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 847 records · Page 47Linked to original sources
PubMed1995

Noradrenergic regulation of immediate early gene expression in rat forebrain: differential effects of alpha 1- and alpha 2-adrenoceptor drugs.

Noradrenergic (NAergic) transmission in the rat cerebral cortex has recently been shown to be involved in the regulation of the basal expression of NGFI-A, an immediate early gene (IEG) which encodes a zinc-finger transcription factor. The present study further investigated the role of the NAergic system in mediating cortical IEG expression and possible topographical changes in expression of NGFI-A mRNA in rat forebrain after alpha 1- and alpha 2-adrenoceptor (AR) agonist and antagonist treatment. Expression of c-fos and c-jun, which encode leucine-zipper class transcription factors, was also studied. Male Sprague-Dawley rats were injected intraperitoneally with either an alpha 1-AR agonist (methoxamine, 5 or 10 mg/kg); an alpha 1-AR antagonist (prazosin, 5 mg/kg); an alpha 2-AR agonist (clonidine, 0.5 mg/kg); or an alpha 2-AR antagonist (methoxyidazoxan, 5 mg/kg) and killed after 1 h. IEG mRNA levels were detected by quantitative in situ hybridization histochemistry using 35S-labelled oligonucleotides. High basal levels of NGFI-A mRNA were present in cortical layers IV and VI, hippocampal CA1, piriform cortex, amygdala and caudate putamen. alpha 1-AR agonist and antagonist treatment had essentially no effect on IEG mRNA, despite producing characteristic behavioral and peripheral effects at the doses used. Methoxyidazoxan significantly increased (mean%) NGFI-A mRNA in: cerebral cortex (44); caudate putamen (82); amygdala (92); and CA1 of hippocampus (48), while clonidine significantly decreased NGFI-A mRNA in the various cortical layers to a similar extent (27-37%). Basal c-fos mRNA expression was lower than that for NGFI-A in forebrain areas including cortex, caudate putamen and hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Olfactory bulb networks revealed by lateral olfactory tract stimulation in the in vitro isolated guinea-pig brain.

Olfactory information processing is mediated by synaptic connections between the olfactory bulbs (OBs) and piriform-limbic cortices. Limited accessibility using common in vivo and in vitro preparations has hindered previous attempts to define these synaptic interactions. We utilized the isolated guinea-pig brain preparation to overcome these experimental limitations. Previous studies demonstrated extensive functional preservation in this preparation maintained in vitro by arterial perfusion. Field potential laminar profiles were performed with multi-channel probes in the OB following stimulation of both the lateral olfactory tract (LOT) and the anterior piriform cortex (APC). Current-source density analysis was carried out on laminar profiles to reconstruct current sinks/sources associated with intrinsic synaptic activities. LOT stimulation induced sequentially i) an antidromic population spike (at 2.66+/-0.39 ms) located in the mitral cell layer that was resistant to 100 Hz high-frequency stimulation (HFS) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM), ii) a component located in the external plexiform layer at 3.85+/-0.63 ms that was unaffected by HFS, iii) a large amplitude potential (peak amplitude at 5.84+/-0.58 ms) generated in the external plexiform layer, abolished by HFS and CNQX, but not by bicuculline (50 microM), iv) a late response (onset at 20.00+/-2.94 ms) abolished by CNQX and enhanced by bicuculline. Stimulation of the APC also induced a late potential abolished by HFS and CNQX. Both APC-evoked and late LOT-evoked responses were abolished by a transverse cut to separate OB from APC. These results demonstrate in an isolated mammalian brain preparation the presence of reciprocal synaptic interactions between the OB and piriform cortical structures.

2-Amino-5-phosphonovalerate↗
PubMed1994

Expression of c-fos protein in rat brain elicited by electrical and chemical stimulation of the hypothalamic paraventricular nucleus.

The functional connectivity of the paraventricular nucleus of the hypothalamus (PVN) was studied by assessing the expression of the immediate early gene, c-fos, after unilateral stimulation of this structure in urethane-anesthetized rats. Electrical stimulation for 1 h (10 s on, 10 s off; 15-40 microA at 20 Hz) was accompanied by increases in mean arterial pressure (13-29 mm Hg). In these animals, ipsilateral increases in numbers of neurons with Fos-like immunoreactivity (FLI) were immunohistochemically demonstrated in the insular cortex, lateral septum, medial amygdala, hypothalamus, lateral division of the parabrachial nucleus (PBN) of the pons and the nucleus of the tractus solitarius (NTS) and ventrolateral medulla (VLM). Numbers of cells with FLI were quantitated in five areas known for their roles in autonomic function: arcuate nucleus, ventromedial hypothalamus, lateral PBN, NTS (at three levels) and VLM (caudal and rostral). In each case, stimulation of the PVN led to significant differences in number of neurons with FLI on the side ipsilateral to the stimulation compared to the contralateral side. To eliminate effects associated with stimulation of fibers of passage in the vicinity of the PVN, the results after electrical stimulation were compared to those obtained in animals in which the PVN was chemically stimulated unilaterally with the excitatory amino acid L-glutamate (5 one-minute infusions of 50 nl, 0.5 M glutamate over 1 h). Mean arterial pressure was increased after each injection (7-13 mm Hg), and significant differences in numbers of neurons with FLI between sides were maintained in all five areas except the NTS caudal to, and at, the level of the area postrema. An increase in neurons with FLI in the piriform cortex of all animals including controls may be due to injury-induced activation of target neurons from the PVN. These data illustrate that electrical and chemical stimulation of the PVN leads to simultaneous activation of neurons in many targets. All of the target areas studied receive direct projections from the PVN, although multisynaptic projections may also contribute to activation of target neurons.

Animals↗
PubMed2003

The medial prefrontal cortex differentially regulates stress-induced c-fos expression in the forebrain depending on type of stressor.

The medial prefrontal cortex (mPFC) plays an important inhibitory role in the hypothalamic-pituitary-adrenal (HPA) axis response. The involvement of the mPFC appears to depend on the type of stressor, preferentially affecting 'psychogenic' stimuli. In this study, we mapped expression of c-fos mRNA to assess the neural circuitry underlying stressor-specific actions of the mPFC on HPA reactivity. Thus, groups of mPFC-lesioned and sham-operated rats were restrained for 20 min or exposed to ether fumes for 2 min. In both cases, the animals were killed at 40 min from the onset of stress. Interestingly, bilateral lesions of the mPFC significantly enhanced c-fos mRNA expression in the hypothalamic paraventricular nucleus of restrained animals, an effect that was paralleled by potentiation of circulating ACTH concentrations in these animals. On the other hand, lesions of the mPFC did not affect neither PVN c-fos mRNA expression nor plasma ACTH concentrations in animals exposed to ether. Lesions of the mPFC also enhanced c-fos activation in the medial amygdala following restraint, but not following ether exposure. Additional regions whose activity was affected by mPFC lesions or stressor differences included the ventrolateral division of the bed nucleus of the stria terminalis, CA3 hippocampus, piriform cortex, and dorsal endopiriform nucleus. Expression of c-fos mRNA was nearly absent in the central amygdala of all stressed animals, regardless of lesion. Furthermore, prefrontal cortex lesions did not change stress-induction levels of c-fos in the CA1 hippocampus, dentate gyrus, anteromedial division of the bed nucleus of the stria terminalis, lateral septum, and claustrum. Taken together, this study indicates that the medial prefrontal cortex differentially regulates cellular activation of specific stress-related brain regions, thus exerting stressor-dependent inhibition of the HPA axis.

Adrenocorticotropic Hormone↗
PubMed1996

Developmental and plasticity-related differential expression of two SNAP-25 isoforms in the rat brain.

In this article we study the relationship between the expression pattern of two recently identified isoforms of the 25-kD synaptosomal-associated protein (SNAP-25a and SNAP-25b) and the morphological changes inherent to neuronal plasticity during development and kainic acid treatment. SNAP-25 has been involved in vescicle fusion in the nerve terminal, and most likely participates in different membrane fusion-related processes, such as those involved in neurotransmitter release and axonal growth. In the adult brain, SNAP-25b expression exceeded SNAP-25a in distribution and intensity, being present in most brain structures . Moderate or high levels of SNAP-25a hybridization signal were found in neurons of the olfactory bulb, the layer Va of the frontal and parietal cortices, the piriform cortex, the subiculum and the hippocampal CA4 field, the substantia nigra/pars compacta, and the pineal gland, partially overlapping SNAP-25b mRNA distribution. In restricted regions of cerebral cortex, thalamus, mammillary bodies, substantia nigra, and pineal glands the two isoforms were distributed in reciprocal fashion. During development SNAP-25a mRNA was the predominant isoform, whereas SNAP-25b expression increased postnatally. The early expression of SNAP-25a in the embryo and the decrease after P21 is suggestive of a potential involvement of this isoform in axonal growth and/or synaptogenesis. This conclusion is indirectly supported by the observation that SNAP-25a mRNA, but not SNAP-25b mRNA, was upregulated in the granule cells of the adult dentate gyrus 48 hours after kainate-induced neurotoxic damage of the hippocampal CA3-CA4 regions. Increase of SNAP-25 immunoreactivity was observed as early as 4 days after kainate injection within the mossy fiber terminals of the CA3 region, and in the newly formed mossy fiber aberrant terminals of the supragranular layer. These data suggest an isoform-specific role of SNAP-25 in neural plasticity.

Animals↗
PubMed1996

Distribution of alpha 2C-adrenergic receptor-like immunoreactivity in the rat central nervous system.

The distribution of alpha 2C-adrenergic receptors (ARs) in rat brain and spinal cord was examined immunohistochemically by using an affinity purified polyclonal antibody. The antibody was directed against a recombinant fusion protein consisting of a 70-amino-acid polypeptide portion of the third intracellular loop of the alpha 2C-AR fused to glutathione-S-transferase. Selectivity and subtype specificity of the antibody were demonstrated by immunoprecipitation of [125I]-photoaffinity-labeled alpha 2-AR and by immunohistochemical labeling of COS cells expressing the individual rat alpha 2-AR subtypes. In both cases the antibody recognized only the alpha 2C-AR subtype, and immunoreactivity was eliminated by preadsorption of the antibody with excess antigen. In rat brain, alpha 2C-AR-like immunoreactivity (alpha 2C-AR-LI) was found primarily in neuronal perikarya, with some labeling of proximal dendrites; analysis by confocal microscopy revealed the intracellular localization of some of the immunoreactivity. Areas of dense immunoreactivity include anterior olfactory nucleus, piriform cortex, septum, diagonal band, pallidum, preoptic areas, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus, amygdala, hippocampus (CA1 and dentate gyrus), substantia nigra, ventral tegmental area, raphe (pontine and medullary), motor trigeminal nucleus, facial nucleus, vestibular nucleus, dorsal motor nucleus of the vagus, and hypoglossal nucleus. Labeling was found in specific laminae throughout the cortex, and a sparse distribution of very darkly labeled cells was observed in the striatum. At all levels of the spinal cord there were small numbers of large, darkly labeled cells in layer IX and much smaller cells in layer X. In general, the pattern of alpha 2C-LI throughout the neuraxis is consistent with previously published reports of the distribution of receptor mRNA detected by hybridization histochemistry.

Animals↗
PubMed1996

Distribution of neurotensin-containing neurons in the central nervous system of the pigeon and the chicken.

Neurotensin is widely located in neurons of the central and peripheral nervous systems among mammalian species. To obtain a comparative evaluation, we examined the distribution of neurotensin-containing cell bodies and fibers in the central nervous system of the pigeon and the chicken. The pattern of localization of neurotensin immunoreactivity was similar in the two species. Abundant accumulations of neurotensin-containing cell bodies were found in the dorsolateral corticoid area, the piriform cortex, the parahippocampal area, the medial part of the frontal neostriatum, the lateral part of the caudal neostriatum, nucleus accumbens, the bed nucleus of the stria terminalis, ventral paleostriatum, the preoptic area, the ventromedial hypothalamic nucleus, the inferior hypothalamic nucleus, the infundibular hypothalamic nucleus, and the mammillary nuclei. Extremely dense networks of neurotensin-containing fibers were found in the pallial commissure, the lateral septal nucleus, the preoptic area, the periventricular gray around the third ventricle, the dorsalis hypothalamic area, the hypothalamic nuclei, the parabrachial nucleus, the locus ceruleus, and the dorsal vagal complex. Major differences of immunoreactivity between the two species were as follows. 1) The chicken neurohypophysis contained an extremely large accumulation of immunoreactive fibers, but there were few in the median eminence. The reverse was found in the pigeon. 2) The optic tectum in the pigeon contained immunoreactive cells and fibers in layers 2 and 4, but no immunoreactivity was seen in the chicken optic tectum. 3) The cerebellar cortex in the pigeon contained a small number of immunoreactive fibers, whereas that in the chicken did not. 4) The pigeon spinal cord contained immunoreactive neurons in the subependymal layer, but the chicken spinal cord did not. Our observations suggest the presence of a very wide network of neurotensin-containing neurons in the avian brain and spinal cord, which is also the case in mammals.

Anatomy, Artistic↗
PubMed1996

Anatomy of rat semaphorin III/collapsin-1 mRNA expression and relationship to developing nerve tracts during neuroembryogenesis.

Semaphorin III/collapsin-1 (semaIII/coll-1) is a chemorepellent that exhibits a repulsive effect on growth cones of dorsal root ganglion neurons. To identify structures that express semaIII/coll-1 in developing mammals, we cloned the rat homologue and performed in situ hybridization on embryonic, neonatal, and adult rats. The relationship between semaIII/coll-1 mRNA distribution and developing nerve tracts was studied by combining in situ hybridization with immunohistochemistry for markers of growing nerve fibers. At embryonic day 11, semaIII/coll-1 expression was restricted to the olfactory pit, the basal and rostral surface of the telencephalic vesicle, the anlage of the eye, the epithelium of Rathke's pouch, and the somites. At later developmental stages, semaIII/coll-1 mRNA was found to be widely distributed in neuronal as well as in mesenchymal and epithelial structures outside the nervous system. Strong expression was found in the olfactory bulb, retina, lens, piriform cortex, amygdalostriatal area, pons, cerebellar anlage, motor nuclei of cranial nerves, and ventral spinal cord. After birth, mesenchymal staining decreased rapidly and expression became progressively restricted to specific sets of neurons in the central nervous system (CNS). In the mature CNS, semaIII/coll-1 mRNA remains detectable in mitral cells, neurons of the accessory bulb and cerebral cortex, cerebellar Purkinje cells, as well as a subset of cranial and spinal motoneurons. The temporal and spatial expression pattern of semaIII/coll-1 mRNA and its relationship to emerging nerve tracts suggests that semaIII/coll-1 is involved in guiding growing axons towards their targets by forming a molecular boundary that instructs axons to engage in the formation of specific nerve tracts.

Animals↗
PubMed1997

Distribution of alpha1A adrenergic receptor mRNA in the rat brain visualized by in situ hybridization.

Norepinephrine has been implicated in a number of physiological, behavioral, and cellular modulatory processes in the brain, and many of these modulatory effects are attributable to alpha1 adrenergic receptors. At least three alpha1 receptor subtypes have been identified by molecular criteria, designated alpha1A, alpha1B, and beta1D. The distributions of alpha1B and alpha1D receptor mRNA expression in rat brain have been described previously, but the cDNA for the rat alpha1A receptor has only recently been cloned and characterized. In the present study, we used a radiolabelled riboprobe derived from the rat alpha1A receptor cDNA to describe the distribution of alpha1A message expression in the rat brain. The highest levels of alpha1A adrenergic receptor mRNA expression were seen in the olfactory bulb, tenia tectae, horizontal diagonal band/magnocellular preoptic area, zona incerta, ventromedial hypothalamus, lateral mammillary nuclei, ventral dentate gyrus, piriform cortex, medial and cortical amygdala, magnocellular red nuclei, pontine nuclei, superior and lateral vestibular nuclei, brainstem reticular nuclei, and several cranial nerve motor nuclei. Dual in situ hybridization combining a radioactive riboprobe for choline acetyltransferase mRNA with a digoxigenin-labeled alpha1A riboprobe in the fifth and seventh cranial nerve motor nuclei showed that the alpha1A mRNA is expressed in cholinergic motor neurons. Prominent alpha1A hybridization signal was also seen in the neocortex, claustrum, lateral amygdala, ventral cochlear nucleus, raphe magnus, and in the ventral horn of thoracic spinal cord. This overall pattern of expression, considered in comparison with that previously described for the other alpha1 adrenergic receptor subtypes, may shed light on the different roles of the alpha1 receptors in mediating the neuromodulatory effects of norepinephrine in processes such as arousal, neuroendocrine control, sensorimotor regulation, and the stress response.

Animals↗
PubMed1997

Distribution of radial glia in the developing telencephalon of chicks.

Radial glia are known to have a sparse and uneven distribution in the telencephalon of adult birds. The present study utilizes antibodies against vimentin to reveal a more extensive, and more clearly radial, set of radial glia in the chicken telencephalon during the first half of embryogenesis. This initially extensive radial glial fiber system becomes distorted and reduced between 10 and 14 days of incubation. This reduction coincides with the cytoarchitectural differentiation of the telencephalon into its major adult subdivisions. Because developing neurons tend to migrate along radial glial fibers in both birds and mammals, a topological projection of these major subdivisions onto the embryonic ventricular zone along the radial glial fibers suggests hypotheses about lineage relationships that can be tested by subsequent experimental methods. This analysis suggests that the major components of the avian dorsal ventricular ridge, i.e., the ventral hyperstriatum, the neostriatum with its various subdivisions, part of the archistriatum, and probably also the piriform cortex, all derive from overlapping portions of the lateral pallial ventricular zone. Staining with antibodies against neurofilament suggests that this developmental parcellation of the lateral pallial complex is associated with the development of neuronal fiber systems.

Animals↗
PubMed1996

Neuronal expression of hippocampal cholinergic neurostimulating peptide (HCNP)-precursor mRNA in rat brain.

The expression of hippocampal cholinergic neurostimulating peptide (HCNP)-precursor mRNA in rat brain was examined by Northern blot and in situ hybridization analyses. Northern blot analysis using rat HCNP-precursor cDNA revealed a 1.1-kilobase (kb) transcript. A message of identical size was also detected with the antisense precursor riboprobe. In situ hybridization disclosed that HCNP-precursor mRNA was expressed in many areas of the brain, including the basal forebrain cholinergic system, the olfactory system, and the cerebellum. Very high levels were seen in the pyramidal cells of the CA3 region and in the hilus of the dentate gyrus of the hippocampal formation. High levels were also found in the septal area, piriform cortex, entorhinal cortex, thalamic nuclei, subthalamic nuclei, medial habenular nuclei, substantia nigra, Purkinje cells of the cerebellum, and choroid plexus. By contrast, glial cells were not labeled by the antisense HCNP-precursor riboprobe. The expression of HCNP-precursor mRNA by a variety of neurons suggests that HCNP and its precursor protein play significant roles in the stimulation of cholinergic activity, as well as in other not yet defined functions.

Animals↗
PubMed1998

Seizure suppression in kindling epilepsy by grafts of fetal GABAergic neurons in rat substantia nigra.

Compared with studies on models of neurodegenerative diseases, considerably less work has been performed with neural grafts in experimental epilepsy. The potential value of this approach, however, is already shown by evidence that noradrenergic grafts implanted bilaterally into the hippocampus or amygdala-piriform cortex can suppress seizure development in the kindling model of temporal lobe epilepsy. We previously showed that amygdala kindling results in a significant decrease of GABA and its synthesizing enzyme glutamate decarboxylase in substantia nigra (SN), i.e., a region thought to be critically involved in seizure propagation in various models of epilepsy. Thus, transplantation of fetal GABAergic neurons into SN might be an effective means of permanently blocking seizure generalization in kindling epilepsy and probably also other types of epilepsy. To test this hypothesis, three groups of female Wistar rats (n = 10 per group) were kindled by electrical stimulation via a bipolar electrode in the basolateral amygdala. After all rats were fully kindled, one group was implanted with GABA-rich cells prepared from the striatal eminence of Wistar rat fetuses at embryonic day 14. The striatal neurons were bilaterally microinjected at various sites over the anterior-posterior axis of the SN, aimed at the pars reticulata. The second group received microinjections of spinal cord cell preparations, whereas the third group received microinjections of cell-free medium only. In all rats, the threshold for focal discharges (afterdischarge threshold [ADT]) as well as afterdischarge duration and severity and duration of seizures occurring at ADT current were determined once weekly before and after transplantation. Eleven to 12 weeks following transplantation, the rats were killed, and location and integration of grafts were examined by immunohistological methods. Rats with GABAergic grafts in SN exhibited a significant increase in ADT and marked reduction in seizure severity compared with pretransplantation values, whereas no such alteration was seen in the other groups. However, the seizure-suppressing effect of GABAergic grafts was not permanent but slowly disappeared over the weeks after transplantation. Although the data indicate that intranigral transplantation of GABA-producing cells is no effective means of inducing long-lasting anticonvulsant effects in experimental epilepsy, this approach may be an initial step to develop more efficient strategies for seizure suppression.

Animals↗
PubMed1998

Immunohistochemical localization of the neural cannabinoid receptor in rat brain.

The cannabinoid receptor family consists of two inhibitory G-protein-coupled receptors, CB1 and CB2. CB1 is distributed primarily in neural tissue, whereas CB2 is distributed predominantly in immune cells. The distribution of cannabinoid receptors in neural tissue has been demonstrated by using ligand binding autoradiography with CP55,940, a high-affinity cannabinoid receptor ligand, and in situ hybridization. However, the localization of CB1 within individual cells in the brain remains to be defined. In the present study, domain-specific polyclonal antibody to amino acids 83-98 of CB1 was used to define the expression of the neural cannabinoid receptor at the histochemical level. The use of CB1-specific antiserum is advantageous in view of recent reports that CB2 also is expressed in the brain and binds CP55,940. Thus, utilization of anti-CB1 antiserum would allow for the specific detection of CB1 protein expression. The regional staining pattern for CB1 in rat brain was consistent with that reported for CB1 using ligand binding autoradiography and in situ hybridization. Intense immunoreactivity was present in the hippocampal formation, the basal ganglia, and the molecular layer of the cerebellum. Moderate immunohistochemical staining was observed in the olfactory bulb, piriform cortex, cerebral cortex, and the granular layer of the cerebellum. In addition, immunoreactive staining was concentrated on afferent projections and dendritic processes of neuronal cells and was present within cell bodies and on cell surfaces. These data indicate that the anti-CB1 antibody is a sensitive probe for the unequivocal histological discrimination of CB1 protein expression.

Animals↗
PubMed1998

Anatomical distribution of the chemorepellent semaphorin III/collapsin-1 in the adult rat and human brain: predominant expression in structures of the olfactory-hippocampal pathway and the motor system.

Alterations in neuronal connectivity of the mature central nervous system (CNS) appear to depend on a delicate balance between growth-promoting and growth-inhibiting molecules. To begin to address a potential role of the secreted chemorepulsive protein semaphorin(D)III/collapsin-1 (semaIII/coll-1) in structural plasticity during adulthood, we used high-resolution nonradioactive in situ hybridization to identify neural structures that express semaIII/coll-1 mRNA in the mature rat and human brain. SemaIII/coll-1 was expressed in distinct but anatomically and functionally linked structures of the adult nervous system. The olfactory-hippocampal pathway displayed semaIII/coll-1 expression in a continuum of neuronal structures, including mitral and tufted cells of the olfactory bulb, olfactory tubercle, and piriform cortex; and distinct nuclei of the amygdaloid complex, the superficial layers of the entorhinal cortex, and the subiculum of the hippocampal formation. In addition, prominent labeling was found in neuronal components of the motor system, particularly in cerebellar Purkinje cells and in subpopulations of cranial and spinal motoneurons. Retrograde tracing combined with in situ hybridization also revealed that the staining of semaIII/coll-1 within the entorhinal cortex was present in the stellate neurons that project via the perforant path to the molecular layer of the dentate gyrus. Like in the rat, the human brain displayed discrete expression of semaIII/coll-1. Among the structures examined, the most prominent staining was observed in the cellular islands of the superficial layers of the human entorhinal cortex. The constitutive expression of the chemorepellent semaIII/coll-1 in discrete populations of neurons in the mature rat and human CNS raises the possibility that, in addition to its function as repulsive axon guidance cue during development, semaIII/coll-1 might be involved in restricting structural changes that occur in the wiring of the intact CNS.

Adult↗
PubMed1998

Abnormal astrocyte development and neuronal death in mice lacking the epidermal growth factor receptor.

Stimulation of the epidermal growth factor receptor (EGF-R) produces numerous effects on central nervous system (CNS) cells in vitro including neuronal survival and differentiation, astrocyte proliferation and the proliferation of multipotent progenitors. However, the in vivo role of EGF-R is less well understood. In the present study, we demonstrate that EGF-R null mice generated on a 129Sv/J Swiss Black background undergo focal but massive degeneration the olfactory bulb, piriform cortex, neocortex, and thalamus between postnatal days 5 and 8 which is due, at least in part, to apoptosis. Some of the neuronal populations that degenerate do not normally express EGF-R, indicating an indirect mechanism of neuronal death. There were also delays in GFAP expression within the glia limitans and within structures outside the germinal zones in early postnatal ages. At or just prior to the onset of the degeneration, however, there was an increase in GFAP expression in these areas. The brains of EGF-R (-/-) animals were smaller but cytoarchitecturally normal at birth and neuronal populations appeared to be intact, including striatal GABAergic and midbrain dopaminergic neurons which have previously been shown to express EGF-R. Multipotent progenitors and astrocytes derived from EGF-R (-/-) mice were capable of proliferating in response to FGF-2. These data demonstrate that EGF-R expression is critical for the maintenance of large portions of the postnatal mouse forebrain as well as the normal development of astrocytes.

Animals↗
PubMed2000

Immunocytochemical mapping of Fos protein following seizures in gerbils indicates the activation of hippocampal neurons.

The expression of the proto-oncogene, c-fos, and its protein, Fos, has been shown to be a useful marker for elevated levels of neuronal activity generated in the brain following different stimuli, including seizures. Since previous studies indicated hippocampal involvement in seizure activity in gerbils, Fos immunocytochemistry was used to determine whether hippocampal neurons become activated following environmentally induced seizures in this animal. Gerbils with maximal seizures showed many Fos-immunolabeled neurons in the granule cell layer and hilus of the dentate gyrus, as well as in CA3 and CA1 of the hippocampus. These gerbils had significantly greater numbers of Fos-immunolabeled dentate granule cells than gerbils with less severe seizures or no seizures. The number of dentate granule cells and CA3 pyramidal cells with Fos immunolabeling increased in an exponential manner with increased seizure severity. Many Fos-immunolabeled neurons were found in several regions of the neo- and paleocortex and in other limbic structures including the piriform cortex, cortical amygdaloid nucleus, and arcuate nucleus of the hypothalamus. These results indicate that hippocampal neurons are activated following seizures in a genetic model, and provide further proof that the hippocampal formation is involved in the circuitry for seizures in gerbils.

Animals↗
PubMed2000

Basal telencephalic regions connected with the olfactory bulb in a Madagascan hedgehog tenrec.

In an attempt to gain insight into the organization and evolution of the basal forebrain, the region was analysed cytoarchitecturally, chemoarchitecturally, and hodologically in a lower placental mammal, the lesser hedgehog tenrec. Particular emphasis was laid on the subdivision of the olfactory tubercle, the nuclear complex of the diagonal band, and the cortical amygdala. The proper tubercule and the rostrolateral tubercular seam differed from each other with regard to their immunoreactivity to calbindin and calretinin, as well as their afferents from the piriform cortex. Interestingly, the tubercular seam showed similar properties to the dwarf cell compartment, located immediately adjacent to the islands of Calleja. The most prominent input to the olfactory bulb (OfB) originated from the diagonal nuclear complex. This projection was ipsilateral, whereas the bulbar afferents from the hypothalamus and the mesopontine tegmentum were bilateral. The amygdala projected only sparsely to the OfB, but received a prominent bulbar projection. An exception was the nucleus of the lateral olfactory tract, which was poorly connected with the OfB. Unlike other species with an accessory OfB, the projections from the tenrec's main OfB did not show a topographic organization upon the lateral and medial olfactory amygdala. However, there was an accessory amygdala, which could be differentiated from the lateral nuclei by its intense reaction to NADPh-diaphorase. This reaction was poor in the diagonal nuclear complex as in monkey but unlike in rat. The variability of cell populations and olfactory bulb connections shown here may help to clarify both phylogenetic relationships and the significance of individual basal telencephalic subdivisions.

Amygdala↗
PubMed2000

Human cocaine- and amphetamine-regulated transcript (CART) mRNA is highly expressed in limbic- and sensory-related brain regions.

Cocaine- and amphetamine-regulated transcript (CART) is a novel putative peptide neurotransmitter. We studied the expression of CART mRNA throughout the human postmortem brain by using in situ hybridization histochemistry. The cortical expression was distinct with high mRNA expression levels in the piriform cortex, dorsolateral prefrontal cortex, lateral orbital prefrontal cortex, medial orbitofrontal cortex, and middle temporal cortex, but extremely low levels in immediately adjacent cortical areas, e.g., the medial prefrontal cortex, subcallosal gyrus, and superior temporal cortex. Within the striatum, CART mRNA was only detected in the nucleus accumbens, primarily in the most medial area. No positive CART mRNA-expressing neurons were found in the dorsal caudate nucleus and putamen. High mRNA expression levels were evident within the bed nucleus of the stria terminalis as well as the amygdala (central, cortical, and medial nuclei). In the hippocampus, intense expression was found within the uncal gyrus and moderate to high levels in the CA3 and polymorphic layer of the dentate gyrus. CART mRNA expression was also detected in the locus coeruleus and dorsal raphe, but no positive labeling was apparent in the substantia nigra. Overall, the most abundant CART mRNA expression levels in the human brain were detected within in the hypothalamus (posterior, paraventricular nucleus, premammillary, tuberomamillary, dorsomedial, arcuate) and the thalamus (mediodorsal, pulvinar, anterior, zona incerta, geniculate). Rat brain specimens were also studied and many similarities to the human CART mRNA expression were evident. However, the most marked species difference was the virtual absence of the CART mRNA in the rat thalamus.

Adult↗