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PubMed1984

[Axospinal synapses in the forebrain cortex of aquatic and terrestrial turtles].

An electron microscopical investigation of synaptic organization of the superficial plexiform layer of three forebrain cortical zones (hippocampal, dorsal and piriform) in two aquatic and two land Chelonia species has been performed. As demonstrate the data obtained and those from the literature, the main elements of the axo-spinal complexes (spines--synapses--neural terminals) possess both stability properties, contributing to structural firmness of the contacts and their reliability during activities, and plastisity ensuring the maintenance of dynamic equilibrium and a possibility for adequate rearrangements. Under normal conditions, the functional shifts in ultrastructure of the synaptic apparatuses are, possibly, so negligible that they cannot mask certain specific fractures of the synaptic organization of the neural centers. When comparing structures of the axo-spinal complexes in functionally dissimilar cortical zones, more constant, common for all species of Chelonia studied signs are definitely revealed. They characterize a certain level of the neural processes integration. There are signs more variable, evidently, ensuring adaptive rearrangements within limits of the given level of the interneuronal connections organization which can be considered as ecological and species-specific peculiarities.

Animals↗
PubMed1998

[Structural organization and Lugaro neuron connections in the cat cerebellar cortex].

Two types of intermedial Lugaro cells are distinguished in the cat cerebellum: fusiform (horizontal, vertical and obliquely oriented at angles 60-70 to longitudinal axis of folia cerebelli at different levels of granular layer) and those with triangular somata, sparsely branching dendrites and small number of spines. Both fusiform and triangular neuron axons do not stretch out beyond the borders of cerebellar cortex and may be thought of as recurrent interneurons as they contain GABA and glycine. Lugaro cells form numerous contacts almost with all cortical nervous elements: piriform (Purkinje) and Golgi cells, granular and basket neurons, parallel and mossy fibres and even unipolar, (brush) cells. At light microscopic level they are represented as axosomatic and axodendritic contacts. Lugaro cells are the only cerebellar cortical interneurons with dendritic arborizarion oriented in horizontal plane in contrast to vertical orientation of the other interneurons of cerebellar cortex.

Animals↗
PubMed2000

Characterization of benzodiazepine receptor binding in immature rat brain after kainic acid administration.

PURPOSE: To evaluate the effects of status epilepticus on benzodiazepine (BDZ) receptor binding in immature rat brain. METHODS: Twenty-four immature (15 days old) and six adult (90 days old) rats were used in this study. Status epilepticus was induced in immature animals by administration of kainic acid (7 mg/kg intraperitoneal), whereas adults rats received saline. Animals were killed 72 hours or 35 days after treatment, and their brains were used for in vitro autoradiography experiments to determine BDZ binding. RESULTS: In basal conditions and compared with the adult group, immature animals presented reduced BDZ binding in the entorhinal cortex, substantia nigra pars reticulata, and periaqueductal gray. Seventy-two hours after kainic acid-induced status epilepticus, immature rats showed significantly increased BDZ in the frontal (48%), cingulate (39%), sensorimotor (39%), piriform (57%), and entorhinal (59%) cortices, the medial (84%) and basolateral (27%) amygdaloid nuclei, the dentate gyrus (51%), and the substantia nigra pars reticulata (43%). Thirty-five days after status epilepticus, immature rats displayed decreased BDZ binding in the entorhinal cortex (48%), dentate gyrus (36%), and fields CA1, CA2, and CA3 of Ammon's horn (30%). CONCLUSIONS: The present study demonstrates that status epilepticus and temporal lobe epilepsy produce a characteristic pattern of BDZ binding changes in the immature rat brain that differs from the one previously seen in adults.

Age Factors↗
PubMed2000

Localization of the CB1 cannabinoid receptor in the rat brain. An immunohistochemical study.

The presence of central cannabinoid receptor (CB1), involving the N-terminal 14 amino acid peptide, was demonstrated in the rat brain by immunohistochemistry. Intensely stained neurons were observed in the principal neurons of the hippocampus, striatum, substantia nigra, cerebellar cortex, including the Purkinje cells. Moderate CB1-IR cell bodies and fibers were present in the olfactory bulb, cingulate, entorhinal and piriform cortical areas, amygdala and nucleus accumbens. The perivascular glial fibers have shown moderate to high density CB1-IR in olfactory and limbic structures. Low density was detected in the thalamus and hypothalamus and area postrema. The CB1 receptor was widely distributed in the forebrain and sparsely in the hindbrain. These new data support the view that the endogenous cannabinoids play an important role in different neuronal functions as neuromodulators or neurotransmitters.

Amygdala↗
PubMed1991

Focal ischemia in rats causes time-dependent expression of c-fos protein immunoreactivity in widespread regions of ipsilateral cortex.

c-Fos protein expression was examined in brain by immunohistochemistry following permanent middle cerebral artery (MCA) occlusion above the rhinal fissure and ipsilateral common carotid artery (CCA) occlusion in Long-Evans rats. In sham-operated animals, c-fos protein-like immunoreactivity (CFPLI) was confined to neuronal nuclei of the hypothalamus and was not present in other regions including cerebral cortex. In the core territory of the MCA, CFPLI was not detected when examined at 15 and 30 min, 1, 4 and 8 h and 1, 2, 4 and 7 days after occlusion. Focal ischemia induced two temporal and spatial patterns of CFPLI. At 1 h, c-fos protein was expressed in the nuclei of many neurons in layers II-V of the ipsilateral cortex both immediately adjacent to and remote from the ischemic territory. Within regions outside the MCA territory (e.g. cingulate gyrus and piriform cortices), CFPLI in these neurons peaked at 2-4 h and was undetectable after 2 days. Neurons in the zone immediately surrounding the ischemic core within MCA territory also expressed CFPLI, but in contrast, continued to express c-fos up to 4 days after ischemia. Immunoreactivity surrounding the ischemic core was found in neuronal nuclei predominantly, although from 1 to 4 days, CFPLI was found in perikarya and dendrites as well. MK-801 (3 mg/kg, i.p., 30 min prior to occlusion) completely blocked the early c-fos protein induction in all regions but expression within neurons surrounding the ischemic core was present 1 day after a single injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

The limbic zone of the rabbit and rat claustrum: a study of the claustrocingulate connections based on the retrograde axonal transport of fluorescent tracers.

The claustrum is a subcortical structure lying under the insular and piriform cortices, whose function is still not clear. Although data exist on connections of the claustrum and the limbic cortex, the topography of the limbic zone in the rabbit and rat claustrum has not been studied extensively. The study was performed on 17 adult Wistar rats and 12 New Zealand rabbits. Two percent water solutions of fluorescent retrograde tracers fast blue and nuclear yellow were injected into the various regions of the limbic cortex. The limbic zone is localized throughout the whole rostrocaudal extent of the claustrum, mainly in its ventromedial portion lying close to the external capsule. Although this zone of the claustrum is localized similarly in both rat and rabbit, some differences between these two species exist. In the rat, neurons projecting to all limbic areas are localized mainly in the anterior and central parts of the claustrum, whereas in the rabbit, the majority of the neurons projecting to the cingulate cortex are present in the anterior and central parts of this structure, while neurons sending axons to the retrosplenial cortex are localized in the central and posterior parts. In both species, double-labeling study showed that neurons projecting to various limbic regions are intermingled and that neurons sending axons into two different limbic regions are seen only occasionally. Our findings give support to the role of the claustrum in integrating information between different areas of the cerebral cortex and the limbic system.

Animals↗
PubMedDate not supplied

[Comparison of the effects of the administration of fluoxetine and sertraline on the immune markers of the mu opioid receptor in the rat brain].

INTRODUCTION: Chronic fluoxetine or imipramine administration in rats can generate a similar increase in the number of neural cells immunostained for mu opioid receptors in several prosencephalic regions. OBJECTIVE: The aim of the present work was to describe the effects of chronic sertraline administration on mu opioid receptor immunostaining in several rat brain prosencephalic regions, in order to compare with previously described fluoxetine effects. MATERIALS AND METHODS: Experimental animals were chronically administered with sertraline (i.p.). An immunocytochemical method, with the aid of a computerized image analysis system, was used in order to measure the number of neural cells immunostained for mu opioid receptors in several prosencephalic regions. RESULTS: Although chronic sertraline administration in rats generates a significant increase in the number of neural cells immunostained for mu opioid receptors in the caudatus-putamen, dentate gyrus, lateral septum and the frontal, parietal and piriform cortices, slight regional differences, with respect to fluoxetine action, were found. Thus, a more marked action on parietal cortex and lateral septum, and a lesser action on the frontal cortex, were found. CONCLUSION: Regional differences in sertraline effects, with respect to fluoxetine, could be related to a lesser incidence of psychomotor impairment.

Animals↗
PubMed2005

Bilateral, vascular and perivascular glial upregulation of heat shock protein-27 after repeated epileptic seizures.

Heat shock protein-27 (HSP-27) is an inducible stress response protein. It inhibits apoptotic cell death and is a reliable marker for oxidative stress. We studied the induction of HSP-27 in rat brains on days 1, 4 and 14 after repeated, pentylenetetrazole (PTZ)-induced seizures using immunohistochemisty. Saline treated control rats showed no induction of HSP-27. HSP-27 reactive astrocytes were rarely seen 1 or 4 days after PTZ injection. When present, single astrocytes were located in the cortex and/or the hippocampus. After 14 days PTZ treatment, a bilateral distribution of HSP-27 immunoreactive glia was present in piriform and entorhinal cortices and in the dentate gyrus of most brains. Rats with most intense HSP-27 upregulation showed HSP-27 in amygdala and thalamic nuclei. Astrocytes associated with blood vessels presented strongest HSP-27 staining, but did not show upregulation of gial fibrillary acidic protein and none responded with HSP-47 expression. Additionally, HSP-27 immunoreactivity increased in the endothelial cells of blood vessels in the affected brain regions, although no neuronal induction occurred. Contrastingly, a subconvulsive dose of the glutamine synthetase inhibitor L-methionine sulfoxime, which acts directly on astrocytes, resulted in a rapid, homogeneous astrocyte-specific HSP-27 upregulation within 24 h. Thus, repeated PTZ-induced seizure activity elicits a focal "heat shock" response in endothelial cells and astrocytes of selected cerebral regions indicating that expression of HSP-27 occurred in a seizure-dependent manner within the affected cerebral circuitries. Therefore, this PTZ-model of repeated seizure activity exhibited a cortical pattern of HSP-27 expression which is most comparable to that known from patients with epilepsy.

Animals↗
PubMed1983

Opiate receptor localization in rat cerebral cortex.

The differential distributions of [3H]naloxone-labeled and [3H]D-Ala-D-Leu-enkephalin-labeled opiate receptors in rat cerebral cortex were localized autoradiographically and quantified by grain counting and computerized densitometry. In addition, receptor distributions were compared to terminal patterns of thalamocortical projections labeled by axoplasmic transport of [3H]amino acids. Opiate receptors labeled with [3H]naloxone in a mu ligand selectivity pattern show striking laminar heterogeneity and are densest in limbic cortical areas, intermediate in the motor cortex, and fewest in the primary sensory areas. By contrast, opiate receptors labeled with [3H]D-Ala2-D-Leu5-enkephalin in a delta ligand selectivity pattern are much more homogeneously distributed across both regions and laminae within regions. Mu receptors in most cortical areas have density peaks in layers I and VI and each peak shows a density gradient that is sloped within the layer so that the highest densities are at the most superficial and the deepest portions of cortex. In addition, there is an intermediate peak whose laminar position varies depending on the area in which it is found. In rostral agranular cortex, including limbic and motor areas, the [3H]naloxone binding peaks are in layers I, III, and VI. In primary somatosensory cortex, the intermediate peak is in layer Va and in most of remaining homotypical cortex it is in layer IV. Some areas have only bilaminar labeling, in superficial and deep layers; these include portions of the sulcal and retrosplenial cortices. Piriform and entorhinal cortices have dense [3H]naloxone binding only in the deepest layer and show a descending gradient of density toward the superficial layer. The positions of the mu receptor peaks were compared with termination patterns of projections originating in the thalamus. Close correspondence was found between receptor binding in the prelimbic, primary somatosensory, and entorhinal areas and projection terminations arising from the thalamic mediodorsal, posterior, and central medial nuclei, respectively. Although regional variations in [3H]D-Ala2-D-Leu5-enkephalin-labeled receptor density are uncommon, a gradual decrease in the number of sites along the dorsomedial wall of the cortex from anterior cingulate to caudal retrosplenial limbic cortex can be observed. Laminar variations in binding density are small as well; higher concentrations of the peptide binding sites are usually found in the deep cortical layers. These findings emphasize aspects of opiate receptor architecture which may be relevant to identifying cortical "opiatergic" neurocircuitry and raise the possibility of opiate modulation of thalamocortical transmission.

Animals↗
PubMed1992

Paucity of glutaminase-immunoreactive nonpyramidal neurons in the rat cerebral cortex.

Glutaminase has been considered to be a synthesizing enzyme of transmitter glutamate in pyramidal neurons of the cerebral cortex. In the present study, an attempt was made to examine with a double immunofluorescence method whether or not nonpyramidal neurons of the cerebral cortex are immunoreactive for glutaminase. Glutaminase was stained with mouse anti-glutaminase IgM and FITC-labeled anti-[mouse IgM] antibody. In the same section, parvalbumin (PA), calbindin (CB), choline acetyltransferase (CAT), vasoactive intestinal polypeptide (VIP), corticotropin releasing factor (CRF), cholecystokinin (CCK), somatostatin (SS), or neuropeptide Y (NPY) was visualized as a marker for nonpyramidal neurons with an antibody to each substance, biotinylated secondary antibody and Texas Red-labeled avidin. Virtually no glutaminase immunoreactivity was seen in PA-, CB-, CAT-, VIP-, CRF-, CCK-, SS-, or NPY-immunoreactive neuronal perikarya in the neocortex and mesocortex (cingulate and retrosplenial cortices), although it was detected in a few PA-, CB-, VIP-, CCK-, SS-, or NPY-immunoreactive nonpyramidal neurons in the piriform, entorhinal, and hippocampal cortices. PA- and CB-positive neurons have been reported to constitute the major population of GABAergic neurons in the cerebral cortex. Thus, the present results, together with the previous reports, suggest that most GABAergic, cholinergic and peptidergic nonpyramidal neurons in the neo- and mesocortex do not contain glutaminase.

Animals↗
PubMed1991

Distribution of the beta-2 adrenergic receptor messenger RNA in the rat brain by in situ hybridization histochemistry: effects of chronic reserpine treatment.

We studied the distribution of the rat brain beta-2 adrenergic receptor (AR) mRNA, and the effects of monoamine depletions by chronic reserpine treatment using in situ hybridization histochemistry. In the control group, high level signals of beta-2 AR mRNA were observed in the parietal, frontal and piriform cortices, the medial septal nuclei, the olfactory tubercle, and the midbrain. Moderate signals were found in the striatum, the retrosplenial cortex, the hippocampus, and the thalamic nuclei. After chronic reserpine treatment, beta-2 AR mRNA levels were increased in many brain regions. The large increases were seen in the hippocampus, all thalamic nuclei, the amygdaloid nuclei, and the midbrain, followed by the striatum and the occipital cortex. The receptor up-regulation resulting from chronic monoamine depletion may be due to these increases in beta-2 AR mRNA, indicating that this up-regulation may be caused by increased receptor production rather than decreased receptor degradation.

Animals↗
PubMed2003

Olfactory input to the parahippocampal region of the isolated guinea pig brain reveals weak entorhinal-to-perirhinal interactions.

The processing of olfactory inputs by the parahippocampal region has a central role in the organization of memory in mammals. The olfactory input is relayed to the hippocampus via interposed synapses located in the piriform and entorhinal cortices. Whether olfactory afferents directly or indirectly project to other areas of the parahippocampal region beside the entorhinal cortex (EC) is uncertain. We performed an electrophysiological and imaging study of the propagation pattern of the olfactory input carried by the fibres that form the lateral olfactory tract (LOT) into the parahippocampal region of the in vitro isolated guinea pig preparation. Laminar analysis was performed on field potential depth profiles recorded with 16-channel silicon probes at different sites of the insular-parahippocampal cortex. The LOT input induced a large amplitude polysynaptic response in the lateral EC. Following appropriate LOT stimulation, a late response generated by the interposed activation of the hippocampus was observed in the medial EC. LOT stimulation did not induce any local response in area 36 of the perirhinal cortex (PRC), while a small amplitude potential with a delay similar to the lateral EC response was inconsistently observed in PRC area 35. No PRC potentials were observed following the responses evoked by LOT stimulation in either the lateral or the medial EC. These findings were substantiated by current source density analysis of PRC laminar profiles. To further verify the absence of EC-to-PRC field interactions after LOT stimulation, high-resolution optical imaging of neuronal activity was performed after perfusion of the isolated brain with the voltage-sensitive dye RH-795. The optical recordings confirmed that olfactory-induced activity in the EC does not induce massive PRC activation. The present findings suggest that the olfactory input into the parahippocampal region is confined to the entorhinal cortex. The results also imply that, as demonstrated for the PRC-to-EC pathway, the propagation of neuronal activity from the EC to the PRC is hindered, possibly by a powerful inhibitory control generated within the EC.

Animals↗
PubMed2004

The potion's magic.

During remembering, a perception of the past is constructed that includes sensory details of the original episode. In this issue of Neuron, Gottfried and colleagues provide evidence for selective piriform activation during recognition of visual cues previously paired with scents. These data provide evidence of sensory-specific reactivation of olfactory cortex during remembering.

Auditory Cortex↗
PubMed1987

Immunocytochemical localization and morphology of GABA-containing neurons in the prefrontal and frontoparietal cortex of the rat.

The distribution and morphology of gamma-aminobutyric acid (GABA)-containing neurons in the rat prefrontal, frontal and parietal cortex were examined using a specific polyclonal antiserum directed against GABA and the immunoperoxidase method. The reaction product was present in the cell bodies, as well as in terminals and some processes without using colchicine. The immunoreactive neurons were observed in all layers but their laminar distribution was different in each cortical area. The immunoreactive cells were more numerous: in layer II and layer V-VI of the frontal cortex, in the deep layers (IV, V, VI) of the parietal cortex and in layer II and layer VI of the prefrontal cortex. The neurons displaying a labelling both in perikarya and processes were classified as multipolar and bipolar neurons. We distinguished various subtypes in each category. Multipolar neurons: cells with a large round soma and thin dendrites radiating in all directions; small neurons with ovoid or angular soma; large neurons with multiangular soma; neurons with a piriform soma. Bipolar neurons: horizontal bipolar cells with ovoid soma and vertical bipolar neurons with fusiform soma.

Animals↗
PubMed1997

Induction of NADPH-diaphorase activity in the forebrain in a model of intracerebral hemorrhage and its inhibition by the traditional Chinese medicine complex Nao Yi An.

Induction of NADPH-diaphorase (NDP) activity in the rat cerebral cortex was studied after autologous blood injection into the internal capsule as experimental model of intracerebral hemorrhage. The potential inhibitory effect on NDP induction by Nao Yi An (NYA), a complex derived from materials of animal and plant origin used in the treatment of intracerebral hemorrhage in traditional Chinese medicine, was also investigated. In animals without therapeutic treatment 2 and 4 days after injection of autologous blood, NDP activity was highly induced in pyramidal neurons in the neocortex, piriform, and entorhinal cortices, in astrocytes and in phagocytes in the hematoma and the area surrounding it, as well as in the subcortical white matter, and in endothelial cells in both the cortex and subcortical white matter bilaterally. Oral administration of NYA failed to inhibit NDP induction in endothelial cells but demonstrated a strong inhibitory effect on NDP activity induced in pyramidal neurons and astrocytes. NDP induction in phagocytes was also inhibited by the administration of NYA. Altogether the present results suggest that intracerebral hemorrhage in the internal capsule may induce nitric oxide synthase activity in different cell populations in the cortex and that administration of NYA can selectively inhibit such induction and, thus, potentially play a neuroprotective role.

Animals↗
PubMed1996

Effects of chronic morphine pretreatment on amygdaloid kindling development, postictal seizure and suppression and benzodiazepine receptor binding in rats.

Effects of chronic morphine pretreatment on the development of amygdaloid kindling, seizure suppression and benzodiazepine (BDZ) receptor binding in rats were evaluated. The morphine-pretreated animals showed faster acquisition of seizure activity. Further evaluation of the postictal seizure suppression immediately after a fully kindled seizure demonstrated that morphine-pretreated rats had a decreased sensitivity to subsequent kindling stimulations. Twenty-four hours after the last electrical stimulation, saline-pretreated fully kindled rats showed enhanced BDZ receptor binding in dentate gyrus, and decreased binding in cingulate cortex ipsilateral to the stimulation site, compared to saline controls. Morphine-pretreated amygdala-kindled rats had significantly higher BDZ binding in piriform, entorhinal and sensorimotor cortices, basolateral and cortical amygdaloid nuclei, dentate gyrus, CAI-3 areas, substantia nigra pars reticulata and periaqueductal gray. The present study indicates that the previous experience with chronic morphine modifies the kindling process and that the enhanced BDZ receptor binding detected in our experiments may be involved in the enhanced postictal seizure suppression observed in these animals.

Amygdala↗
PubMed1999

FOS induction in brain associated with seizure and sustained cortical vasodilation in anesthetized rat.

PURPOSE: By estimating the anatomical distribution of neurons expressing c-fos protein, we sought to establish whether the intrinsic neural systems known to be implicated in the cerebrovascular regulation were activated during the increase in cortical blood flow associated with epileptic seizures. METHODS: A single unilateral microinjection of the cholinergic agonist, carbachol, in the thalamic generalized convulsive seizure area was used in anesthetized rats to elicit recurrent episodes of electrocortical epileptiform activity and an increase in cortical blood flow. Neuronal expression of Fos protein was analyzed to identify activated brain regions. RESULTS: We identified two cortical vasodilatory responses: a sustained cortical vasodilatory response associated with the continuous low-frequency, high-amplitude spiking and a transient cortical vasodilatory response invariably related to the recurrent spike-burst activity. The sustained cortical blood flow began to increase at 55-65 min, remaining significantly (p < 0.05) increased and reaching at the end of the experiment < or =182+/-17% of the prestimulated control. The electrocortical epileptic activity and the cerebral cortical vasodilation were associated with a marked increase in Fos immunoreactivity in the entorhinal and piriform cortices, the dentate gyrus, the hippocampus, and the amygdala. Fos-positive neurons also were found in specific thalamic nuclei, the cerebral cortex, the caudate-putamen, the hypothalamus, the pontine parabrachial nuclei, the dorsal raphe, and the rostral ventrolateral medulla. CONCLUSIONS: These results provide evidence that convulsive seizures elicited by cholinergic stimulation of the thalamus, in addition to limbic and somatic motor systems, activate central autonomic nuclei and their pathways, including those implicated in cerebrovascular regulation.

Animals↗
PubMed2005

Divergent regulatory mechanisms governing BDNF mRNA expression in cerebral cortex and substantia nigra in response to striatal target ablation.

We have studied the regulation of BDNF mRNA expression in the corticostriatal and nigrostriatal systems following neurotoxin ablation of striatal targets induced by quinolinic acid (QA) or 2S:2'R:3'R:-2-(2'3'-dicarboxycyclopropyl)glycine (DCG-IV) injections. Striatal lesions were verified by quantifying the loss of glutamic acid decarboxylase (GAD) mRNA expression. Levels of BDNF mRNA were analyzed at 6, 12, and 24 h postlesion. Both lesions paradigms highly induced BDNF mRNA in the ipsilateral cerebral cortex at 6 and 12 h postlesion to drop to control levels at 24 h postlesion. These inductions were mostly restricted to cortical layers II/III and V and ipsilateral insular and piriform cortices, which provide the main cortical inputs to the striatum. Analysis of neuronal activation on these areas demonstrated high levels of cFos mRNA in response to the excitotoxic striatal lesions. Dual labeling of cFos and BDNF mRNAs demonstrated a positive correlation between cortical neuronal activation and expression of BDNF mRNA. Consequently, expression of BDNF in cortical areas projecting to striatum is dependent on both target integrity and neuronal activity. Regulation of BNDF mRNA in substantia nigra, the second major source of BDNF to striatal cells, highly differed from that seen in cerebral cortex. Analysis of cellular expression alone or in combination of BDNF, cFos, tyrosine hydroxylase and GAD mRNAs demonstrated that expression of BDNF in substantia nigra is dependent on target integrity and independent of neuronal activity. In addition, we have studied regulatory mechanisms of BDNF mRNA in the subthalamic nucleus.

Animals↗