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A Represa

Publications and source records attributed to A Represa.

At least 73 records · Page 4Linked to original sources
PubMed1991

Transient cerebral ischemia induces changes in SRIF mRNA in the fascia dentata.

A transient cerebral ischemia produced in rats by 4-vessel occlusion, produces with a delay of 24 h a fall in the number of somatostatin-containing neurons. In the present study we show that this loss is preceded by a loss of somatostatin mRNA that starts as soon as 30 min after the anoxic episode. By 24 h of revascularization the surviving somatostatinergic hilar cells present a transient recovery of hybridization signal. This effect could be related to a previously reported increase in intracellular calcium.

Animals↗
PubMed1991

Effects of neonatal gamma-ray irradiation on rat hippocampus--I. Postnatal maturation of hippocampal cells.

The axons of dentate granule cells, the mossy fibres, establish synaptic contacts with the thorny excrescences of the apical dendrite of CA3 pyramidal neurons. Dentate granule granule cells develop postnatally in rats, whereas the CA3 pyramidal cells are generated before birth. In the present studies, using unilateral neonatal gamma-ray irradiation to destroy the granule cells in one hemisphere, we have studied the effect of mossy fibre deprivation on the development of their targets. We show that such "degranulation" prevents the normal development of giant thorny excrescences, suggesting that the development of thorny excrescences in CA3 pyramidal neurons is under the control of mossy fibres. In contrast, irradiation of the hippocampus of the neonatal rat does not affect the development of the dendritic arborization of CA3 pyramidal cells and their non-mossy dendritic spines.

Animals↗
PubMed1991

Effects of neonatal gamma-ray irradiation on rat hippocampus--II. Development of excitatory amino acid binding sites.

In the rat, neonatal irradiation produces a destruction of dentate granule cells and prevents the development of the mossy fibre-CA3 pyramidal cell synapse. The developmental increase of high affinity kainate binding sites in the stratum lucidum was reduced on the irradiated side as compared with the control side. This suggests that a proportion of high affinity kainate binding sites is associated with mossy fibres. In contrast, the developmental profile of N-methyl-D-aspartate binding sites, which are associated with associational and commissural synapses in CA3, was not affected by irradiation. The role that afferent fibres may play in the development of pyramidal cells is discussed in connection with the modulatory effects of glutamate receptors on the development of neurons.

Animals↗
PubMed1990

Effects of kainic acid-induced seizures and ischemia on c-fos-like proteins in rat brain.

We have analyzed the brain pattern and time-course of c-fos-like proteins expression in kainic acid-induced seizures in the rat. C-fos-like immunoreactivity increased initially in the hippocampus, notably in the dentate gyrus, at the time of the first limbic motor seizure (90 min after kainate). C-fos-like labelling progressively involved different structures of the limbic system when the rats manifested a permanent epileptic state (3-6 h). The labelling was still conspicuous 12 h after kainate treatment and progressively declined to reach control levels 48 h after kainate. This time-course is similar to that produced by kainic acid on 2-deoxyglucose consumption and correlates with the electrographic changes previously described, supporting the idea that c-fos-like immunostaining may provide a useful marker of neuronal activity, with a cellular resolution. Since anoxic-ischemic treatment produces a very slight and transient increase in c-fos-like immunostaining restricted to the fascia dentata, c-fos-like expression is seizure-related and not due to a local hypoxia or ischemia.

Amino Acid Sequence↗
PubMed1990

Brief seizure episodes induce long-term potentiation and mossy fibre sprouting in the hippocampus.

Much of our present understanding of the cellular mechanisms of learning and memory derives from studies on the hippocampus in which long-term potentiation (LTP) of synaptic transmission is produced by a train of high-frequency electrical stimulation or by potassium channel blockers. The hippocampus is also a seizure-prone region and recent studies have revealed that brief seizure episodes produce remarkably long-lasting changes which are reminiscent of 'classical' LTP. A brief seizure episode also sets in motion a cascade of events that includes changes in gene expression, sprouting of fibres and the establishment of new synaptic contacts. This paper reviews this use-dependent structural rearrangement of the neuronal network and discusses its possible role in epilepsy and as a model of plasticity in the adult nervous system.

Animals↗
PubMed1990

Neurogranin: immunocytochemical localization of a brain-specific protein kinase C substrate.

The developmental expression and the cellular localization of neurogranin (formerly designated p17), a brain-specific protein kinase C (PKC) substrate, were investigated. The developmental expression of neurogranin was studied by immunoblotting of rat brain and neuronal cell-culture extracts using neurogranin polyclonal antibodies. Neurogranin synthesis was found to be developmentally regulated, with no expression in the embryonic and neonatal period and an abrupt increase between 2 and 3 weeks of age. By immunohistochemistry, neurogranin was found essentially in the adult rat telencephalon, specifically located in the cell bodies and dendritic processes of neurons of the cerebral cortex, hippocampus, striatum, and a few other discreet areas. Neurogranin immunoreactivity was nearly absent in the thalamus, cerebellum, and brain stem. The late developmental expression and the dendritic localization of neurogranin in neurons are 2 features that also characterize the type I PKC isozyme. The specific localization of the protein in integrative areas of the rat brain suggests a highly specialized function of neurogranin in the CNS. A possible role for neurogranin in the transduction of the PKC activation signals at the postsynaptic level is suggested.

Animals↗
PubMed1989

Selective destruction of mossy fibers and granule cells with preservation of the GABAergic network in the inferior region of the rat hippocampus after colchicine treatment.

Lesions induced by colchicine injection into the rat hippocampus were investigated by means of electron microscopy and GABA immunocytochemistry. Granule cells were nearly completely destroyed 3 days after colchicine injection; since the necrosis of their axonal endings was delayed, an anterograde degeneration of the mossy fibers had probably taken place. The selectivity of the lesions was not limited to granule cells, for some pyramidal neurons in CA1 pyramidal layer were damaged. It was, however, striking to observe that throughout the hippocampal structure GABAergic neurons were spared from the effects of colchicine. For instance, GABAergic neurons were found in the vicinity of the completely destroyed granule cell layer. GABAergic neurons and terminals were also present in the CA3 region where the GABA-containing terminals formed a dense network of synapses with somata and dendrites of pyramidal cells. It was interesting to note that, consistent with previous studies, the GABAergic neurons in CA3 are innervated by mossy fibers. We conclude that after colchicine treatment the destruction of the granule cells was not associated with a lesion of the GABAergic network. This selective lesion provides a useful model with which to study the properties of CA3 neurons deprived of their major excitatory input but with an intact inhibitory network.

Animals↗
PubMed1989

Hippocampal plasticity in the kindling model of epilepsy in rats.

Histochemical and autoradiographic techniques were used to study mossy fiber sprouting which occurs in the hippocampus of kindled rats. In rats kindled by daily stimulation of amygdala or entorhinal cortex, the mossy fibers sprout to innervate the supragranular zone of fascia dentata; this synaptic reorganization was associated with a significant increase in the density of high-affinity kainic acid binding sites. Amygdala but not entorhinal kindling also induces sprouting of mossy fibers in the stratum infrapyramidale of CA3.

Amygdala↗
PubMed1989

Hippocampal plasticity in childhood epilepsy.

Quantitative autoradiography was used to study changes in high affinity (Kd = 12 nM) binding sites for kainic acid, a marker of mossy fibers, in the hippocampus of childhood epileptics. We found a highly significant increase in the density of kainate binding sites in the CA3 region and in the fascia dentata in childhood epileptics as compared to age matched controls. We suggest that anatomical plasticity occurs in the hippocampus of human epileptics as in experimental models of epilepsy. The increase in kainate binding sites may contribute to the development of epileptic seizures.

Adolescent↗
PubMed1989

Development of the cholinergic system in control and intra-uterine growth retarded rat brain.

The activity of choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and muscarinic receptors was studied in control rats and in rats growth-retarded in utero because of reduction of the blood supply 5 days before birth. The different markers of the cholinergic system were estimated at P (postnatal day) 6, 9, 12, 15, 22 and 60 in cerebellum, hypothalamus, septum, striatum and CA1, CA3 and fascia dentata of the hippocampus. In control rats, there was a transient increase in ChAT activity in the septum during the second week of postnatal development. In the intrauterine growth retarded rats there was a marked delay in this developmental rise in CA1, CA3 at P6 and P9 and in the fascia dentata at P14 respectively. This delayed rise enzyme activity was associated with a significant reduction of muscarinic binding sites [( 3H]QNB) in the hippocampus. AChE staining showed a similar development in both groups. Therefore, the undernutrition produced by a reduction of the blood supply 5 days before birth is associated with a delayed maturation of cholinergic functions.

Acetylcholinesterase↗
PubMed1989

Transient increase of NMDA-binding sites in human hippocampus during development.

In the human hippocampus, the density of glutamate and N-methyl-D-aspartate (NMDA) binding sites follows during development a bell-shaped curve with a peak at 23-27 fetal weeks. We suggest that there is a transient increased density of NMDA binding sites during a restricted period of hippocampal development; this may play an important role in developmental plasticity.

Adult↗
PubMed1989

Effects of colchicine treatment on the cholinergic septohippocampal system.

The influence of hippocampal target cells on the septohippocampal cholinergic system was studied using immunocytochemical and autoradiographic procedures. The destruction of dentate granular cells by colchicine injection promotes a significant increase in the density of acetylcholinesterase staining and cholinergic-muscarinic receptors in the zone denervated by the terminal axons of granular cells, which supports the hypothesis of a proliferation of cholinergic fibers in CA3. In the septal region the number of choline acetyl transferase positive cells was significantly lower (by 23%) ipsilaterally to the colchicine injection as compared to the contralateral side; when the hippocampus is almost completely destroyed by colchicine treatment this cell loss is more important (by over 50%). The present results agree with those of earlier studies and suggest that target-derived trophic factors are important for the maintenance of the basal forebrain cholinergic system and that the fascia dentata provides a significant source of such factors.

Acetylcholine↗
PubMed1989

Hippocampal damage induced by ischemia and intra-amygdaloid kainate injection: effect on N-methyl-D-aspartate, N-(1-[2-thienyl]cyclohexyl)piperidine and glycine binding sites.

The N-methyl-D-aspartate receptor channel-complex is widely distributed in the hippocampus, particularly in the CA1 region, in the terminal field of CA3 pyramidal axons and in the fascia dentata, in the terminal field of the perforant pathway. In the present study, we have examined, in the rat, the effect of specific lesions of various neuronal populations of the hippocampus on the distribution of several markers of the N-methyl-D-aspartate receptor-channel complex. Anoxic-ischemic treatment produced a destruction of CA1 pyramidal cells (postsynaptic element): this was associated with a 50% loss of N-methyl-D-aspartate, glycine and N-(1-phenylcyclohexyl)piperidine binding sites. In contrast, the destruction of CA3 pyramidal cells and their axons (presynaptic element) by kainate treatment did not induce significant changes in the density of binding sites. The present results therefore strongly support an exclusively postsynaptic localization of the N-methyl-D-aspartate receptor-channel complex in CA1; the possibility of a localization of the remaining binding sites on glial cells or interneurons is discussed. In the molecular layer of the fascia dentata, the anoxic-ischemic treatment produced a partial destruction of the median perforant pathway (presynaptic element) associated with a decrease in the density of N-methyl-D-aspartate, N-(1-[2-thienyl]cyclohexyl)piperidine and glycine binding sites; this suggests that, in contrast to CA1, in the molecular layer of the fascia dentata, N-methyl-D-aspartate receptor-binding sites are located both pre- and postsynaptically.

Amygdala↗
PubMed1988

Transient increased density of NMDA binding sites in the developing rat hippocampus.

Using quantitative autoradiography and membrane preparations, the density of specific glutamate and N-methyl-D-aspartic acid (NMDA) binding sites have been determined in the developing rat hippocampus. We found an abrupt reduction in the density of NMDA binding sites after P8 (postnatal day) without change in affinity. The transient expression of NMDA receptors during maturation suggests that they may play a particularly important role in synaptogenesis.

Aging↗
PubMed1988

Is senile dementia of the Alzheimer type associated with hippocampal plasticity?

The density of binding sites for excitatory amino acids in the hippocampus of SDAT (senile dementia of the Alzheimer type) patients has been investigated. This was compared to that found in younger and old non-dement cases. In the SDAT hippocampi there was a significant decrease in the glutamate and kainate binding. This reduction correlated positively with the degree of the severity of neurological and pathological disease. In spite of an extensive denervation of SDAT hippocampi, there was no sign of sprouting of mossy fibers; this observation indicates a loss of plasticity in the hippocampus of SDAT patients.

Adult↗