocampus. Since the piriform cortex is also populated by PSA-NCAM immunoreactive neurons during adulthood, we sought to characterize them in detail and to test whether NMDA receptor antagonists also modulate PSA-NCAM in this cortical region. PSA-NCAM immunoreactivity is located mainly in layer II, where many neurogliaform and some pyramidal-semilunar transitional neurons are labeled. Many large neurons in layer III and endopiriform nucleus also express PSA-NCAM. Interestingly, some small labeled cells resembling migratory neuroblasts appear in these layers and in the ventral end of the corpus callosum subjacent to the piriform cortex. These putative migratory cells and some neurogliaform neurons in layer II do not express NeuN, a marker of differentiated neurons. Many of these PSA-NCAM immunoreactive cells also express doublecortin, a molecule involved in neuronal migration. The number of PSA-NCAM immunoreactive neurogliaform neurons increases significantly 7 days after the administration of an NMDA receptor antagonist. Moreover, 21 days after the treatment we observe a significant increase in the number of doublecortin expressing cells in the deep layers of the piriform cortex. These results expand the current knowledge of the neuronal populations expressing PSA-NCAM in the piriform cortex, suggesting that some of these cells could be involved in structural plastic events such as axonal outgrowth, synaptogenesis or even neuronal migration. Similar to the hippocampus, NMDA receptors appear to play a critical role in these processes in the adult piriform cortex.

Animals↗
PubMed1999

Essential amino acids affect interstitial dopamine metabolites in the anterior piriform cortex of rats.

The anterior piriform cortex (APC) is essential for the anorectic reactions to an amino acid-imbalanced diet, and it also responds to repletion of the limiting amino acid. In the present study, we examine the dynamic changes of the interstitial dopamine metabolites in the APC following feeding of either an amino acid-corrected or -imbalanced diet. Microdialysates, collected from the APC, were analyzed using HPLC with electrochemical detection. The concentrations were 19.7 +/- 4.8 microg/L for 3, 4-dyhydroxyphenylacetic acid and 25.1 +/- 4.4 microg/L for homovanillic acid, respectively, in the baseline dialysates. After diet treatments, no significant changes occurred in 3, 4-dyhydroxyphenylacetic acid in the corrected (n = 7) or imbalanced (n = 9) groups vs. the basal group (n = 7). However, after feeding the threonine-corrected diet, the concentration of homovanillic acid was significantly less (P < 0.01) than after the basal and imbalanced diets. The homovanillic acid level in the corrected group was already significantly lower than in the basal group by 20 min (P < 0.05), and reached its lowest level at 70 min (P < 0.05). The concentrations of homovanillic acid in the corrected group remained at this low level until the end of the experiment. The present results introduce the idea that the dopaminergic system is involved in the feeding responses to essential amino acid repletion.

3,4-Dihydroxyphenylacetic Acid↗