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.

SourceResearch connectionFrom yearThrough year

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

At least 1,099 records · Page 61Linked to original sources

PubMed2006

KCC3 and KCC4 expression in rat adult forebrain.

Potassium chloride ion cotransporters (KCCs) are part of a family of transporters classically described as being involved in cell volume regulation. Recently, KCC2 has been shown to have a role in the development of the inhibitory actions of amine transmitters, whereas KCC3 also plays a fundamental role in the development and function of the central and peripheral nervous system. We have re-assessed the expression of each of the known KCCs in the rat forebrain using RT-PCR and in situ hybridisation histochemistry. As well as confirming the widespread expression of KCC1 and KCC2 throughout the brain, we now show a more restricted expression of KCC3a in the hippocampus, choroid plexus and piriform cortex, as well as KCC4 in the choroid plexus and the suprachiasmatic nucleus of the hypothalamus. The expression of KCC4 in the latter and KCC2 in the lateral hypothalamic and ventromedial hypothalamic nuclei suggests that these cotransporters may have selective roles in neuroendocrine or homeostatic functions. Finally, we demonstrate the existence of a truncated splice variation of KCC3a in the rat that appears to be expressed exclusively in neurons (as is KCC2), whereas the native form of KCC3a and KCC4 appears to be expressed in glial cells.

Animals↗

PubMed2007

Enzymatic properties and localization of motopsin (PRSS12), a protease whose absence causes mental retardation.

Motopsin (PRSS12) is a mosaic protease expressed in the central nervous system. Truncation of the human motopsin gene causes nonsyndromic mental retardation. Understanding the enzymatic properties and localization of motopsin protein in the central nervous system will help identify the molecular mechanism by which the loss of motopsin function causes mental retardation. Recombinant motopsin showed amidolytic activity against the synthetic substrate benzyloxycarbonyl-l-phenylalanyl-l-arginine 4-methyl-coumaryl-7-amide. Motopsin activated the single-chain tissue plasminogen activator precursor and exhibited gelatinolytic activity. This enzymatic activity was inhibited by typical serine protease inhibitors such as aprotinin, leupeptin, and (4-amidinophenyl) methanesulfonyl fluoride. Immunocytochemistry using anti-motopsin IgG revealed that both human and mouse motopsin proteins were distributed in discrete puncta along the dendrites and soma as well as axons in cultured hippocampal neurons. In the limbic system, including the cingulate and hippocampal pyramidal neurons and piriform cortex, high level of motopsin protein was expressed at postnatal day 10, but a very low level at 10-week-old mice. Motopsin and tissue plasminogen activator were co-expressed in the cingulate pyramidal neurons at postnatal day 10 and were distributed along dendrites of cultured pyramidal neurons. In cranial nuclei, a moderate level of motopsin protein was detected independently on the developmental stage. Our results suggest that motopsin has multiple functions, such as axon outgrowth, arranging perineuronal environment, and maintaining neuronal plasticity, partly in coordination with other proteases including tissue plasminogen activator.

Animals↗

PubMed2004

Cue valence representation studied by Fos immunocytochemistry after acquisition of a discrimination learning task.

The piriform cortex (PCx) and related structures such as hippocampus and frontal cortex could play an important role in olfactory memory. We investigated their involvement in learning the biological value of an odor cue, i.e. predicting reward or non-reward in a two-odor discrimination task. Rats were sacrificed after stimulation by either rewarded or non-rewarded odor and Fos immunocytochemistry was performed. The different experimental groups of rats did not show strongly differentiated Fos expression pattern in either the PCx or the hippocampus. A few differences were noted in frontal areas. In the ventro-lateral orbital cortex, rats, ramdomly rewarded during the conditionning had a higher Fos level in comparison with other groups. In infralimbic cortex, rats, which learned the reward value of the olfactory cue and were water-reinforced the day of sacrifice, showed a higher Fos expression. Data are discussed in view of the olfactory learning paradigm and of the accuracy of the control groups used in the present experimental design. The behavioural conditions leading to Fos expression are further discussed since Fos is a marker of learning-induced plasticity as well as a general activity marker which can be activated by a wide range of stimuli not directly linked to memory.

Animals↗

PubMed2005

Pallial expression of Enc1 RNA in postnatal mouse telencephalon.

We analysed the pallial expression pattern of Enc1 (a member of the kelch family of genes) in postnatal mice (P1-P10). At early developmental stages this gene plays a role in the histogenesis of cortical structures [M.C. Hernández, P.J. Andrés-Barquin, S. Martínez, A. Bulfone, J.L.R. Rubenstein, M.A. Israel, Enc1: novel mammalian kelch-related gene specifically expressed in the nervous system encodes an actino-binding protein, J. Neurosci. 17 (1997) 3038-3051]. A restricted expression of Enc1 was found in the mouse pallium, notably within claustroamygdaloid derivatives of the lateral pallium and in some cortical layers in the lateral, dorsal and medial pallium sectors, with distinct regional differences. The strongest cortical expression was found in isocortical layer II and in the piriform cortex, anterior olfactory area and olfactory bulb mitral cells. The lowest signal occurred in the retrosplenial cortex. The subgranular layers V/VI were also positive, particularly layer V, with clearcut areal differences. The hippocampal CA3/CA4 areas and the dentate gyrus were strongly positive. The dorsolateral (core) portion of the claustrum and dorsal endopiriform nucleus were moderately positive, as were the amygdaloid lateral and basolateral nuclei.

Age Factors↗

PubMed2005

In vivo preparation and identification of mitral cells in the main olfactory bulb of the mouse.

The mouse main olfactory bulb (MOB) is commonly used as a mammalian model to study olfactory processing. The genetic techniques available with the mouse make its MOB a powerful model for analysis of neuronal circuitry. The mouse has been used as a mammalian model for all types of MOB neurons, but especially to study the activity of mitral cells. However, mouse mitral cell activity is most commonly studied in vitro. Therefore, we aimed to develop a protocol to record the activity of antidromically identified mitral cells in mouse in vivo. Currently, such a protocol does not exist. Using extracellular techniques, we report a protocol that is able to record neurons from all mouse MOB layers. Specifically, mitral cell single-units were identified by antidromic activation from the posterior piriform cortex, and their spontaneous activity was recorded for more than 30 min. This protocol is stable enough to record from single-units while buprenorphine was applied both topically to the surface of the MOB and injected systemically.

Analgesics, Opioid↗

PubMed2005

The GCN2 kinase biases feeding behavior to maintain amino acid homeostasis in omnivores.

To insure an adequate supply of nutrients, omnivores choose among available food sources. This process is exemplified by the well-characterized innate aversion of omnivores to otherwise nutritious foods of imbalanced amino acid content. We report that brain-specific inactivation of GCN2, a ubiquitously expressed protein kinase that phosphorylates translation initiation factor 2 alpha (eIF2alpha) in response to intracellular amino acid deficiency, impairs this aversive response. GCN2 inactivation also diminishes phosphorylated eIF2alpha levels in the mouse anterior piriform cortex following consumption of an imbalanced meal. An ancient intracellular signal transduction pathway responsive to amino acid deficiency thus affects feeding behavior by activating a neuronal circuit that biases consumption against imbalanced food sources.

Amino Acids↗

PubMed2005

Ontogeny of cortical synaptic depression underlying olfactory sensory gating in the rat.

Sensory gating is the ability to filter irrelevant or redundant sensory input and is a critical function of all sensory systems that allows efficient processing of important stimuli. The present results demonstrate that a form of activity-dependent synaptic depression recently found to be involved in both cortical and behavioral olfactory sensory gating, is functional by at least the first postnatal week in the rat piriform cortex, and shares a common metabotropic glutamate receptor mechanism.

Animals↗

PubMed2006

Optimal window for ictal blood flow mapping. Insight from the study of discrete temporo-limbic seizures in rats.

RATIONALE: Measurement of local cerebral blood flow (LCBF) is routinely used to locate the areas involved in the generation and spread of seizures in epileptic patients. Since the spatial distribution and extent of ictal LCBF depends on the epileptogenic network, but also on the timing of injection of tracer, we used a rat model of amygdala kindled seizures to follow time-dependent changes in the distribution of seizure-induced LCBF changes. METHODS: Rats were implanted with a left amygdala electrode and were stimulated until reaching stage 1. LCBF was measured by the quantitative [14C]iodoantipyrine autoradiographic technique. The tracer was injected either at 15 s before seizure induction (early ictal) or simultaneously with the amygdala stimulation (ictal) in rats undergoing a stage 0 or 1 seizure. RESULTS: During stage 0 seizures, LCBF rates increased significantly ipsilaterally in medial and central amygdala and substantia nigra. During stage 1 seizures, LCBF increased unilaterally in amygdala, piriform cortex, substantia nigra, ventral tegmental area and cerebellum and bilaterally in several limbic and subcortical structures, excepted in hippocampus and pallidum. When pooling stages 0 and 1 but considering only tracer injection time, discrete LCBF changes occurred ipsilaterally in amygdala and substantia nigra at early ictal time. At true ictal time, significant changes occurred in several subcortical structures bilaterally while limbic structures displayed more localized and lateralized changes. CONCLUSION: LCBF mapping appears unable to identify in rats the ictal onset zone of clinically significant amygdala-triggered seizures (stage 1), while the study of sub-clinical seizures (stage 0) allowed to correctly locate the amygdala onset of the seizures within the limbic network. Compared to human SPECT studies, this work confirms that some ictal hyperperfused areas belong to the spreading network rather than to the epileptogenic zone. The spatial recruitment of remote subcortical structures could be further investigated to strengthen the rationale of therapeutic stimulation of basal ganglia in drug-resistant epilepsies.

Amygdala↗

PubMed2005

Combination of adenosine A1 and A2A receptor blocking agents induces caffeine-like locomotor stimulation in mice.

The spontaneous locomotor activity of C57BL/6J mice was examined, using an automated detection system based on infra-red beams, after administration of caffeine (3-30 mg/kg, i.p.), the adenosine A(2A) receptor selective antagonist SCH 58261 (0.312-2.5 mg/kg, i.p.) and the A(1) selective antagonist DPCPX (1.25-5 mg/kg, i.p.). SCH 58261 failed to influence motor activity in mice habituated to the test environment. DPCPX produced a small increase in motility and locomotion (significant at the dose of 5.0 mg/kg), much weaker than that produced by caffeine. Combined administration of DPCPX (1.2 mg/kg, i.p.) and SCH 58261 (1.2 mg/kg, i.p.) produced stimulation of motility and locomotion comparable with the effect of caffeine (15 mg/kg, i.p.). In contrast to motility and locomotion, rearing counts were not significantly influenced by DPCPX, SCH 58261, their combination, or by caffeine. Caffeine (15 mg/kg, i.p.) caused an increase in NGFI-A mRNA (an immediate early gene was chosen as an index of neuronal activation) in the piriform cortex 4 h after injection. This effect was reproduced by the combination of A(1) and A(2A) receptor antagonist. It is hypothesised that the stimulatory effect of low doses of caffeine in C57BL/6J mice is due to concomitant blockade of both A(1) and A(2A) adenosine receptors.

Adenosine A1 Receptor Antagonists↗

PubMed2006

Distinct regulation of metabotropic glutamate receptor (mGluR1 alpha) in the developing limbic system following multiple early-life seizures.

The effects of repeated neonatal seizures on metabotropic glutamate receptors (mGluRs) during critical periods of brain development are unknown. Therefore, we characterized the expression of Group I (mGluR1 and mGluR5) and Group II (mGluR2/3) metabotropic glutamate receptor proteins in the developing limbic system in response to a varied neonatal seizure history. Status epilepticus was induced with kainic acid (KA) either once (1x KA) on postnatal (P) day (P13), twice (2x KA) on P6 and P9 or P13, or three times (3x KA) on P6, P9, and P13. In control hippocampus, mGluR1alpha protein expression differed at all stages of development examined, whereas mGluR2/3 and mGluR5 protein expression patterns were mature by P15. After KA-induced status epilepticus, there was a significant elevation in mGluR1alpha protein expression within a select group of inhibitory interneurons of the CA1 stratum oriens-alveus that was enhanced with increasing number of neonatal seizures. mGluR2/3 and mGluR5 subtypes were unchanged. Increases were also observed within neurons of the amygdala and piriform cortex. Selective increases of mGluR1alpha subtypes within limbic structures may contribute to the resistance and tolerance of the immature hippocampus from damage. This may occur by excessive stimulation of excitatory synapses to collectively enhance the inhibitory drive of the immature brain by increasing GABA release. Data suggest that the mGluR1alpha subtype plays an important role in regulating hippocampal network activity after early-life seizures.

Age Factors↗

PubMed2006

Antidepressant-mediated reversal of abnormal behavior and neurodegeneration in mice following olfactory bulbectomy.

Olfactory bulbectomy is an established animal model of depression that has been mostly investigated in rats. As in human major depression, bulbectomy induces behavioral alterations that can be ameliorated by chronic antidepressant treatment. Furthermore, bulbectomy in rats is known to induce neurodegeneration in some brain areas. The aim of the present study was to evaluate patterns of behavioral alterations and neurodegeneration, and their drug-induced reversibility, in bulbectomized mice. Our results reveal that in mice bulbectomy increases locomotor activity and induces deficits in the passive avoidance test, comparable to the effects seen in rats. Bulbectomy also induced neuronal degeneration, visualized by incorporation of Fluoro-Jade B, in the piriform cortex and the posterolateral cortical amygdaloid nucleus (PLCo). Chronic treatment with the antidepressant amitriptyline protected neurons in both areas and efficiently reversed abnormal locomotor activity induced by bulbectomy. Treatment with citalopram was effective in reversing the behavioral deficits induced by bulbectomy, but did not protect against neurodegeneration. Our data indicate significant overlap between mice and rats in terms of behavioral alterations and neurodegeneration following olfactory bulbectomy. However, there are differences in drug-mediated reversibility of neurodegeneration suggesting that neurodegeneration and protection may be "second-order" features in this animal model of depression. This may also be relevant in the context of studies using genetically altered mice.

Amitriptyline↗

PubMed2006

Accumulated increase in neuropeptide Y and somatostatin gene expression of the rat in response to repeated electroconvulsive stimulation.

The mechanisms by which electroconvulsive therapy (ECT) causes its antidepressive effect are unknown. Because ECT requires repeated induction of electroconvulsive seizures, adaptive changes in the brain and regulation of gene expression, are likely to be the fundamental basis on which ECT acts. Neuropeptide Y (NPY) gene expression is increased after multiple electroconvulsive stimulations (ECS) and since it also has anticonvulsant and antidepressant properties, it has led to the hypothesis that the beneficial effect of ECT is mediated via its activation of NPY-dependent neurotransmission. We have therefore examined in detail the temporal profile of NPY gene expression, using in situ hybridisation histochemistry in the rat dentate gyrus and piriform cortex - two brain areas centrally involved in seizure regulation. NPY mRNA in both regions was found to increase gradually with the number of ECS, reaching a maximum (550-700%) after approximately 14 ECS where no further increase was achieved by additional ECS. A number of 14 ECS was also shown to exert anticonvulsant activity against kainic acid seizures. In the dentate gyrus, repeated ECS also caused a gradual, but smaller, increase in the expression of somatostatin (SS) - a neuropeptide that is co-localised with NPY and also has anticonvulsant effects. These results shows that NPYergic and, to a lesser extent, SSergic neurotransmission is activated by ECS and support the hypothesis that these neuropeptides could play a central role in the anticonvulsant and antidepressant effect of ECT.

Animals↗

PubMed2005

Comparative study of the PrPBSE distribution in brains from BSE field cases using rapid tests.

The distribution of PrP(BSE) in the brain of nine confirmed BSE field cases was analyzed using immunohistochemistry and compared to the levels of PrP(BSE) determined by two rapid tests (Prionics-Check WESTERN and Prionics-Check LIA). Each brain was dissected into 16 areas: spinal cord, medulla oblongata, pons, mesencephalon, thalamus, hippocampus, cerebellar vermis, cerebellar medulla, cerebellar hemispheres, occipital cortex, temporal cortex, parietal cortex, striatum, frontal cortex, piriform lobe and olfactory bulbs. The highest levels of PrP(BSE) were detected in the medulla oblongata, spinal cord and pons, and correspondingly both rapid tests showed 100% correlation with the immunohistochemistry with regard to sensitivity and specificity. Some inconsistencies between the levels of PrP(BSE) determined either by immunohistochemistry or by the rapid tests were found in brain areas with medium to low levels of PrP(BSE). These brain areas included the cerebellar hemisphere, olfactory bulb, and the temporal and parietal cortices. A brain PrP(BSE) distribution curve (BPDC) was designed by plotting the PrP(BSE) signals obtained from the two rapid tests versus the anatomical region along the caudal-rostral axis of the brain. Comparison of the BPDC of the nine BSE cases showed that all cases had a similar PrP(BSE) distribution in the brain but with variable intensities, which could be explained by different stages in the progression of the disease. We propose that the BPDC could be used as a tool to differentiate classical cases of BSE from the recently identified atypical BSE cases.

Animals↗

PubMed2005

NAPOR-3 RNA binding protein is required for apoptosis in hippocampus.

NAPOR-3 is a central nervous system RNA binding protein that is associated with downstream mRNA targets and has been demonstrated to be selectively overexpressed during apoptotic cell death. In this study, we first examined the regional distribution of NAPOR-3 mRNA in the adult rat brain by in situ hybridization: the transcript was abundantly expressed in many brain regions, mostly in gray matter, including the CA1-CA4 regions and dentate gyrus of the hippocampus, the piriform cortex and the cerebellar granule cell layer. We then investigated the role of NAPOR-3 in neuronal cell death by monitoring its mRNA and protein expression levels using semiquantitative RT-PCR and Western blotting, respectively. NAPOR-3 was overexpressed in rat organotypic slices exposed to staurosporine and to oxygen-glucose deprivation (OGD), an in vitro model of apoptotic cerebral ischemia, but not when exposed to glutamate toxicity. Our results also demonstrate that NAPOR-3 gene overexpression is an early step in the chain of signaling events leading to apoptosis, taking place upstream of caspase-3 activation. Finally, antisense-mediated downregulation of NAPOR-3 gene expression protected hippocampal cultures against OGD-induced apoptosis and prevented caspase-3 activation. Our results demonstrate that NAPOR-3 gene overexpression is necessary for the execution of OGD-induced programmed cell death.

Animals↗

PubMed2004

Lipoprotein lipase and endothelial lipase expression in mouse brain: regional distribution and selective induction following kainic acid-induced lesion and focal cerebral ischemia.

Lipoprotein and endothelial lipases are members of the triglyceride lipase gene family. These genes are expressed in the brain, where the encoded proteins are fulfilling functions that have yet to be elucidated. In this study, we examined the distribution of their respective mRNAs in the C57BL/6 mouse brain by in situ hybridization. In control mice, we observed widespread expression of lipoprotein lipase (LPL) mRNA mainly in pyramidal cells of the hippocampus (CA1, CA2 and CA3 areas), in the striatum and in several cortical areas. Endothelial lipase (EL) mRNA expression was restricted to CA3 pyramidal cells of the hippocampus, to ependymal cells in the ventral part of the third ventricle and to some cortical cell layers. To gain insight into the role played by lipases in the brain, neurodegeneration was induced by intraperitoneal injection of kainic acid (KA) or by occlusion of the middle cerebral artery (MCA). Upon injection of KA, a rapid increase in EL mRNA expression was observed in the piriform cortex, hippocampus, thalamus and neocortex. However, the levels of LPL mRNA were unaffected by KA injection. Remarkably, after focal cerebral ischemia, the expression of EL was unaffected whereas a dramatic increase in LPL expression was observed in neocortical areas of the lesioned side of the brain. These results show that LPL and EL transcripts are selectively upregulated in function of the type of brain injury. LPL and EL could thus fulfill a function in the pathophysiological response of the brain to injury.

Animals↗

PubMed2005

Transient changes in the limbic histaminergic system after systemic kainic acid-induced seizures.

Increased brain histamine is reported to protect against convulsions. We used systemic kainic acid (KA) administration to study possible changes of the histaminergic system in rat brain in status epilepticus (SE). Robust increases in brain histamine concentrations and numbers of histamine-immunoreactive nerve fibers were detected in the piriform cortex (Pir) and amygdala after KA injection, suggesting a reactive increase, which is opposite to other published aminergic transmitter responses. These changes, lasting several weeks, might be coupled to a mechanism unrelated to the anticonvulsive function of histamine. Transient increases in mRNA expression of H(3) receptor isoforms with a full-length third intracellular loop, coupled to mitogen-activated protein kinase pathway, were detected first in the hippocampal CA3c area, followed by the Pir and amygdala and then the hippocampal CA1 area. These results suggest that histamine and H3 receptors, which also control the release of GABA and glutamate, might be involved in convulsive SE.

Amygdala↗

PubMed2006

Oral uridine pro-drug PN401 is neuroprotective in the R6/2 and N171-82Q mouse models of Huntington's disease.

Previously, uridine pro-drug 2',3',5'-tri-O-acetyluridine (PN401) was shown to be protective in the mitochondrial complex II inhibitor 3-nitropropionic acid model of Huntington's disease (HD). In this study, PN401 increased survival and improved motor function on the rotarod in both R6/2 and N171-82Q polyglutamine repeat mouse models of HD. PN401 significantly decreased neurodegeneration in both the piriform cortex and striatum although PN401 decreased huntingtin protein aggregates only in the striatum. Cortical and striatal brain-derived neurotrophic factor (BDNF) protein levels were reduced in the +/- compared to the -/- N171-82Q mice and PN401 treatment significantly increased cortical BDNF in both +/- and -/- mice, but PN401 did not affect striatal BDNF. These results suggest that PN401 may have beneficial effects in the treatment of neurodegenerative diseases such as HD.

Acetates↗

PubMed2004

Localization of DJ-1 mRNA in the mouse brain.

DJ-1 is mutated in autosomal recessive, early onset Parkinson's disease but the exact localization of the DJ-1 gene product in the mammalian brain is largely unknown. We aimed to evaluate the DJ-1 mRNA expression pattern in the mouse brain. Serial coronal sections of brains of five male and five female adult mice were investigated by using in situ hybridization with a DJ-1 specific 35S-labeled oligonucleotide probe. Hybridized sections were analyzed after exposure to autoradiography films and after coating with a photographic emulsion. DJ-1 was heterogeneously expressed throughout the mouse central nervous system. A high expression of DJ-1 mRNA was detected in neuronal and non-neuronal populations of several structures of the motor system such as the substantia nigra, the red nucleus, the caudate putamen, the globus pallidus, and the deep nuclei of the cerebellum. Furthermore, DJ-1 mRNA was also highly expressed in non-motor structures including the hippocampus, the olfactory bulb, the reticular nucleus of the thalamus, and the piriform cortex. The high expression of DJ-1 mRNA in brain regions involved in motor control is compatible with the occurrence of parkinsonian symptoms after DJ-1 mutations. However, expression in other regions indicates that a dysfunction of DJ-1 may contribute to additional clinical features in patients with a DJ-1 mutation.

Animals↗