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PubMed1992

The organization of the thalamocortical connections of the mediodorsal thalamic nucleus in the rat, related to the ventral forebrain-prefrontal cortex topography.

The medial and central segments of the mediodorsal nucleus of the thalamus (MD) receive afferents from the ventral forebrain, including the piriform cortex, the ventral pallidum, and the amygdaloid complex. Because MD is reciprocally interconnected with prefrontal and agranular insular cortical areas, it provides a relay of ventral forebrain activity to these cortical areas. However, there are also direct projections from the piriform cortex and the amygdala to the prefrontal and agranular insular cortices. This study addresses whether this system has a "triangular" organization, such that structures in the ventral forebrain project to interconnected areas in MD and the prefrontal/insular cortex. The thalamocortical projections of MD have been studied in experiments with injections of retrograde tracers into prefrontal or agranular insular cortical areas. In many of the same experiments, projections from the ventral forebrain to MD and to the prefrontal/insular cortex have been demonstrated with anterograde axonal tracers. The connections of the piriform cortex (PC) with MD and the prefrontal/insular cortex form an organized triangular system. The PC projections to the central and medial segments of MD and to the lateral orbital cortex (LO) and the ventral and posterior agranular insular cortices (AIv and AIp) are topographically organized, such that more caudal parts of PC tend to project more medially in MD and more caudally within the orbital/insular cortex. The central and medial portions of MD also send matching, topographically organized projections to LO, AIv and AIp, with more medial parts of MD projecting further caudally. The anterior cortical nucleus of the amygdala (COa) also projects to the dorsal part of the medial segment of MD and to its cortical targets, the medial orbital area (MO) and AIp. The projections of the basal/accessory basal amygdaloid nuclei to MD and to prefrontal cortex, and from MD to amygdaloceptive parts of prefrontal cortex, are not as tightly organized. Amygdalothalamic afferents in MD are concentrated in the dorsal half of the medial segment. Cells in this part of the nucleus project to the amygdaloceptive prelimbic area (PL) and AIp. However, other amygdaloceptive prefrontal areas are connected to parts of MD that do not receive fibers from the amygdala. Ventral pallidal afferents are distributed to all parts of the central and medial segments of MD, overlapping with the fibers from the amygdala and piriform cortex. Fibers from other parts of the pallidum, or related areas such as the substantia nigra, pars reticulata, terminate in the lateral and ventral parts of MD, where they overlap with inputs from the superior colliculus and other brainstem structures.(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗
PubMed1992

Regional distribution of DARPP-32 (dopamine- and adenosine 3',5'-monophosphate-regulated phosphoprotein of Mr = 32,000) mRNA in mouse brain.

DARPP-32 (dopamine- and adenosine 3',5'-monophosphate-regulated phosphoprotein of Mr = 32,000) mRNA distribution was examined in adult mouse central nervous system by in situ hybridization. In general, DARPP-32 mRNA was found in regions of brain where cells express the dopamine D1 subtype receptor. Cells of the olfactory tubercle, caudate-putamen, and nucleus accumbens had the highest levels of DARPP-32 mRNA, as did choroid plexus and Purkinje cells. Relatively high levels were found in medial habenula and lateral piriform cortex. Moderate levels were seen in cerebral cortex layer VI, medial piriform cortex, lateral entorhinal cortex, tenia tecta, anterior olfactory nucleus, and lateral bed nucleus of the stria terminalis. Low levels were observed in hippocampus, cerebral cortex layers II and III, olfactory bulb, and the nucleus of the lateral olfactory tract. DARPP-32 mRNA levels in the amygdaloid nuclei varied greatly.

Animals↗
PubMed2001

Ex vivo MR microimaging of neuronal damage after kainate-induced status epilepticus in rat: correlation with quantitative histology.

The present study was designed to investigate whether T(2)-weighted signal changes obtained by microimaging of paraformaldehyde-fixed brain correlate with the histologically quantified damage in a model of status epilepticus (SE) induced by kainic acid in the rat. Animals were killed at several time points up to 8 weeks after a single intraperitoneal kainate (KA) injection (9 mg/kg). Perfusion-fixed brains were embedded in gelatin for MR microimaging at 9.4T. After the MRI analysis, the gelatin was removed and the brains were cryoprotected and processed for quantitative histology. Severity of neuronal damage and gliosis were assessed from thionin-stained serial sections. Correlative analysis of microimaging and histology data was done in the hippocampus, amygdala, parietal rhinal cortex (PaRH), piriform cortex (Pir), and entorhinal cortex. The relative signal intensities in T(2)-weighted images correlate with the severity of neuronal damage in the matched histological sections (correlation coefficients of 0.752-0.826). Our data show that MR microimaging ex vivo detects the degree of neuronal damage and its anatomical distribution after KA-induced SE, thus providing a useful tool for detecting the dynamics of progressive neuronal damage after prolonged seizures.

Animals↗
PubMed1988

Amygdala kindling and c-fos protein(s).

c-fos protein was visualized immunohistochemically in the brains of rats after partial amygdala seizures and generalized amygdala-kindled seizures and in seizure-free amygdala-kindled rats. Four hours following partial amygdala seizures there was a massive induction of c-fos protein in the ipsilateral piriform cortex, entorhinal cortex, and amygdala. Following generalized amygdala-kindled seizures there was a massive bilateral induction of c-fos in the entire cerebral cortex, amygdala, piriform and entorhinal cortices, hippocampus, and dentate gyrus. However, there did not appear to be any change in the basal levels of c-fos in the brains of amygdala-kindled rats that had been seizure free for 7 days. These results show that kindled seizures induce c-fos in neurons, but that the permanence of kindling is not related to altered basal c-fos levels.

Amygdala↗
PubMed1989

Effect of cysteamine on somatostatin-like immunoreactivity in the amygdala-kindled rat brain.

Previous studies have shown that a somatostatin-depleting drug, cysteamine (CYS), suppresses kindled seizures. However, no data is available concerning the levels of somatostatin-like immunoreactivity (SLI) in the kindled rat brain after CYS administration. In the present study, we used radioimmunoassay to measure SLI in the frontal cortex, amygdala + piriform cortex, hippocampus, striatum and hypothalamus: 1) in control rats, 2) in amygdala-kindled rats decapitated 14 days after the last stimulus, and 3) in amygdala-kindled rats decapitated 14 days after the last stimulus but treated either 11 days or 4) 4 hours before decapitation with CYS (100 mg/kg, subcutaneously). The results showed that, compared to controls, in kindled rats SLI was elevated both in the ipsi lateral (28%, p = 0.0372) and contralateral (17%, p = 0.0078) frontal cortex. Compared to kindled rats, CYS given 4 hours before decapitation decreased SLI in the frontal cortex (to 71%, p = 0.0066) and hippocampus (to 72%, p = 0.0027), but compared to the controls, only in the hippocampus. In rats given CYS 11 days before decapitation, SLI did not differ from either the controls or from the kindled rats. In conclusion, the somatostatinergic system is affected in amygdala-kindling; but the relationship of anatomical localization and the magnitude of CYS-induced decrease of SLI to elevated seizure threshold needs to be studied further.

Amygdala↗
PubMed1993

Immunocytochemical detection of insulin receptor substrate-1 (IRS-1) in rat brain: colocalization with phosphotyrosine.

In peripheral insulin-sensitive tissues, insulin receptor substrate (IRS-1) undergoes tyrosine phosphorylation immediately after cells are stimulated by insulin or insulin-like growth factor-1 (IGF-1), and may function as a molecular link between insulin/IGF-1 receptor tyrosine kinases and enzymes regulating cell growth and metabolism. A fundamental question pertaining to insulin/IGF-1 action in the brain is whether IRS-1 is expressed by neurons. In this study, the distribution of cells containing immunoreactivity to IRS-1 in the brain was determined by immunocytochemistry with polyclonal IRS-1 antiserum, and compared to the localization of immunostaining for phosphotyrosine using polyclonal phosphotyrosine antiserum. The immunostaining results with ABC-peroxidase method and cryostat sections showed the presence of IRS-1 immunoreactivity in many neuron cell bodies throughout the rat forebrain, particularly in the habenula, cerebral cortex and piriform cortex. In the hypothalamus, IRS-1 immunostaining was present in neurons of the paraventricular nucleus, supraoptic nucleus, and arcuate nucleus. The choroid plexus stained intensely for IRS-1. The populations of cells that stained for IRS-1 also showed strong immunostaining for phosphotyrosine. Studies at the cellular level are needed to verify coexpression of IRS-1 and receptors for insulin or IGF-1 by the same neurons, as well as in cells of the choroid plexus. The present results are the first demonstration of IRS-1 expression by neurons in adult mammalian brain. These findings are consistent with the hypothesis that insulin and IGF-1 actions in the brain involve signal transduction mechanisms common to those found in peripheral tissues.

Animals↗
PubMed1994

Anodal polarization induces protein kinase C gamma (PKC gamma)-like immunoreactivity in the rat cerebral cortex.

Protein kinase C gamma (PKC gamma)-like immunoreactivity was examined in the rat brain, employing the monoclonal antibody 36G9 raised against purified PKC gamma, after an application of weak anodal direct current to the surface of the sensorimotor cortex. Anodal polarization with 3.0 microA for 30 min resulted in a pronounced increase in the number of PKC gamma-like-positive neurons in accordance with the intensity of PKC gamma-like immunostaining in the neocortex, cingulate cortex and piriform cortex ipsilateral to the polarization. The number of PKC gamma-like-positive neurons began to increase at 1 h after polarization, peaked at 3 h, and thereafter decreased to the control levels by 72 h. The increase in expression of PKC gamma-like immunoreactivity in specific areas of the cerebral cortex is suggested to serve as a basis for the long-lasting hyperexcitability in situ following anodal polarization.

Animals↗
PubMed1994

Lactation-induced deficits in NMDA receptor-mediated cortical and hippocampal activation: changes in NMDA receptor gene expression and brainstem activation.

During lactation, there is an inhibition of cortical and hippocampal activation in response to N-methyl-D,L-aspartate (NMA), but not kainate, as assessed by induction of c-Fos expression. To study whether changes in NMDA receptor function may account for this inhibition, NMDA receptor subunit (NMDAR1) mRNA levels were measured by both Northern analysis and in situ hybridization. Analysis of NMDAR1 gene expression by Northern blot analysis did not reveal significant differences between cycling and lactating rats. Using in situ hybridization, NMDAR1 mRNA levels in several cortical and hippocampal areas appeared to be smaller in lactating rats, compared to cycling rats, although these differences reached significance only in the fronto-parietal cortex and piriform cortex. These subtle changes in NMDAR1 receptor subunit gene expression during lactation are not likely to account for the global lack of neuronal activation in response to NMA. However, it is possible that there may be changes in other NMDA receptor subunits that could account for the deficits in NMDA receptor activation. We also examined the activation state of afferent pathways in the brainstem that provide excitatory input to the cortex and hippocampus. During lactation, NMA induced c-Fos expression in similar areas of the brainstem as during the cycle, except in the locus coeruleus and dorsal raphe, where c-Fos expression was significantly less than that observed during the cycle. In contrast, no differences in the pattern of c-Fos expression in the brainstem in response to kainate were observed between cycling and lactating rats. The lack of NMA-induced activation of the locus coeruleus and dorsal raphe may contribute to the lack of cortical activation during lactation.

Animals↗
PubMedDate not supplied

Neurotoxic effects of neonatal triethyltin (TET) exposure are exacerbated with aging.

Neonatal Long-Evans rats dosed with TET (5 mg/kg; IP) or saline on postnatal day (PND) 10 were examined across the life span for neural damage and performance on spatial learning tasks. A subset of rats were sacrificed to assess early damage with Nissl-staining, Timm's histochemistry, and glial fibrillary acidic protein (GFAP) immunohistochemistry 2, 7, or 14 days after dosing. Littermates were tested behaviorally in a T-maze spatial delayed alternation task on PND 23 or PND 90, and in a Morris water maze place learning task at 3, 12, or 24 months postdosing and then sacrificed for histological analysis. In neonatal rats, histological analysis indicated gliosis in discrete cortical regions, loss of Nissl-stained neurons in the hippocampal formation, entorhinal cortex and piriform cortex, and loss of Timm's staining in the entorhinal cortex. The behavioral assessment at PND 23 indicated a significant impairment in the T-maze. However, no significant impairments were observed in the T-maze at 3 months or the water maze at 3 or 12 months postdosing. At 24 months, TET-treated rats showed significant deficits in acquisition and retention of the water maze task compared with age-matched controls. Both groups of 24 months old rats were significantly impaired compared with young controls. At 24 months, there was a general age-related decrease in the optical density of Timm's staining in cortical regions (9%), compounded by a further decrease in the entorhinal cortex and outer molecular layer of the dentate gyrus of the hippocampus in TET treated rats (30%). These data indicate that early developmental exposure to an organometal resulted in morphological damage that was apparent behaviorally only during early postnatal development and with advanced aging.

Aging↗
PubMed1994

Differential expression of messenger RNAs for somatostatin receptor subtypes SSTR1, SSTR2 and SSTR3 in adult rat brain: analysis by RNA blotting and in situ hybridization histochemistry.

The messenger RNAs encoding three somatostatin receptor subtypes, SSTR1, SSTR2 and SSTR3, were detected in rat by RNA blotting and in situ hybridization histochemistry to identify the sites of synthesis and expression of these somatostatin receptor subtypes. RNA blotting revealed that SSTR1 messenger RNA of 3.8 kilobases was highly expressed in cerebral cortex, hippocampus, midbrain and hypothalamus. In situ hybridization histochemistry revealed that SSTR1 messenger RNA was localized to discrete layers of the cerebral cortex, the piriform cortex and the dentate gyrus of the hippocampus. SSTR1 messenger RNA was expressed at low levels in the cerebellum and pituitary and was not detectable in striatum or other peripheral organs. At least two SSTR2 messenger RNAs were detected by RNA blotting of 2.4 and 2.8 kilobases which correspond to the size of the spliced and unspliced forms of this receptor messenger RNA. SSTR2 messenger RNA detected by in situ hybridization is diffusely expressed in cerebral cortex and amygdala but is discretely localized to dentate gyrus in the hippocampus, medial habenula and ventromedial and dorsomedial nuclei and arcuate nucleus of the hypothalamus. The levels of SSTR2 messenger RNA are very low in the cerebellum and were not observed in the striatum or peripheral tissues other than the pituitary or adrenal gland. A single SSTR3 messenger RNA of 4.0 kilobases was seen in hippocampus, cerebral cortex, midbrain, hypothalamus and pituitary. However, the tissue with the highest levels of SSTR3 messenger RNA is the cerebellum with messenger RNA localized to the granule cell layer. The expression of the three different somatostatin receptor messenger RNAs are distinct but overlapping. Such distinct expression may contribute to the selective biological roles of the receptor subtypes.

Animals↗
PubMed1986

Cholinergic limbic projections and behavioral role of basal forebrain nuclei in the rat.

The purposes of the present study were to identify cholinergic non-neocortical projections of the basal forebrain and to determine the role of this region in the regulation of estrogen-dependent reproductive behaviors in the rat. Bilateral electrolytic lesions were placed in an area encompassing the horizontal limb of the diagonal band, as well as portions of the substantia innominata and magnocellular preoptic nucleus, and choline acetyltransferase (CAT) activity was assayed in microdissected brain areas seven days after lesion. Compared to sham surgery, lesions of this region significantly reduced CAT activity in the basal amygdala (34%), dorsal hippocampus (14%), cingulate cortex (25%), piriform cortex (36%), and entorhinal cortex (34%). Other limbic and midbrain structures do not appear to receive significant cholinergic innervation from this locus since no reductions in CAT were detected after bilateral lesions. These included the anterior hypothalamus, ventromedial hypothalamus, mammillary nucleus, habenula, subiculum, ventral hippocampus, insular cortex, central gray, and interpeduncular nucleus. Behaviorally, female rats with bilateral lesions of the basal forebrain displayed an unusually high incidence of rejection behavior in response to attempted mounts by stimulus male rats in sexual behavior tests. There was no effect of basal forebrain lesions on the incidence of lordosis exhibited by these females. The dissociation of rejection and lordosis suggests that distinct neural pathways mediate the occurrence of these reproductive behaviors and that rejection behavior may be regulated by basal forebrain pathways.

Animals↗
PubMed2006

Chronic antidepressant treatment selectively increases expression of plasticity-related proteins in the hippocampus and medial prefrontal cortex of the rat.

Antidepressants protect against hippocampal volume loss in humans and reverse stress-induced atrophic changes in animals thus supporting the hypothesis that the pathophysiology of stress-related disorders such as depression involves reductions in neuronal connectivity and this effect is reversible by antidepressant treatment. However, it is unclear which brain areas demonstrate such alterations in plasticity in response to antidepressant treatment. The aim of the present study was to examine the effect of antidepressant treatment on the expression of three plasticity-associated marker proteins, the polysialylated form of nerve cell adhesion molecule (PSA-NCAM), phosphorylated cyclic-AMP response element binding protein (pCREB) and growth-associated protein 43 (GAP-43), in the rat brain. To this end, rats were treated either acutely (60 min) or chronically (21 days) with imipramine (30 and 15 mg/kg, respectively) and the expression of PSA-NCAM, pCREB, and GAP-43 was assessed using immunohistochemistry. Initial mapping revealed that chronic imipramine treatment increased expression of these plasticity-associated proteins in the hippocampus, medial prefrontal cortex and piriform cortex but not in the other brain regions examined. Since PSA-NCAM and pCREB are expressed in recently-generated neurons in the dentate gyrus, it is likely that chronic imipramine treatment increased their expression in the hippocampus at least partially by increasing neurogenesis. In contrast, since chronic imipramine treatment is not associated with neurogenesis in the medial prefrontal cortex, increased expression of PSA-NCAM and pCREB in the prelimbic cortex implicates changes in synaptic connectivity in this brain region. Acute treatment with imipramine increased the number of pCREB positive nuclei in the hippocampus and the prefrontal cortex but did not alter expression of GAP-43 or PSA-NCAM in any of the brain regions examined. Taken together, the results of the present study suggest that antidepressant treatment increases synaptic plasticity and connectivity in brain regions associated with mood disorders.

Animals↗
PubMed2005

Immunohistochemical localization of toluene-induced c-Fos protein expression in the rat brain.

Although toluene is a widely abused substance, the neuronal populations and pathways mediating its effects are not well understood. Using c-Fos protein as a marker for neuronal activation, the present study investigated the pattern of c-Fos induction at 1h after various doses (0, 300, 750, and 1000 mg/kg, i.p.) of toluene injection in adult male rats. Quantitative analysis of Fos-immunoreactive neurons indicated toluene dose-related induced c-Fos immunoreactivity in the majority of structures examined. The structures included several cortex subareas (primary motor cortex, secondary motor cortex, somatosensory cortex, frontal association cortex, cigulate cortex area 1, cigulate cortex area 2, prelimbic cortex, infralimbic cortex, retrosplenial agranular cortex, ventral orbital cortex, lateral orbital cortex, and piriform cortex), ventral tegmental area, nucleus accumbens shell, thalamic nuclei (mediodorsal, lateral posterior, and laterodorsal ventrolateral) and pontine nuclei. However, the substantia nigra, caudate putamen, nucleus accumbens core, subthalamic nucleus, hippocampus and cerebellum were almost unaffected. The data demonstrate that toluene dose-related induced a unique pattern of c-Fos immunoreactivity. The widespread distribution of toluene-induced c-Fos expression seen in this study can be linked to the profound alterations in physiological function and behavior produced by this solvent.

Animals↗
PubMed2003

Characterization of zetin 1/rBSPRY, a novel binding partner of 14-3-3 proteins.

14-3-3 proteins are ubiquitously expressed proteins which serve as central adaptors in different signal transduction cascades. In this study, yeast two-hybrid screening of a rat brain cDNA library identified a novel gene product termed zetin 1/rBSPRY that interacts with 14-3-3 zeta. The zetin 1/rBSPRY gene is ubiquitously expressed in a variety of rat tissues, with highest expression being found in testis. In adult brain, high levels of zetin 1/rBSPRY mRNA were observed in the hippocampus, cerebral cortex, and piriform cortex. Biochemical studies confirmed zetin 1/rBSPRY to interact with 14-3-3 zeta. Transient co-transfection in COS 7 cells caused a partial redistribution of zetin 1/rBSPRY into 14-3-3 zeta enriched submembranous foci at leading edges. Our results suggest a role for zetin 1/rBSPRY-14-3-3 interactions at specialized submembrane domains.

14-3-3 Proteins↗
PubMed1998

Visualization of specific angiotensin II binding sites in the rat limbic system.

The present study examined the distribution of angiotensin-binding cells by using a fluorescence-coupled angiotensin II in fixed horizontal sections that contained several limbic structures. In normal female rats, dense staining was found in the CA3 and CA1 regions and the dentate gyrus of the hippocampus--in the subiculum as well as in the entorhinal cortex and piriform cortex. Moderate staining was found in the CA2 region, in the central and medial nuclei of the amygdala. Low-level staining was obtained in the basolateral and lateral nucleus of the amygdala as well as in the bed nucleus of the stria terminalis. The co-incubation of fluorescence-coupled angiotensin II together with angiotensin II in excess and with saralasin, respectively, suppressed the angiotensin staining in structures investigated.

Amygdala↗
PubMed1998

Mapping of angiotensin AT1 receptors in the rat limbic system.

The AT1 receptor is one of the two receptor subtypes able to bind angiotensin II. In the present study, immunohistochemical examination of the distribution of the AT1 receptor in several limbic structures of female rats has been done, revealing new aspects of the distribution of AT1-positive cells. The presence of AT1 receptor expressing cells in the hippocampus and the amygdala is described, but their distribution in these regions has not been examined in a detailed way. We found some notable differences in the distribution of these cells: in female rats, we detected high amounts of labeled cells in the hippocampus, the entorhinal cortex and piriform cortex. In somewhat lower amounts, stained cells could be found in several nuclei of the amygdala (in the basomedial, basolateral, lateral, central and medial nucleus of the amygdala, in the amygdalopiriform transition area and in the amygdalohippocampal transition area as well as in the bed nucleus of the stria terminalis).

Amygdala↗
PubMed2002

Seizure-mediated neuronal activation induces DREAM gene expression in the mouse brain.

Various transcriptional activators are induced in neurons concomitantly with long-lasting neural activity, whereas only a few transcription factors are known to act as neural activity-inducible transcription repressors. In this study, mRNA of DREAM (DRE-antagonizing modulator), a Ca(2+)-modulated transcriptional repressor, was demonstrated to accumulate in the mouse brain after pentylenetetrazol (PTZ)-induced seizures. Accumulation in the mouse hippocampus reached maximal level in the late phase (at 7-8 h) after PTZ injection. Kainic acid induced the same response. Interestingly, the late induction of DREAM expression required new protein synthesis and was blocked by MK801 suggesting that Ca(2+)-influx via NMDA receptors is necessary for the PTZ-mediated DREAM expression. In situ hybridization revealed that PTZ-induced DREAM mRNA accumulation was observed particularly in the dentate gyrus, cerebral cortex, and piriform cortex. The results of the present study demonstrate that DREAM is a neural activity-stimulated late gene and suggest its involvement in adaptation to long-lasting neuronal activity.

Animals↗
PubMed1997

Autoradiographic visualization of the receptor subclasses for vasoactive intestinal polypeptide (VIP) in rat brain.

Vasoactive Intestinal Polypeptide (VIP) exerts its biological effects through interaction with two high affinity receptors named the VIP1- and the VIP2 receptors. Their messenger RNAs have been mapped in rat brain by in situ hybridization. A cyclic peptide (RO 25-1553) and a secretion analogue ([R16]chicken secretin) were identified as selective agonist peptides for the VIP2- and VIP1 receptors, respectively. The iodinated peptides retained the high affinity and selectivity of the unlabelled peptides and were used for the mapping of each receptor subclass in rat brain. VIP1 receptors were present in the cerebral cortex, the piriform cortex, the claustrum, the caudate-putamen, the dentate gyrus, the lateral amygdaloïd nucleus, the anteroventral thalamic nucleus, the rhomboïd nucleus, the supraoptic nucleus and the choroïd plexus. VIP2 receptors were present in the cerebral cortex, the claustrum, the caudate-putamen, the nucleus accumbens, the lateral septal nuclei, the bed nucleus of the stria terminalis, the basolateral amygdaloïd nucleus, the Ammon's horn, the thalamic nuclei except some centromedial nuclei, the medial habenula, the suprachiasmatic nucleus, the periventricular nucleus, the mammilary nucleus, the superior colliculus and the choroïd plexus.

Animals↗