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 955 records · Page 53Linked to original sources
PubMed2003

Cu2+, Co2+, and Mn2+ modify the gating kinetics of high-voltage-activated Ca2+ channels in rat palaeocortical neurons.

The effects of three divalent metal cations (Mn2+, Co2+, and Cu2+) on high-voltage-activated (HVA) Ca2+ currents were studied in acutely dissociated pyramidal neurons of rat piriform cortex using the patch-clamp technique. Cu2+, Mn2+, and Co2+ blocked HVA currents conducted by Ba2+ ( IBa) with IC50 of approximately 920 nM, approximately 58 micro M, and approximately 65 micro M, respectively. Additionally, after application of non-saturating concentrations of the three cations, residual currents activated with substantially slower kinetics than control IBa. As a consequence, the current fraction abolished by the blocking cations typically displayed, in its early phase, an unusually fast-decaying transient. The latter phenomenon turned out to be a subtraction artifact, since none of the pharmacological components (L-, N-, P/Q-, and R-type) that constitute the total HVA currents under study showed a similarly fast early decay: hence, the slow activation kinetics of residual currents was not due to the preferential inhibition of a fast-activating/inactivating component, but rather to a true slowing effect of the blocker cations. The percent IBa-amplitude inhibition caused by Mn2+, Co2+, and Cu2+ was voltage-independent over the whole potential range explored (up to +30 mV), hence the slowing of IBa activation kinetics was not due to a mechanism of voltage- and time-dependent relief from block. Moreover, Mn2+, Co2+, and Cu2+ significantly reduced I(Ba) deactivation speed upon repolarization, which also is not compatible with a depolarization-dependent unblocking mechanism. The above results show that 1) Cu2+ is a particularly potent HVA Ca2+-channel blocker in rat palaeocortical neurons; and 2) Mn2+, Co2+, and Cu2+, besides exerting a blocking action on HVA Ca2+-channels, also modify Ca2+-current activation and deactivation kinetics, most probably by directly interfering with channel-state transitions.

Animals↗
PubMed2001

Ni2+ slows the activation kinetics of high-voltage-activated Ca2+ currents in cortical neurons: evidence for a mechanism of action independent of channel-pore block.

The effects of Ni2+ were evaluated on slowly-decaying, high-voltage-activated (HVA) Ca2+ currents expressed by pyramidal neurons acutely dissociated from guinea-pig piriform cortex. Whole-cell, patch-clamp recordings were performed with Ba2+ as the charge carrier. Ni2+ blocked HVA Ba2+ currents (IBas) with an EC50 of approximately 60 microM. Additionally, after application of nonsaturating Ni2+ concentrations, residual currents activated with substantially slower kinetics than both total and Ni2+-sensitive I(Ba)s. None of the pharmacological components of slowly decaying, HVA currents activated with kinetics significantly different from that of total currents, indicating that the effect of Ni2+ on I(Ba)s kinetics cannot be attributed to the preferential inhibition of a fast-activating component. The effect of Ni2+ on I(Ba) amplitude was voltage-independent over the potential range normally explored in our experiments (-60 to +20 mV), hence the Ni2+-dependent decrease of I(Ba) activation rate is not due to a voltage- and time-dependent relief from block. Moreover, Ni2+ significantly reduced I(Ba) deactivation speed upon repolarization, which also is not compatible with a depolarization-dependent unblocking mechanism. The dependence on Ni2+ concentration of the I(Ba) activation-rate reduction was remarkably different from that found for I(Ba) block, with an EC50 of approximately 20 microM and a Hill coefficient of approximately 1.73 vs. approximately 1.10. These results demonstrate that Ni2+, besides inhibiting the I(Ba)s under study probably by exerting a blocking action on the pore of the underlying Ca2+ channels, also interferes with Ca2+-channel gating kinetics, and strongly suggest that the two effects depend on Ni2+ occupancy of binding sites at least partly distinct.

Animals↗
PubMed2004

Expression of neurochondrin in the developing and adult mouse brain.

Here we describe a detailed analysis of the expression of neurochondrin ( ncdn) in the developing and adult mouse brain. Ncdn is first expressed in the hindbrain and spinal cord at embryonic day 10.5 (E10.5) followed by expression in the midbrain at E11.5. By E18 ncdn is also expressed in the diencephalon and telencephalon. However, strongest expression is still observed in the hindbrain. In adults, the expression in the forebrain is as strong as in the hindbrain. Ncdn is highly expressed in the hippocampus, piriform cortex, septum, amygdaloid complex, medial geniculate nucleus, inferior colliculus, cerebellar nuclei and the nuclei of the Vth, VIIth, and XIIth cranial nerves.

Animals↗
PubMed2000

The subrhinal paleocortex in the hedgehog tenrec: a multiarchitectonic characterization and an analysis of its connections with the olfactory bulb.

In the Madagascan hedgehog tenrec, Echinops telfairi, the entire paleocortical region (PCx) subjacent to the rhinal indentation is composed of three layers and occupies up to two thirds of the lateral hemisphere. A clear differentiation of PCx into its presumed constituents, the piriform cortex and the entorhinal cortex, as seen in other mammals, has not been obtained so far. To gain insight into location and intrinsic organization of these areas in a basal placental mammal we investigated the tenrec's PCx using cyto-, myelo- and chemoarchitectural criteria (zinc, acetylcholinesterase, NADPh-diaphorase, Wisteria floribunda agglutinin, parvalbumin, calbindin, calretinin) and analysed its connections with the olfactory bulb. The layers 2 and 3 of the tenrec's PCx differed from the corresponding layers in the rat. The layer 2 showed a complex distribution of corticobulbar cells but could not be subdivided, in contrast to layer 3. Additional cell groups in the depth of PCx were tentatively compared with subdivisions of the endopiriform region. The architectural and connectional features varied clearly along the rostrocaudal and dorso-ventral extents of PCx and gave hints for the presence of different paleocortical subdivisions. With the possible exception of an area located at the most caudal tip of the dorsomedial hemisphere, however, no conclusive evidence was obtained for the presence of a multilayered, entorhinal region. The bulbar projections to the PCx were very extensive and almost exclusively ipsilateral. The laterality of the projection is similar to that in higher mammals, but differs from that in the erinaceous hedgehog.

Animals↗
PubMed1998

Cellular localization of neuropeptide Y mRNA and peptide in the brain of the Japanese quail and domestic chicken.

Neuropeptide Y (NPY) has been implicated in the control of a number of physiological functions in birds including food intake and reproduction. In the present study, sites of NPY synthesis were localized in the brains of Japanese quail and domestic chickens by in situ hybridization histochemistry using a digoxigenin-labelled riboprobe. NPY mRNA was detected in three main cell groups in both species. The most prominent group was associated with structures in the lateral thalamus including the anterior lateral thalamic nucleus, lateral forebrain bundle, rotund nucleus, pretectal nucleus and occipitomesencephalic tract. Other major cell groups were detected in the hippocampus, and in the caudal linear nucleus and raphe nucleus of the brainstem. NPY mRNA was also present in the piriform cortex and taenial nucleus. Double-labelling of NPY mRNA and peptide was demonstrated in individual cells of the hippocampal, thalamic and brainstem cell groups, suggesting that NPY is synthesized and stored in these areas. However, the identity of other cell groups, notably in the hyperstriatal, archistriatal and neostriatal regions of the telencephalon, which exhibit NPY-immunoreactive cell bodies but no NPY mRNA, remains to be determined.

Animals↗
PubMed2005

Peripheral ChE inhibition modulates brain monoamines levels and c-fos oncogene in mice subjected to a stress situation.

The present study examined, in mice, whether regional patterns of brain monoamines concentrations (DA, 5-HT and their metabolites) and expression of c-Fos protein, that may represent a prolonged functional change in neurons, could be changed after a combined exposure to stress and the peripheral cholinesterase reversible inhibitor pyridostigmine (PYR). Animals were subjected every day to a random combination of mild unescapable electric footshocks and immobilization over a 12-day period, resulting in a significant increase of glucocorticoids levels and an activation of c-fos in hippocampus, thalamus and piriform cortex. This stress protocol induced a significant increase of 5-HT levels in striatum, hippocampus and ponto mesencephalic area (PMA) but failed to induce any DA activation. When PYR (0.2 mg/kg s.c. inducing 19-35% inhibition of the plasmatic ChE activity) was administered twice a day during the last 5 days of the stress session, 5-HIAA levels and expression of c-fos oncogene were significantly increased in the most of the brain areas studied. DA levels were also enhanced in striatum/hippocampus as a result of a possible activation of mesolimbic and nigrostriatal dopamine systems. Taken together, these results suggest that a combined exposure to certain stress conditions and PYR leads, in mice, to functional changes in neurons and may affect centrally controlled functions. The mechanisms underlying these modifications and their behavioral implications remain to be further investigated.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Direct mapping of beta-adrenergic receptors in the rat central nervous system by a novel fluorescent beta-blocker.

DL-N-(2-Hydroxy-3-napthyloxypropyl)-N'-dansylethylenediamine, dansyl analogue of propranolol (DAPN) is a novel fluorescent beta-adrenergic antagonist with high affinity to beta-receptors. The distribution pattern of DAPN fluorescence was studied in the rat central nervous system subsequent to its intravenous administration to living rats. DAPN distinctly labels specific regions and cells in the central nervous system (CNS). Highly dense DAPN fluorescence was observed in the pyramidal cell layer of the hippocampus, the granule cell layer of the dentate gyrus, the basal layers of the piriform cortex and the neocortex, the cerebellar Purkinje cell layer, and the spinal a-motoneurons. Pretreatment of control rats with DL-and L-propranolol markedly decreased the intensity and density of DAPN fluorescence in the tissue sections, whereas prior administration of D-propranolol had almost no effect. Pretreatment with large doses of reserpine did not alter the pattern of DAPN fluorescence. These findings were identical to those observed with another fluorescent beta-blocker, 9-aminoacridino-propranolol (9-AAP). Our data suggest that fluorescent beta-adrenergic antagonists may be used in vivo for the direct probing of the beta-receptors within the mammalian CNS.

Animals↗
PubMed1981

Anatomical distribution of estrogen target neurons in turtle brain.

Autoradiographic studies with [3H]estradiol-17 beta in red-eared turtle (Pseudemys scripta elegans) show concentration and retention of radioactivity in nuclei of neurons in certain regions. Accumulations of estrogen target neurons exist in the periventricular brain with relationships to ventral extensions of the forebrain ventricles, including parolfactory, amygdaloid, septal, preoptic, hypothalamic and thalamic areas, as well as the dorsal ventricular ridge, the piriform cortex, and midbrain-pontine periaqueductal structures. The general anatomical pattern of distribution of estrogen target neurons corresponds to those observed not only in another reptile (Anolis carolinensis), but also in birds and mammals, as well as in teleosts and cyclostomes. In Pseudemys, which appears to display an intermediate degree of phylogenetic differentiation, the amygdaloid-septal-preoptic groups of estrogen target neurons constitute a continuum. In phylogenetic ascendency, e.g. in mammals, these cell populations are increasingly separated and distinct, while in phylogenetic descendency, e.g. in teleosts and cyclostomes, an amygdaloid group appears to be absent or contained within the septal-preoptic target cell population.

Amygdala↗
PubMed1982

Immunohistochemical localization of choline acetyltransferase in rabbit forebrain.

uinea pig antiserum specific to the purified bovine choline acetyltransferase was used to demonstrate the localization of this enzyme in rabbit forebrain by the peroxidase-antiperoxidase immunohistochemical method. Choline acetyltransferase was localized in olfactory bulb, olfactory tract, olfactory tubercle, piriform cortex, septum, diagonal band, basal ganglia, thalamus, hypothalamus, subthalamus, habenula, cerebral cortex, hippocampal region, corpus callosum, internal capsule, fornix, longitudinal striae and other areas. The findings reflect the distribution of cholinergic axons and, possibly, their terminals. These observations correlate well with biochemical determinations of choline acetyltransferase and with previously proposed cholinergic pathways.

Animals↗
PubMed1982

Some observations on hypothalamo-amygdaloid connections in the monkey.

The projections of the hypothalamus to the amygdala have been studied autoradiographically in a series of eleven cynomolgus monkeys (Macaca fascicularis) in which injections of [3H]amino acids had been made in different regions of the caudal two-thirds of the hypothalamus. The most prominent projection arises from the ventromedial nucleus of the hypothalamus and terminates most heavily in the medial, magnocellular division of the central nucleus. Injections confined to the ventromedial nucleus also result in labeling of the piriform cortex, the periamygdaloid cortex, the anterior amygdaloid area, the medial amygdaloid nucleus and the parvocellular divisions of both the basal and basal accessory nuclei. All these projections are bilateral (although the contralateral component is much smaller) and show evidence of a rostro-caudal topographic organization. Isotope injections that involve the caudal part of the lateral hypothalamic area label projections to the medial division of the central amygdaloid nucleus, to the medial and cortical nuclei and to the anterior amygdaloid area. When such caudally placed injections also involved the lateral mamillary nucleus, the lateral division of the central amygdaloid nucleus was additionally labeled. Although the medial mamillary nucleus does not project to the amygdala, there is evidence for a minor projection from the supramamillary region to the medial amygdaloid nucleus. The ventral tegmental area appears to project to the lateral division of the central nucleus and the medial portion of the substantia nigra has a small projection to both divisions of the central nucleus. All of these projections reach the amygdala by way of the so-called ventral amygdalofugal pathway, but at least some of the fibers that arise in the ventromedial nucleus run in the stria terminalis.

Afferent Pathways↗
PubMed1984

Histofluorescent identification of indoleamine-concentrating brain loci associated with intraspecies, reflexive biting and locomotor behavior in olfactory-bulbectomized mice.

The histofluorescent identification of indoleamine (serotonin)-concentrating neurons and the changes induced by olfactory bulbectomy (Obx) were correlated with reflexive biting and locomotor behavioral activities in grouped male mice. Between 2 and 35 days post-Obx, an increase in the number and fluorescent-intensity of indoleamine-containing neurons was identified in the olfactory tubercle, lateral olfactory tract (bed neurons) and piriform cortex. Neurons in the nucleus accumbens and anterior olfactory nucleus also demonstrated increased histofluorescence by Day 35 post-Obx as compared with controls, but to a lesser extent than observed in the other olfactory loci. The increase in serotonin concentration was inversely related to locomotor activity and directly correlated to biting behavior in Obx mice. These results demonstrate that the development of this type of intraspecies aggression is temporally correlated with an enhanced serotonin histofluorescence in specific forebrain, olfactory regions in mice.

Animals↗
PubMed1985

Quantitative autoradiographic mapping of serotonin receptors in the rat brain. II. Serotonin-2 receptors.

The distribution of serotonin-2 (5-HT2) receptors in the rat brain was studied by light microscopic quantitative autoradiography. Receptors were labeled with four ligands: [3H]ketanserin, [3H]mesulergine, [3H]LSD and [3H]spiperone, which are reported to show high affinity for 5-HT2 receptors. Co-incubation with increasing concentrations of several well-known 5-HT2-selective drugs, such as pirenperone, cinanserin and ketanserin, resulted in an inhibition of the binding of the four 3H-labeled ligands to the same areas. However, all of them recognized, in addition to 5-HT2 sites, other populations of binding sites. Receptor densities were quantified by microdensitometry with the aid of a computer-assisted image-analysis system. Our results reveal a heterogeneous distribution of 5-HT2 receptor densities in the rat brain. Very high concentrations were localized in the claustrum, olfactory tubercle and layer IV of the neocortex. The anterior olfactory nucleus, piriform cortex and layer I of neocortex were also rich in 5-HT2 receptors. Intermediate concentrations of receptors were found in caudate putamen, nucleus accumbens, layer V of neocortex, ventral dentate gyrus and mammillary bodies. Areas containing only low concentrations of receptors included the thalamus, hippocampus, brainstem, medulla, cerebellum and spinal cord. The specificity of the different ligands used is discussed in terms of the other populations of sites recognized by them. The distribution of 5-HT2 receptors here reported is discussed in correlation with (a) the known distribution of serotoninergic terminals, (b) the specific anatomical systems and (c) the central effects reported to be mediated by 5-HT2-selective drugs.

Animals↗
PubMed1985

Kainic acid responses and toxicity show pronounced Ca2+ dependence.

Responses of pyramidal neurons to ionophoretic kainate, quisqualate and N-methyl aspartate were studied in a submerged rat piriform cortex slice as a function of Ca2+ and Mg2+ concentrations. The results suggest that the channel activated by kainate is unusually influenced by Ca2+, excitotoxicity is Ca2+-dependent and a function of Ca2+ concentration, and the excitotoxic actions of various amino acid agonists are correlated with the Ca2+ dependence of their responses.

Animals↗
PubMed1987

Effect of intravenous heroin and naloxone on regional cerebral blood flow in the conscious rat.

Regional cerebral blood flow (RCBF) was measured with the [14C]iodoantipyrine technique and quantitative autoradiography in awake, restrained rats shortly after intravenous injection of heroin, naloxone or naloxone before heroin. The RCBF observed in these animals was compared to those obtained in similarly treated, saline-injected rats. In an identically treated series of animals, no significant change in arterial blood gases, pH or bicarbonate was seen following any of the drug treatments at the equivalent time RCBF was determined. Blood flow increased an average 36% in 37 of the 40 areas measured 1 min after heroin injection. Significant increases were found in 21 areas including visual and piriform cortex, basal ganglia, diencephalon, limbic system, midbrain tegmentum, superior colliculus, periaqueductal gray, internal capsule and fornix. These elevations in blood flow were reversed in rats receiving heroin following naloxone pretreatment. RCBF decreased in 35 areas (mean = -12%) 4 min after naloxone injection; a 40% decrease in blood flow to entorhinal cortex was significant. These results suggest that opiate receptor stimulation by heroin increases functional activity within selected brain areas, and this effect is not limited to regions with dense populations of opiate receptors.

Animals↗
PubMed1988

A monoclonal antibody, WCC4, recognizes a developmentally regulated ganglioside containing alpha-galactose and alpha-fucose present in the rat nervous system.

A monoclonal antibody, WCC4, raised against PC12 cells, recognizes a ganglioside which is present in low concentrations in the postnatal rat nervous system. The antigen is also present in the adrenal and kidney, as determined immunohistochemically, but is not detectable in liver or spleen. A neutral glycosphingolipid is also immunoreactive. In the present report, the chemical characterization of this ganglioside, isolated from PC12 cells, and the anatomical distribution of the antigens recognized by the WCC4 antibody are described. By enzymatic cleavage of terminal saccharide moieties, the ganglioside is identified as alpha-galactosyl, (alpha-fucosyl) GM1. The ganglioside increases in concentration postnatally to day 35 (P35) and is present in a slightly diminished concentration in the adult. Immunohistochemical studies revealed that this glycolipid is also present on neuronal cell soma throughout the cerebrum, cerebellum and spinal cord. It is expressed in highest concentration in the molecular layer of the dentate gyrus and is also present in the olfactory bulb, the molecular layer of the hippocampus, the piriform cortex, the olfactory tubercle and the entorhinal cortex. The dentate molecular layer receives most of its innervation from neurons in the entorhinal cortex, and gangliosides are known to have an effect on plasticity following entorhinal cortical lesions. Therefore, the WCC4 antibody should prove to be a useful tool for the study of the role of endogenous gangliosides in this region of the nervous system.

Adrenal Gland Neoplasms↗
PubMed1989

Limbic seizures without brain damage after injection of low doses of kainic acid into the amygdala of freely moving rats.

Kainic acid (KA, 8-15 ng) was injected into the amygdala of conscious freely moving rats via chronically implanted fused silica cannulas. At 15-25 min after the injection, most rats suffered a limbic seizure attack of short duration, consisting of mastication, forelimb clonus, and raising on hind limbs, behaviorally indistinguishable from kindled seizures. Typically, the attack was followed by stereotypies, intense exploration, and by 1 or 2 more attacks. About 60 min after the injection, most rats appeared normal again and histopathological changes in their brains did not exceed those seen in vehicle-injected rats. In 3 cases, however, recurrent seizures culminated in behavioral status epilepticus 60-90 min after the injection. The status epilepticus was stopped by i.p. injection of diazepam (10 mg/kg) after a duration of 10 min (1 case) and 30 min (2 cases), respectively. After 10 min status epilepticus, we observed marginal neuronal damage with slight gliosis in both hippocampi (CA3 and CA1); after 30 min, hippocampal histopathology was more pronounced, with additional necrosis of the ipsilateral piriform cortex. After 0.8 microgram KA, a hundredfold higher dose, the incidence of limbic seizures during the first 40 min was not significantly higher (9/12) than after the lower KA doses (13/19). However, a significantly higher proportion of rats exhibited long-lasting seizure activity, associated with confluent destruction of CA3 pyramidal cells and additional seizure-related brain damage. Our results show that limbic motor seizures do not inevitably lead to histopathological changes in the brain, provided they do not culminate in a state of permanent seizure activity.

Amygdala↗
PubMed1989

Widespread expression of corticotropin-releasing factor messenger RNA and immunoreactivity in the rat olfactory bulb.

Immunohistochemical, in situ hybridization histochemical, and Northern blot methods were used to demonstrate and characterize the distribution of corticotropin-releasing factor immunoreactivity (CRF-IR) and mRNA in the rat olfactory system. Northern analysis demonstrated the presence of an mRNA species in the olfactory bulb indistinguishable from, and in greater abundance than, CRF mRNA isolated from whole hypothalamus. Results from hybridization histochemical and immunohistochemical studies converged to indicate that CRF is expressed in a majority of mitral and tufted cells in the main and accessory bulbs, and in subsets of granule and periglomerular cells. Consistent with cellular localizations in primary output neurons, a dense network of fine CRF-immunoreactive varicosities was demonstrated in the external plexiform layer of the olfactory bulb and in layer Ia of piriform cortex. Other acknowledged terminal fields of the projection neurons of the main and accessory bulbs also displayed CRF-IR. The results suggest that CRF is the most broadly distributed neuroactive agent yet charted in olfactory bulb somata. This peptide may serve as a modulator or co-transmitter of importance in several cell types in the main and accessory olfactory bulbs, including the principal output neurons.

Animals↗
PubMed1990

Loss of dopamine receptors in the olfactory bulb of patients with Alzheimer's disease.

The presence and localization of dopamine D2 receptors was studied by means of in vitro autoradiography with [3H]N-n-propylnorapomorphine in olfactory bulbs obtained postmortem from Alzheimer patients and age-matched controls. It appeared that, in 5 age-matched controls, the greatest density of dopamine D2 receptors was found in the glomerular layer of the bulb. In 6 of 7 Alzheimer patients, the labeling of the glomerular layer was decreased so that glomerular and granular layer did not differ in labeling density. Tangles, as revealed by Thioflavin S staining, were present in all different layers of the bulbus in Alzheimer patients. Observation of Nissl-stained preparations revealed that mitral cell bodies in bulbs of these patients were not present. Since mitral cells are projection neurons with targets in the entorhinal and piriform cortex, the observation of loss of these cells supports the hypothesis of early involvement of the olfactory system in Alzheimer's disease and the spread from the olfactory mucosa and bulb to the cerebral cortex and hippocampus via degeneration of interconnecting neurons. Moreover, in vivo detection of bulbar dopamine receptors might in the future provide a diagnostic tool for the early detection of senile dementia of the Alzheimer type.

Aged↗