Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Piriform Cortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1997

Immunolocalization of metabotropic glutamate receptor 7 in the rat olfactory bulb.

Metabotropic glutamate receptors (mGluRs) constitute a large family of G-protein-coupled receptors that are subdivided into three groups based on sequence similarity, pharmacological profiles, and coupling to second messengers. Although mRNAs for seven of the eight mGluRs are expressed in the olfactory system, the localization and function of specific subtypes have not been fully characterized. Mitral cells of the olfactory bulb express mRNA for several mGluRs, including mGluR7, which has been suggested as a presynaptic glutamate autoreceptor. To investigate the immunolocalization of mGluR7 in the olfactory system, we used a polyclonal antiserum specific for the carboxy terminus of the receptor. Mitral cell somata and proximal dendrites were strongly labeled by the mGluR7 antibody. Electron microscopic analysis revealed that most of the mitral cell somatic staining was cytoplasmic. In olfactory bulb glomeruli, immunoreactivity was present in axons and dendrites. In the piriform cortex, diffuse staining was present in layer Ia that was markedly reduced following bulbectomy, consistent with expression of mGluR7 in mitral cell axon terminals. Electron microscopic analysis of this region confirmed the presence of mGluR7 in multiple axon terminals. Distinct labeled fibers in all levels of layer I appeared to originate from labeled piriform cortex pyramidal cells in layers II and III. Our results indicate that mGluR7 is primarily presynaptic at olfactory bulb synapses. However, the postsynaptic localization of mGluR7 at selected synapses indicates that mGluR7 is not targeted exclusively to axonal compartments.

Animals↗
PubMed2005

Transient and widespread astroglial activation in the brain after a striatal 6-OHDA-induced partial lesion of the nigrostriatal system.

The authors have previously described astroglial activation in the ipsilateral nigrostriatal system and ventral tegmental area following small doses of 6-hydroxydopamine (6-OHDA) injected unilaterally in the striatum. This article further evaluated astroglial reactivity in several brain regions after striatal 6-OHDA-induced punctate lesion in the nigrostriatal pathway. Adult male Wistar rats received a unilateral stereotaxical injection of the 6-OHDA (8 microg/4 microl) in the neostriatum and sacrificed 1 or 3 weeks later. Control animals received only solvent. Immunohistochemistry was employed for visualization of the tyrosine hydroxylase (TH), marker for dopamine cells, and glial fibrillary acidic protein (GFAP), marker for astrocytes. TH immunoreactive terminals disappeared in the striatum close to the injection site and a disappearance of a small number of a defined population of dopamine cell bodies was observed in the ipsilateral pars compacta of the substantia nigra (SNc). No dopamine lesion was detected in the contralateral nigrostriatal pathway. Astroglial reaction was seen close to the lesion in the neostriatum and in the ipsilateral SNc of the 1 week 6-OHDA lesioned rats. Specific stereological tools employing point intercepts and rotator, revealed an increased presence of reactive astrocytes in many forebrain regions like frontal, parietal and piriform cortex, septum, neostriatum and SNc, bilaterally, and also corpus callosum after 1 week of 6-OHDA injection. The astroglial activation was characterized by increases in the size of the cell body and/or processes. Astrocytic reaction was found only in the ipsilateral nigrostriatal pathway by 3 weeks of 6-OHDA, a slight activation also remaining in the ipsilateral septum and piriform cortex. Astrocytic reaction was seen in the solvent-injected rats only in the neostriatum close to the needle track. The transient widespread astroglial reaction observed in many brain regions following a striatal injection of 6-OHDA may represent a global paracrine trophic response in the brain.

Animals↗
PubMed1993

Regulation of brain-derived neurotrophic factor messenger RNA and protein at the cellular level in pentylenetetrazol-induced epileptic seizures.

We have examined the effects of pentylenetetrazol-induced epileptic seizures on brain-derived neurotrophic factor messenger RNA and protein and on the messenger RNA of its receptor in the rat. Pentylenetrazol, which acts at the picrotoxin recognition site of the GABAA receptor, was injected intraperitoneally and induced seizures by decreasing the inhibitory GABAergic activity. The effects of a single acute convulsive dose (50 mg/kg) of pentylenetetrazol were analysed at different time points by in situ hybridization or immunohistochemistry. Kindling was induced by daily subconvulsive injections (30 mg/kg) of pentylenetetrazol. At different time points during the kindling process, the messenger RNAs of brain-derived neurotrophic factor and trkB and the protein levels of brain-derived neurotrophic factor were analysed. We showed that brain-derived neurotrophic factor messenger RNA dramatically increased in neurons of the granule cell layer, piriform cortex and amygdala 3 h but not 6 h after an acute high dose of pentylenetetrazol, while brain-derived neurotrophic factor-like immunoreactivity was decreased in the granule cell layer and neurons of the hilus. The trkB messenger RNA was similarly increased 3 h and 6 h after the injection and returned to control levels after 24 h. The first change during the kindling development was seen after the first severe seizure: brain-derived neurotrophic factor messenger RNA was markedly increased in the piriform cortex and amygdala but not in the hippocampus. In fully kindled rats, which had several severe seizures, brain-derived neurotrophic factor messenger RNA and trkB messenger RNA were unaffected 3 h and 24 h after the last pentylenetetrazol injection. However, brain-derived neurotrophic factor-like immunoreactivity was markedly increased in the hippocampal formation 3 h, 24 h and three days after the last pentylenetetrazol injection, and still increased after 10 days. These results suggest that brain-derived neurotrophic factor may be involved in protection mechanisms after damage during seizures and in sprouting responses. The piriform cortex/amygdala seems to be an area of origin for the kindling development.

Amino Acid Sequence↗
PubMed1999

Hypoxia preconditioning attenuates brain edema associated with kainic acid-induced status epilepticus in rats.

Kainic acid (KA)-induced seizures elicit edema associated with necrosis in susceptible brain regions (e.g., piriform cortex and hippocampal CA1 and CA3 regions). To test the hypothesis that hypoxia preconditioning protects against KA-induced edema formation, adult male rats were exposed to a 9% O2, 91% N2 atmosphere for 8 h. KA (14 mg/kg, i.p.) was administered 1, 3, 7, or 14 days later. Regional analysis of edema indicated that hypoxia exposure attenuated edema formation in piriform and frontal cortices and hippocampus when KA was given 1, 3, or 7 days later but not 14 days after hypoxia. Cycloheximide (2 mg/kg s.c.) given 1 h prior to hypoxia prevented the protective effect of hypoxia on KA-induced edema attenuation in the piriform cortex and hippocampus. Thus, hypoxic challenge induces a general adaptive response that protects against the seizure-associated pathophysiology, with no direct relationship to seizure intensity. This response may involve stress-related transcription factors and effector proteins.

Animals↗
PubMed2002

Cognitive deficits and CNS damage after a 4-day binge ethanol exposure in rats.

Impairments of learning and memory are common neuropsychological sequelae of chronic alcohol abuse. Alcoholics often have impairments of anterograde memory, including spatial memory dysfunction, and a tendency toward response perseveration. This study was designed to assess the effects of binge ethanol exposure on neurodegeneration and cognitive function. Rats were given ethanol three times daily for 4 days. Silver staining revealed neurodegeneration in the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and dentate gyrus. After withdrawal, behavioral testing in the Morris water maze revealed significant differences in reversal learning between treatment groups. Ethanol-treated animals required more trials to learn the reversal task, entered the previously trained quadrant more often, and spent more time there than controls. [3H]PK-11195 binding, an index of CNS damage, was elevated in the piriform cortex of ethanol-treated animals. Thus, binge ethanol exposure resulted in neurodegeneration of a corticolimbic circuit with common excitatory inputs from the olfactory bulb and was associated with perseverative responding on a spatial learning task. These studies suggest that a single binge drinking episode could cause neurodegeneration and cognitive dysfunction in humans. The perseverative nature of the behavioral deficit could be related to both cognitive dysfunction and the behavioral components of the addiction process.

Animals↗
PubMed1990

Soman- or kainic acid-induced convulsions decrease muscarinic receptors but not benzodiazepine receptors.

[3H]Quinuclidinyl benzilate (QNB) binding to muscarinic receptors decreased in the rat forebrain after convulsions induced by a single dose of either soman, a potent inhibitor of acetylcholinesterase, or kainic acid, an excitotoxin. A Rosenthal plot revealed that the receptors decreased in number rather than affinity. When the soman-induced convulsions were blocked, the decrease in muscarinic receptors at 3 days was less extensive than when convulsions occurred and at 10 days they approached control levels in most of the brain areas. The most prominent decrements in QNB binding were in the piriform cortex where the decline in QNB binding is probably related to the extensive convulsion-associated neuropathology. The decrements in QNB binding after convulsions suggest that the convulsive state leads to a down-regulation of muscarinic receptors in some brain areas. In contrast to the decrease in QNB binding after convulsions, [3H]flunitrazepam binding to benzodiazepine receptors did not change even in the piriform cortex where the loss in muscarinic receptors was most prominent. Thus, it appears that those neuronal processes that bear muscarinic receptors are more vulnerable to convulsion-induced change than those with benzodiazepine receptors.

Animals↗
PubMed2001

Doublecortin expression in the adult rat telencephalon.

Doublecortin (DCX) is a protein required for normal neuronal migration in the developing cerebral cortex, where it is widely expressed in both radially and tangentially migrating neuroblasts. Moreover, it has been observed in the adult rostral migratory stream, which contains the neuronal precursors traveling to the olfactory bulb. We have performed DCX immunocytochemistry in the adult rat brain to identify precisely the neuronal populations expressing this protein. Our observations confirm the presence of DCX immunoreactive cells with the characteristic morphology of migrating neuroblasts in the subventricular zone, rostral migratory stream and the main and accessory olfactory bulbs. We have also found putative migratory cells expressing DCX in regions were no adult neuronal migration has been described, as the corpus callosum, the piriform cortex layer III/endopiriform nucleus and the striatum. Surprisingly, many cells with the phenotype of differentiated neurons were DCX immunoreactive; e.g. certain granule neurons in the hilar border of the granular layer of the dentate gyrus, some neuronal types in the piriform cortex layer II, granule and periglomerular neurons in the main and accessory olfactory bulbs, and isolated cells in the striatum. Almost all DCX immunoreactive cells also express the polysialylated form of neural cell adhesion molecule and have a similar distribution to rat collapsin receptor-mediated protein-4, two molecules involved in neuronal structural plasticity. Given these results, we hypothesize that DCX expression in differentiated neurons could be related to its capacity for microtubule reorganization and that this fact could be linked to axonal outgrowth or synaptogenesis.

Aging↗
PubMed2006

Fiber connections of the compact division of the posterior pallial amygdala and lateral part of the bed nucleus of the stria terminalis in the pigeon (Columba livia).

The compact division of the posterior pallial amygdala (PoAc) and lateral part of the bed nucleus of the stria terminalis (BSTL) are components of the limbic system in the pigeon brain. In this study, we examined the position and fiber connections of these two nuclei by using Nissl staining and tract-tracing methods. PoAc occupies a central division in the posterior pallial amygdala. BSTL faces the ventral horn of the lateral ventricle and extends between A 7.25 and A 10.50. PoAc and BSTL connect bidirectionally by the stria terminalis. PoAc connects reciprocally with two nuclear groups in the cerebrum: 1) a continuum consisting of the caudoventral nidopallium, lateral part of the caudoventral nidopallium (NCVl), subnidopallium beneath NCVl, and piriform cortex and 2) rostral areas of the hemisphere, including the frontolateral and frontomedial nidopallium and the densocellular part of the hyperpallium. Extratelencephalic projections of PoAc terminate in the dorsomedial thalamic nuclei and reach the lateral hypothalamic area via the hypothalamic part of the occipito-mesencephalic tract. BSTL also connects reciprocally with two main regions: 1) the same continuum as for PoAc projections, except the piriform cortex and 2) rostral areas of the hemisphere, including the olfactory tubercle and nucleus accumbens. Extratelencephalic reciprocal connections are with the substantia nigra, nucleus subceruleus dorsalis, parabrachial nucleus, locus coeruleus, and nucleus of the solitary tract. The dorsomedial subdivision of the hippocampal formation projects massively to PoAc and BSTL. These findings indicate that PoAc and BSTL are important components of an interconnected neural circuit involving widespread regions of the neuraxis and mediating limbic-visceral functions.

Amygdala↗
PubMed1993

Lead blocks LTP by an action not at NMDA receptors.

Exposure of children to low levels of lead results in a reduction in cognitive ability and a series of behavioral deficits. We have studied the effects of PbCl2 on long-term potentiation (LTP), the best available electrophysiologic model of learning and memory, in a rat piriform cortex brain slice preparation in order to test the hypothesis that lead neurotoxicity is a result of actions on LTP. With changes in the composition of the Krebs-Ringer solution normally used in brain slices, it is possible to keep the Pb2+ in solution at concentrations up to 10 microM. In this concentration range, Pb2+ has no effect on the synaptic response elicited in piriform cortex pyramidal neurons upon stimulation of the lateral olfactory tract. We find that Pb2+ blocks LTP by about 75% at 5 microM and completely at 10 microM. At these concentrations, Pb2+ has no effect on posttetanic potentiation. Since it has been reported that Pb2+ blocks N-methyl-D-aspartate (NMDA) responses, and NMDA blockade is known at many sites to block LTP, we studied the effects of Pb2+ on NMDA responses. In the concentration range studied there was no effect of Pb2+ on NMDA responses. The mechanism whereby Pb2+ blocks LTP remains to be determined. While the concentration of Pb2+ found to block LTP in these studies is high relative to concentrations of Pb2+ in blood that are associated with causing cognitive and behavioral effects in children, the sensitivity to Pb2+ may be greater in young animals.

Animals↗
PubMed1995

Neuronal overmaturation in dysraphism: ontogenic expression of neuropeptides in the fetal brain and developmental anomalies in exencephaly.

Starting from knowledge obtained in our previous studies of experimental dysraphism in chick embryos, the entity of neuronal overgrowth observed in exencephaly was further investigated. The ontogenic expression of neuron-specific enolase (NSE), vasoactive intestinal polypeptide (VIP), and somatostatin was analyzed both in chick exencephaly of the natural product and in normal chick fetuses by carrying out immunohistochemical studies. In normal fetuses, immunostained elements positive for NSE first appeared in the spinal gray matter on postincubation day 16 and increased in intensity during the fetal period. By postnatal day 2, the cerebral peduncle, brain stem neurofibers, molecular layer of the cerebellum, corpus striatum, and piriform cortex became immunoreactive. No immunohistochemical reaction to VIP was observed during these stages. Somatostatin-positive elements were not identified during the fetal period, except in limited regions, such as the corpus striatum, which appeared to have weakly positive staining on day 21. The exencephalic fetuses, however, demonstrated extremely advanced neuronal maturation, with intense immunoreactivity already being manifest in various regions, including the corpus striatum, piriform cortex, spinal gray matter, and brain stem nuclei, on day 16 of the fetal period. Somatostatin-positive elements also appeared at this stage in chick exencephaly, but such immunoreactivity was localized, particularly in the overgrown foci. The present study showed that the neuronal maturation process in some neurons of exencephalic brain and spinal cord was definitely further advanced than that in normal controls. A possible clinical application of NSE and somatostatin measurement as markers for dysraphic states in the fetus is suggested.

Amniotic Fluid↗
PubMed2002

Newly generated neurons in the amygdala and adjoining cortex of adult primates.

The subventricular zone remains mitotically active throughout life in rodents. Studies with tritiated thymidine, which is incorporated into the DNA of mitotic cells, have revealed that the rodent subventricular zone produces neuroblasts that migrate toward the olfactory bulb along the rostral migratory stream. A similar migratory stream has been documented in monkeys by using the thymidine analogue BrdUrd. The same approach showed that neurogenesis occurred in the dentate gyrus of adult primates, including humans. In the present study, experiments combining injections of BrdUrd and the dye 1,1'-dioctadecyl-3,3,3',3'-tetramethylindo-carbocyanine, with the immunostaining for molecular markers of neurogenesis (polysialylated neural cell adhesion molecule, beta-tubulin-III, collapsin response mediator protein-4, neuronal nuclear protein) in New World (Saimiri sciureus) and Old World (Macaca fascicularis) monkeys have revealed that new neurons are produced in the amygdala, piriform cortex, and adjoining inferior temporal cortex in adult primates. These newborn neurons expressed the antiapoptotic protein Bcl-2 and formed a more-or-less continuous pathway that extended from the tip of the temporal ventricular horn to the deep portion of the temporal lobe. The production of newborn neurons in the amygdala, piriform cortex, and inferior temporal cortex seems to parallel the continuing addition of neurons in the olfactory bulb. These two concomitant phenomena may ensure structural stability and functional plasticity to the primate olfactory system and temporal lobe.

Amygdala↗
PubMed1993

Photochemically induced focal cerebral ischemia in rat: time dependent and global increase in expression of basic fibroblast growth factor mRNA.

Induction of basic fibroblast growth factor (bFGF) mRNA expression was studied in a Rose bengal induced focal cerebral ischemia during a time course of 2, 4, 24, 72 h and 7 days. Focal cerebral ischemia induced by Rose bengal resulted in a global upregulation in bFGF gene expression at the 24 h time-interval. This upregulation in bFGF gene expression was due to an upregulation in glial bFGF expression in most of the areas studied as seen by means of non-radioactive in situ hybridization in combination with immunocytochemistry for glial fibrillary acidic protein. However, in the piriform cortex a putative neuronal upregulation of bFGF could be detected by combination of non-radioactive in situ hybridization, immunohistochemistry for glial fibrillary acidic protein and nuclear staining with Neutral red. Semiquantitative data concerning bFGF mRNA expression were obtained by use of computer-assisted microdensitometry and revealed substantial increases in bFGF mRNA expression in the cingulate cortex, the neostriatum, a 1 mm marginal zone close to the external capsule and the olfactory tubercle at bregma levels 1 to 2 mm rostral to the lesion. No changes in bFGF gene expression were seen in field CA1 of Ammon's horn on the lesioned side and in dentate gyrus at bregma levels between -2.12 to -3.30 mm. We observed significant changes in bFGF upregulation in the caudate putamen, the piriform cortex and the amygdaloid region and the frontoparietal cortex at bregma levels -2.12 to -3.30 mm. These data indicate that photochemically induced focal cerebral ischemia leads to an early and global response in bFGF gene expression, which is due to an upregulation mainly in astrocytes. The observed widespread upregulation of the bFGF gene transcription rostral and caudal to the lesion is suggested to be due in part to neuronal glutaminergic connections between the areas investigated and in part due to increases in extracellular fluid signals (volume transmission).

Animals↗
PubMed1992

Effect of kainic acid administration to prepubescent rats on cholinergic markers in selected brain regions of adult rats.

Systemic kainic acid administration to prepubescent rats, in a convulsant dose, results in permanent changes in behaviour, learning and memory in adulthood (Holmes et al., 1988, Epilepsia 29, 721-730). With regard to the hypothesis that cholinergic mechanisms play a crucial role in cognitive processes, M1- and M2-muscarinic acetylcholine receptors, choline acetyltransferase, and high-affinity choline uptake as well as benzodiazepine receptors were studied in selected cortical regions (frontal, temporal, somatosensory, visual, piriform cortex), in amygdala, hippocampus, and in the nucleus basalis of Meynert from adult rats, which received at the age of 25 days a single dosage of 11 mg/kg, s.c. kainic acid. Kainic acid treatment of prepubescent rats resulted in the adult brain in decreased numbers of the total population of muscarinic acetylcholine receptors in frontal (by 27%, P < 0.05, two-tailed Student's t-test), temporal (22%, P < 0.05), and piriform cortex (31%, P < 0.05), in amygdala (24%, P < 0.05), and nucleus basalis of Meynert (39%, P < 0.02). The binding affinity was unchanged in these regions. However, in the hippocampus, the dissociation constant was significantly increased following kainic acid treatment, while the receptor numbers remained unchanged. Analysis of competition experiments with the muscarinic antagonist pirenzepine revealed that the reductions of muscarinic acetylcholine receptors in the cortical regions after kainic acid treatment are mainly due to decreases in the number of the muscarinic M1-receptor subtype. In the amygdala, the numbers of both M1- and M2-receptor subtypes are reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1992

Localization of corticotropin-releasing factor-like immunoreactivity in monkey olfactory bulb and secondary olfactory areas.

Electrophysiological and anatomical observations suggest that terminals of olfactory bulb mitral cells ending in rat primary olfactory cortex exert certain postsynaptic effects via an excitatory amino acid neurotransmitter. Recent anatomical studies have shown that several peptides, most notably corticotropin-releasing factor (CRF) (Imaki et al., '89) Brain Res., 496: 35-44), are also localized within rat olfactory bulb projection neurons, thus raising the possibility that there is a peptide cotransmitter in this system. In contrast to the availability of data for rodents, very little is known about the distribution of peptides and other putative transmitters in the olfactory systems of primate species. In the present study, sections through the olfactory bulb and its target areas were obtained from two monkey species (Saimiri sciureus and Macaca fascicularis) and processed for immunohistochemistry with a well-characterized polyclonal antiserum directed against the human form of CRF. Virtually identical results were obtained in the two species. Within the olfactory bulb, nearly all mitral and many tufted cells contained CRF-like immunoreactivity. CRF-positive fibers were seen within the olfactory tract and olfactory stria, which contain the axons of mitral and tufted cells. Within the anterior olfactory nucleus and layer Ia of the olfactory tubercle and piriform cortex, immunoreactivity was seen within fine processes, as well as in coarse, varicose fibers and isolated puncta. CRF-positive cells were seen within layer III of the olfactory tubercle and piriform cortex. Immunoreactive fibers and varicosities were also seen within olfactory-recipient regions of the amygdala and entorhinal cortex. These observations suggest that CRF may act as a transmitter and/or neuromodulator in primate olfactory system.

Amygdala↗
PubMed1994

Isolation and characterization of Bsk, a growth factor receptor-like tyrosine kinase associated with the limbic system.

Neuronal degeneration has been shown to be involved in various neurological disorders. Growth/trophic factors and their receptors are known to be important for the regeneration and survival of neurons. We report here the molecular cloning of a receptor-like protein tyrosine kinase, bsk, (for brain specific kinase). Bsk is highly related to the eph/elk receptor-like kinase family members. Northern blot analysis shows that it is expressed specifically in the brain, with no expression detected in adult heart, spleen, lung, liver, skeletal muscle, and kidney. In situ hybridization analysis of adult mouse brain sections indicates that bsk is expressed at high levels in the hippocampus, tenia tecta, indusium griseum, and the piriform cortex, major components of the limbic system that are important for learning and memory. In addition, elevated levels of expression are found in other areas of the limbic system such as the amygdala, medial septum, and nucleus of the diagonal band, and in the olfactory bulb, which has close connections to the limbic system. The highest level of expression is found in the CA3 region of the hippocampus and the pyramidal cell layer of the piriform cortex. In 16.5 day mouse embryos, bsk is expressed predominantly in the primordial cortex of the telencephalon. An antibody against a C-terminal peptide of bsk recognized a 105 kD protein in the 16.5 day embryonic head extract. Our analysis shows that bsk is a growth factor receptor-like protein tyrosine kinase and that its greatest expression in the adult brain is associated with components of the limbic system.

Amino Acid Sequence↗
PubMed1988

Neuroanatomical regions of the chick brain involved in monitoring amino acid deficient diets.

Chicks fed a diet deficient in tryptophan will reduce food intake dramatically. Chicks will select a balanced diet over one that is deficient in tryptophan (trp). The amygdala and prepiriform cortex have been implicated in monitoring amino acid (AA) balance, and hence food intake in rats. Therefore, comparable regions of the chick brain were studied to determine if they were involved in monitoring AA deficient diets. In each of four experiments, 48 chicks were used (24 experimentally-operated and 24 sham-operated controls). After starting on a commercial diet, chicks were fed semipurified diets: balanced (bal) or trp deficient (def). The following dietary regimen was followed in all experiments in both pre- and postoperatively; 1) bal diet for an adjustment period; 2) bal diet for 1-2 days; 3) def diet for 2-3 days; 4) choice of both diets presented simultaneously. This was followed by ablation of a brain region and then a repetition of the dietary regimen. Brain regions ablated or isolated include the nucleus taeniae (Tn), piriform cortex (CPi), frontal archistriatum (FA) and ventral archistriatum (AV). No differences in selection were observed when lesions ablating the FA, AV or Tn were performed. A significant decrease in selection of the bal diet was observed after knife cuts which isolated the piriform cortex from medial connections. It is suggested that this brain region may be involved in monitoring AA profiles in the plasma.

Amino Acids↗
PubMed2002

Expression of the multidrug transporter P-glycoprotein in brain capillary endothelial cells and brain parenchyma of amygdala-kindled rats.

PURPOSE: Based on data from brain biopsy samples of patients with pharmacoresistant partial epilepsy, overexpression of the multidrug transporter P-glycoprotein (PGP) in brain capillary endothelium has recently been proposed as a potential mechanism of resistance to antiepileptic drugs (AEDs). We examined whether PGP is overexpressed in brain regions of amygdala-kindled rats, a widely used model of temporal lobe epilepsy (TLE), which is often resistant to AEDs. METHODS: Rats were kindled by stimulation of the basolateral amygdala (BLA); electrode-implanted but nonkindled rats and naive (not implanted) rats served as controls. PGP was determined by immunohistochemistry either 1 or 2 weeks after the last kindled seizure, by using a monoclonal anti-PGP antibody. Six brain regions were examined ipsi- and contralateral to the BLA electrode: the BLA, the hippocampal formation, the piriform cortex, the substantia nigra, the frontal and parietal cortex, and the cerebellum. RESULTS: In both kindled rats and controls, PGP staining was observed mainly in microvessel endothelial cells and, to a much lesser extent, in parenchymal cells. The distribution of PGP expression across brain regions was not homogeneous, but significant differences were found in both the endothelial and parenchymal expression of this protein. In kindled rats, ipsilateral PGP expression tended to be higher than contralateral expression in several brain regions, which was statistically significant in the piriform cortex and parietal cortex. However, compared with controls, no significant overexpression of PGP in capillary endothelial cells or brain parenchyma of kindled rats was seen in any ipsilateral brain region, including the BLA. For comparison with kindled rats, kainate-treated rats were used as positive controls. As reported previously, kainate-induced seizures significantly increased PGP expression in the hippocampus and other limbic brain regions. CONCLUSIONS: Amygdala-kindling does not induce any lasting overexpression of PGP in several brain regions previously involved in the kindling process. In view of the many pathophysiologic and pharmacologic similarities between the kindling model and TLE, these data may indicate that PGP overexpression in pharmacoresistant patients with TLE is a result of uncontrolled seizures but not of the processes underlying epilepsy. It remains to be determined whether transient PGP overexpression is present in kindled rats shortly after a seizure, and whether pharmacoresistant subgroups of kindled rats exhibit an increased expression of PGP. Furthermore, other multidrug transporters, such as multidrug resistance-associated protein, might be involved in the resistance of kindled rats to AEDs.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Behavioral, biochemical and histological studies in a model of pilocarpine-induced spontaneous recurrent seizures.

Although the presence of profound cognitive disturbances in lithium-pilocarpine-induced spontaneous recurrent seizures (SRS) has been well documented, much less is known about changes in emotional behavior, in this model of temporal lobe epilepsy. To that end, a lithium-pilocarpine model of SRS was used to evaluate behavior of experimental animals (SRS, non-SRS and saline-treated rats) in different tests of anxiety (open field test, fear conditioning freezing and footshock-induced ultrasonic vocalization). Flinch-jump test, allowing determination of pain threshold, was employed to confirm specificity of data from anxiety tests. Moreover, neurotransmitters' (dopamine, serotonin and their metabolites) concentration was measured in selected brain structures involved in emotional and motor processing (hippocampus, frontal cortex and striatum). Finally, different brain structures were examined histologically in order to determine structures likely to be involved in behavioral changes. It was found that SRS rats, tested in a seizure free period, revealed an increase in motor activity, and a decrease in fear-related reactions (a freezing response to the aversively conditioned context, and a spontaneous, emotion-related ultrasonic vocalization). No changes in the pain threshold were present. The activity of dopamine and serotonin systems in examined brain structures remained unchanged. The neuropathological effects were widespread and involved a loss of neurons, proliferation of astroglial cells and the presence of activated ramified and ameboid microglial cells in the hippocampus proper, piriform cortex, amygdala and lateral posterior thalamic nuclei. The obtained results suggest a prevalence of disinhibitory effects on behavior in SRS rats, as shown by the results of contextual fear and aversive vocalization tests (i.e. a release of rat behavior controlled by fear). It is conceivable that the lesions to the limbic structures involved in the origin of emotions; the hippocampus, amygdala, and piriform cortex, may underlie changes in anxiety reactions in SRS rats. These results indicate that lithium-pilocarpine-induced SRS are also accompanied by profound alteration of animal emotional behavior.

Animals↗