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PubMed1990

Role of NMDA and non-NMDA receptors in synaptic transmission in rat piriform cortex.

The pharmacology of synaptic transmission was studied in slices of rat piriform cortex using the selective non-NMDA glutamate receptor antagonist 6.7-dinitroquinoxaline-2,3-dione (DNQX) and the selective NMDA receptor antagonist D-2-amino-5-phosphonopentanoate (D-AP5). DNQX produced a dose-dependent blockade of synaptic transmission at both lateral olfactory tract and associational system synapses with half-maximal effects at about 2.5 microM. D-AP5 had no significant effects on field potentials recorded in medium containing 2.5 mM Mg++. However in low Mg++ (100-200 microM) medium, D-AP5 did reduce a slow component of postsynaptic responses in both synaptic systems. In Mg(++)-free medium, 20 microM DNQX did not completely block transmission; the remaining response components were blocked by D-AP5. These results suggest that normal synaptic transmission in the two main inputs to the superficial layers of piriform cortex is mediated by non-NMDA receptors but that NMDA receptors can also participate under conditions where the Mg++ block of the NMDA channel is alleviated.

2-Amino-5-phosphonovalerate↗

PubMed1982

Systemic injection of kainic acid: effect on neurotransmitter markers in piriform cortex, amygdaloid complex and hippocampus and protection by cortical lesioning and anticonvulsants.

Systemic injection of kainic acid (12 mg/kg) in rats induces a well established pattern of neuronal lesions in different brain regions. These lesions are accompanied by changes in neurotransmitter markers. In the piriform cortex and amygdaloid complex, the kainic acid lesion was accompanied by a reduction in the high affinity uptake of glutamate and in the activities of glutamate decarboxylase and choline acetyltransferase, whereas in the hippocampus there was a reduction in the high affinity uptake of glutamate and in glutamate decarboxylase activity. Hemidecortication, hemitransection, a caudal knife cut in the cortex, or treatment with diazepam, all protected against the effects of kainic acid in the piriform cortex and amygdaloid complex but not in the hippocampus. Diphenylhydantoin had no effect on the neurotoxicity of kainic acid. The results indicate that the neurotoxic effects of kainic acid in the piriform cortex and amygdala are dependent on an intact cortical structure, probably due to a dependence on specific excitatory circuitry. The neurons involved may be glutamergic/aspartergic.

Afferent Pathways↗

PubMed1995

Strong induction of c-fos in the piriform cortex during focal seizures evoked from different limbic brain sites.

Focal seizures in rats were elicited by electrical stimulation (using parameters necessary for induction of kindling) of the amygdala or two different sites of the piriform cortex, including the previously described 'area tempestas' [26]. Although seizures were behaviorally and electrophysiologically identical, a different pattern of induction of the proto-oncogene c-fos was found. Only the ipsilateral piriform cortex showed strong immunohistochemical labeling of Fos protein, regardless of stimulation site, while the hippocampus was not labeled after focal seizures. It is concluded that the piriform cortex is the epileptogenic focus of limbic seizures, at least during the first stages of electrical kindling.

Animals↗

PubMed1998

Glutamate-like immunoreactivity in axon terminals from the olfactory bulb to the piriform cortex.

A highly specific anti-glutamate monoclonal antibody, mAb2D7, was used together with light and electron microscopy to elucidate the role played by the amino acid glutamate in the projection from the olfactory bulb to the piriform cortex in the rat. By light microscopy, glutamate-like immunoreactivity was observed in neuronal cell bodies and in the neuropil of the piriform cortex. Double labelling experiments which involved injections of wheat germ agglutinin-horse--radish peroxidase into the olfactory bulb and a post-embedding immunogold method for electron microscopy revealed anterogradely labelled terminals making asymmetric synaptic contacts on dendrites in the piriform cortex which contained high levels of glutamate as assessed by quantification. These results further support a role for glutamate as a neurotransmitter in the efferent pathway of the rat olfactory bulb.

Animals↗

PubMed1994

Repeated electroconvulsive shock selectively increases the expression of the neuron specific enolase in piriform cortex.

The effect of repeated electroconvulsive shock (ECS) on the activities of the three enolase isoenzymes present in rat brain: neuron specific enolase (NSE), non-neuronal enolase (NNE) and the hybrid enolase was investigated in piriform cortex. The activities were estimated on isoenzymes separated by agarose gel electrophoresis. Whereas the specific activities of NNE and hybrid enolase were unchanged in piriform cortex or ECS-treated rats the specific activity of NSE was increased by 16.3 percent (P < 0.02). The brain enolase isoenzymes are dimers of alpha- and gamma-enolase subunits. The calculated ratio between the gamma-subunit present in both NSE and hybrid enolase and the alpha-subunits present in both NNE and hybrid enolase was increased by 11.7 percent in piriform cortex of ECS-treated rats (P < 0.05). Previously, it has been shown that the gamma-subunit is only expressed in neurons whereas the alpha-subunit is expressed in both neurons and glial cells. The selectively increased expression of the enolase gamma-subunit in ECS-treated rats might either reflect an increased transcription of a whole group of neuronal genes or rather the trophic role of NSE in ECS-enhanced synaptic remodelling of the rat brain.

Animals↗

PubMed2000

Chronic exposure to ethanol alters GABA(A) receptor-mediated responses of layer II pyramidal cells in adult rat piriform cortex.

This study examined the effect of chronic exposure to ethanol on gamma-aminobutyric acid type-A (GABA(A)) receptor-mediated responses of layer II pyramidal neurons of the piriform cortex. Slices containing the piriform cortex were derived from pair-fed adult rats maintained on ethanol-supplemented or control liquid diet for 30 days. Responses of identified layer II pyramidal neurons to exogenously applied GABA were monitored by whole-cell patch-clamp recording. Chronic exposure to ethanol resulted in a rightward shift in the EC(50) of GABA and a decrease in the amplitude of maximal GABA response. GABA-induced responses were modulated by acutely applied ethanol (10-100 mM) in both chronic ethanol-treated and control groups. No significant difference was found in the average change in GABA response, suggesting that tolerance to acute ethanol exposure did not develop. When the modulatory responses of individual cells were classified and grouped as either being attenuating, potentiating, or having no effect, the incidence of potentiation in the ethanol-treated group was significantly higher. Consistent with the absence of tolerance to acute ethanol, cross-tolerance to diazepam was not observed following 30 days of treatment with ethanol. These results are discussed in light of regionally specific effects of chronic ethanol treatment on GABA(A) receptor-mediated responses of layer II piriform cortical neurons.

Age Factors↗

PubMed1994

Excitation of interneurons in piriform cortex by 5-hydroxytryptamine: blockade by MDL 100,907, a highly selective 5-HT2A receptor antagonist.

Electrophysiological studies have suggested that a subpopulation of interneurons near the border of layer II and III in rat piriform cortex are excited by serotonin (5-hydroxytryptamine; 5-HT) via 5-HT2A (formerly 5-HT2) rather than 5-HT2C (formerly 5-HT1C) receptors. However, the pharmacological agents used in those studies were limited in specificity. In the present study, we tested a new, highly selective 5-HT2A receptor antagonist MDL 100,907 (R-(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl-ethyl)]-4- piperidine-methanol, which has a 300-fold greater affinity for 5-HT2A than 5-HT1C receptors or alpha 1-adrenoceptors) on excitatory responses of interneurons to 5-HT in rat piriform cortex slices. We observed a parallel, reversible rightward shift in the 5-HT concentration-response curve in the presence of 1-10 nM concentrations of MDL 100,907. Schild regression analysis resulted in a slope of 1.13 and a Kd value of 1.17 which is close to the published Ki value of 0.36 for MDL 100,907. These data confirm that 5-HT2A rather than 5-HT2C receptors mediate excitation by 5-HT of interneurons in the piriform cortex. Because of its rapid equilibration and reversibility, MDL 100,907 appears to be an excellent tool for studies of 5-HT2A receptor function in the brain.

Animals↗

PubMed1998

Role of the net architecture in piriform cortex activity: analysis by a mathematical model.

We present a mathematical analysis of the piriform cortex activity in rats. Experimental data were obtained by means of optical recording of fluorescent signals driven by neuronal activity. From these data, we determined the numerical value of the relaxation time for the pyramidal cell activity in layers II and III and the time latency map for bulb activation. Our model for the piriform cortex is based on pairs of excitatory and inhibitory neurons which correspond to pyramidal cells of layers II and III and to their inhibitory associated interneurons respectively; pyramidal cells are also interconnected through short and long range association fiber systems. Under such conditions, the model outputs resemble closely the experimental observations: (1) a double-bumped response to a strong and short stimulation; (2) oscillatory behavior under weak sustained stimulation conditions; (3) propagation of traveling activity waves; and (4) pacemaker activity when clusters of neurons are preferentially coupled.

Animals↗

PubMed2001

Receptive fields in the rat piriform cortex.

Current models of odor discrimination in mammals involve molecular feature detection by a large family of diverse olfactory receptors, refinement of molecular feature extraction through precise projections of olfactory receptor neurons to the olfactory bulb to form an odor-specific spatial map of molecular features across glomerular layer, and synthesis of these features into odor objects within the piriform cortex. This review describes our recent work on odor and spatial receptive fields within the anterior piriform cortex and compares these fields with receptive fields of their primary afferent, olfactory bulb mitral/tufted cells. The results suggest that receptive fields in the piriform cortex are ensemble in nature, highly dynamic, and may contribute to odor discrimination and odor memory.

Animals↗

PubMed1999

Reduced synaptic facilitation between pyramidal neurons in the piriform cortex after odor learning.

Learning-related cellular modifications were studied in the rat piriform cortex after operand conditioning. Rats were trained to discriminate positive cues in pairs of odors. In one experimental paradigm, rats were trained to memorize 35-50 pairs of odors ("extensive training"). In another paradigm, training was continued only until rats acquired the rule of the task, usually after learning the first two pairs of odors ("short training"). "Pseudotrained" and "naive" rats served as controls. We have previously shown that "rule learning" of this task was accompanied by reduced spike afterhyperpolarization in pyramidal neurons in brain slices of the piriform cortex. In the present study, synaptic inputs to the same cells were examined. Pairs of electrical stimuli applied to the intrinsic fibers that interconnect layer II pyramidal neurons revealed significant reduction in paired-pulse facilitation (PPF) in this pathway even after short training. PPF in shortly trained rats was reduced to the same extent as in extensively trained rats. PPF reduction did not result from modification of membrane properties in the postsynaptic cells, change in postsynaptic inhibition, or impairment of the facilitation mechanism. Extracellular field potential recordings showed enhanced synaptic transmission in these synapses. The reduction in PPF became apparent only 3 d after task acquisition and returned to control value 5 d later. PPF evoked by stimulating the afferent fibers to the same neurons was increased 1 d after training for 2 d. We suggest that the transient enhancement in connectivity in the intrinsic pathway is related to the enhanced learning capability and not to memory for specific odors, which lasts for weeks.

Afferent Pathways↗

PubMed2003

Rapid, experience-induced enhancement in odorant discrimination by anterior piriform cortex neurons.

Current views of odorant discrimination by the mammalian olfactory system suggest that the piriform cortex serves as a site of odor object synthesis. Given the enormous number of odorant feature combinations possible in nature, however, it seems unlikely that cortical synthetic receptive fields (RFs) are innate but rather require experience for their formation. The present experiment addressed two issues. First, we made a direct comparison of mitral/tufted cell and anterior piriform cortex (aPCX) neuron abilities to discriminate odorant mixtures from their components to further test whether aPCX neurons can treat collections of features different from the features themselves (synthetic coding). Second, we attempted to determine the minimum duration of experience necessary for formation of cortical synthetic RFs. Single-unit recordings were made from mitral/tufted cells and aPCX layer II/III neurons in urethan-anesthetized rats. Cross-habituation between novel binary mixtures and their novel components was used to determine odor discrimination abilities. The results suggest that after >/=50 s of experience with a binary mixture, aPCX neurons can discriminate the mixture from its components, whereas mitral/tufted cells cannot. However, when limited to 10 s of experience with the mixture, aPCX neurons appear similar to mitral/tufted cells and do not discriminate mixtures from components. These results suggest experience-dependent synthetic processing in aPCX and suggest an important role for perceptual learning in normal odor discrimination.

Action Potentials↗

PubMed1994

Serotonin2 receptor-mediated excitation of interneurons in piriform cortex: antagonism by atypical antipsychotic drugs.

Rat piriform cortex contains a subpopulation of presumed GABAergic interneurons located near the border of layers 2 and 3 that express excitatory serotonin2 receptors. These serotonin2-responsive interneurons send axons to layer 2 pyramidal cells. Using an in vitro brain slice preparation, serotonin2 receptor-mediated excitation can be assessed either by directly recording from the interneurons or by recording the increase in inhibitory postsynaptic potentials in the pyramidal cells. Intracellular recordings from the interneurons demonstrated that compared to pyramidal cells they had a more depolarized resting membrane potential, a higher input resistance and shorter action potential duration. The serotonin2 receptor-mediated excitation was associated with a strong depolarization (range 3-22 mV). We found that the atypical antipsychotic drugs, risperidone and clozapine, which have relatively high affinity for serotonin2 receptors, each dose-dependently inhibited the serotonin2-mediated excitation of the interneurons with IC50 values of 7 nM and 1.4 microM, respectively. This antagonism was specific to the extent that excitation mediated by agonists at excitatory amino acid receptors were not blocked at concentrations of risperidone and clozapine that completely antagonized the serotonin2 receptor-mediated excitation. The typical antipsychotic drug, chlorpromazine, inhibited the serotonin2-mediated excitation of the interneurons with an IC50 of 14 microM. Haloperidol, another typical antipsychotic drug, decreased the serotonin2 response to about half of baseline at a concentration of 10 microM (the exact IC50 could not be calculated because higher concentrations produced non-specific effects on cells). Both risperidone and clozapine blocked the serotonin-elicited inhibitory postsynaptic potentials in layer 2 pyramidal cells at concentrations that approximated the IC50 for antagonizing the serotonin2-mediated excitation of the interneurons. Chlorpromazine and haloperidol, in the concentration range that blocked serotonin2 receptor-mediated excitation of interneurons, also blocked the serotonin-elicited inhibitory postsynaptic potentials in the pyramidal cells. The IC50 values for risperidone and clozapine, but not for chlorpromazine or haloperidol, for blocking serotonin2 receptor-mediated actions in rodent piriform cortical slice are in the range of the plasma concentrations of the drug that are clinically efficacious. Our data suggest that a potential site of action of the atypical antipsychotic drugs risperidone and clozapine could be antagonism of serotonin acting through serotonin2 receptors on GABAergic interneurons in cerebral cortex.

Action Potentials↗

PubMed2003

[Neuronal structure of piriform cortex of anterior amygdaloid body of the rat brain].

The cytoarchitecture and neuronal organization were studied in piriform cortex at rostral and caudal levels of anterior amygdaloid body using the methods of Nissl and Golgi. The division of the piriform cortex into several areas is proposed, including basal area (area basalis), lateral area (area lateralis), and transitional, or terminal area (area terminalis), bordering the insular cortex. It is recommended to subdivide the lateral area into two subareas, L1 and L2. All the areas defined differ in their neuroarchitecture, structure of the layers and neuronal composition.

Amygdala↗

PubMed2004

Bilateral microinjections of vigabatrin in the central piriform cortex retard amygdala kindling in rats.

The piriform cortex (PC) is the largest region of the mammalian olfactory cortex with strong connections to limbic structures, including the amygdala, hippocampus, and entorhinal cortex. Various previous studies in rodents suggest that the PC might be very important in the development and maintenance of limbic kindling, i.e. a widely used model of temporal lobe epilepsy. GABAergic inhibition in the transition zone between the anterior and posterior PC, termed here central PC, seems to be particularly involved in the processes leading to progression of kindled seizures. This prompted us to study whether elevation of GABA levels in this subregion of the PC by bilateral microinjection of vigabatrin is capable of suppressing amygdala kindling. Rats were stimulated once daily until fully kindled (stage 5) seizures had developed. Vigabatrin (10 microg) was injected 24 h before the first stimulation as well as 6 h before the 5th and 10th stimulation, which approximately doubled the number of stimulations required for kindling development compared with controls. This marked retardation of kindling acquisition was predominantly due to a significant inhibition of the progression from stage 1 to stage 2 and stage 3 to stage 4 seizures, demonstrating that microinjection of vigabatrin into the central PC markedly inhibits the progression and secondary generalization of focal seizures emanating from the amygdala.

Amygdala↗

PubMed2000

Development of kindling and spontaneous seizures after massed stimulation of different loci in the rat piriform cortex.

Massed electrical stimulation of the anterior piriform cortex (PC) in rats using short (5 min) interstimulus intervals has previously been reported to induce severe chronic epilepsy with spontaneous seizures and has thus proposed to represent a novel model of temporal lobe epilepsy. In the present study, we used this stimulation protocol to evaluate the frequency and severity of recurrent spontaneous seizures produced in this way. In addition to the locus in the anterior PC previously used for massed stimulation (MS), we also stimulated rats via a locus in the transition zone between anterior and posterior PC ("central PC"), which previously was found to be more sensitive to electrical stimulation than various other loci in the anterior or posterior PC. During MS (71 stimulations for 1 s each at twice afterdischarge threshold), focal and infrequent secondary generalized seizures occurred in both groups, but there was no consistent progressive increase in seizure severity with increasing number of seizures, possibly as a result of postictal inhibitory processes. Following MS, rats were restimulated after 1, 2, 4, and 7 weeks, using five stimuli at 5-min interstimulus periods at each retest period. In both PC-implanted groups, seizure severity and seizure duration progressively increased over the period of the retests, indicating a delayed development of kindling. Spontaneous seizures were only observed rarely, so that MS of the PC is certainly no effective means of producing recurrent spontaneous seizures.

Animals↗

PubMed2002

Secondary generalization of hippocampal kindled seizures in rats: examining the role of the piriform cortex.

A primary feature of epilepsy is the potential for focal seizures to recruit distant structures and generalize into convulsions. Key to understanding generalization is to identify critical structures facilitating the transition from focal to generalized seizures. In kindling, development of a primary site leads progressively to secondarily generalized convulsions. In addition, subsequent kindling of a secondary site results in rapid kindling from that site, presumably because of its facilitated access to the primary kindled network. Here, we investigated the role of the piriform cortex in convulsive generalization from a secondary site kindled in the hippocampus after primary site amygdala kindling. In a necessarily complicated design, rats initially experienced forebrain commissurotomy to lateralize the experiment to one hemisphere. Then the amygdala was kindled and, 3 weeks later, it was electrically-triggered into status epilepticus, which destroyed the ipsilateral piriform cortex. This experience occurred several days before secondary site kindling of the dorsal hippocampus. In rats with complete piriform cortex loss, there was no disruption in kindling or convulsive seizure expression from the hippocampus. However, when damage also involved parts of the perirhinal, insular and entorhinal cortices, convulsive expression was blocked. Although other evidence suggests that piriform lesions affect generalization of primary site kindling, the present study shows that they do not alter secondary site kindling in the dorsal hippocampus. The additional involvement of parahippocampal cortical areas in convulsive expression suggests an important functional association between these cortical regions and the hippocampus in seizure propagation and clinical expression.

Amygdala↗

PubMed1991

Kindling-induced potentiation in the piriform cortex.

At intensities sufficient to induce epileptiform afterdischarges, repeated electrical stimulation of limbic structures can lead to the development of permanent increases in the strength of the epileptiform response (kindling). Field potentials evoked by pulse stimulation are also increased in amplitude in a number of forebrain pathways following kindling. This kindling-induced potentiation effect is similar in many respects to the 'long-term potentiation' (LTP) effect which is produced by non-epileptogenic stimulation. There are, however, some interesting differences. For example, kindling-induced potentiation can far outlast LTP. In these experiments, we attempted to determine the longevity of the kindling-induced potentiation of the response evoked in the piriform cortex by olfactory bulb stimulation, following olfactory bulb kindling. This system was targeted because both the olfactory bulb and the piriform cortex are highly reactive kindling sites. In addition, we used the paired pulse technique to monitor facilitation and inhibition in this system. Kindling was found to induce a potentiation in the piriform field potential that lasted for at least 3 months (the period of the experiment) with little or no decay. Kindling also produced a decrease in paired pulse facilitation. In some animals the net facilitation was changed to a net depression. These results are consistent with the interpretation that kindling produces an increase in recurrent inhibition in the piriform cortex. The paired pulse measures, however, returned to near baseline levels over the 3-month test period.

Animals↗

PubMed1994

Signal propagation from piriform cortex to the endopiriform nucleus in vitro revealed by optical imaging.

Optical signals were recorded from the posterior piriform cortex slices of guinea pigs stained with a voltage-sensitive dye to analyse spatio-temporal spread of neural activity evoked by electrical stimulation of afferent fibers. After propagation of activity along layers II and III, an isolated island of activity appeared deep to the layer III and moved caudally. Histological inspection revealed that the area where the island appeared corresponded well to the endopiriform nucleus. The present results provided an evidence for one of the main outflows of olfactory information from the posterior piriform cortex.

Animals↗