Navegando por Palavras-chave "entorhinal cortex"

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    Effects of pre- or post-training entorhinal cortex AP5 injection on fear conditioning
    (Elsevier B.V., 2005-11-15) Schenberg, E. E.; Soares, JCK; Oliveira, MGM; Universidade Federal de São Paulo (UNIFESP)
    Fear conditioning is one of the most studied paradigms to assess the neural basis of emotional memory. the circuitry involves NNMA receptor activation in the amygdala and, in the case of contextual conditioning, in the hippocampus. Entorhinal cortex is one of the major input/output structures to the hippocampus and also projects to the amygdala, both through glutamatergic transmission. Other learning tasks involving hippocampus and amygdala, such as inhibitory avoidance, require entorhinal cortex during acquisition and consolidation. However, the involvement of NMDA receptors mediated transmission in entorhinal cortex in fear conditioning acquisition and consolidation is not clear. To investigate that issue, rats were trained in fear conditioning to both contextual and tone conditioned stimulus. Immediately before, immediately, 30 or 90 min after training they received NMDA antagonist AP5 or saline injections bilaterally in the entorhinal cortex (AP-6.8 mm, L +/- 5.0 mm DV-6.8 mm). Contextual fear conditioning was measured 24 h after training, and tone fear conditioning 48 h after training. AP5 injections selectively impaired contextual fear conditioning only when injected pre-training. Post-training injections had no effect. These findings suggest that entorhinal cortex NMDA receptors are necessary for acquisition, but not for consolidation, of contextual fear conditioning. On the other hand, both acquisition and consolidation of tone fear conditioning seem to be independent of NMDA receptors in the entorhinal cortex. (c) 2005 Elsevier Inc. All fights reserved.
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    Lack of Fos-like immunoreactivity after spontaneous seizures or reinduction of status epilepticus by pilocarpine in rats
    (Elsevier B.V., 1996-04-19) Mello, LEAM; Kohman, C. M.; Tan, A. M.; Cavalheiro, E. A.; Finch, D. M.; Universidade Federal de São Paulo (UNIFESP); UNIV CALIF LOS ANGELES
    Acute seizures and status epilepticus induced by pilocarpine lead to the expression of Fos-like immunoreactivity in several specific brain areas in a manner similar to that of other models of limbic seizures. Upon development of status epilepticus after systemic pilocarpine injection, animals develop a state where chronic spontaneous seizures recur. Assessment of Fos-like immunoreactivity after such spontaneous seizures or after status epilepticus reinduction reveals either lack of staining or a weak reaction in a few brain areas including the ventral tip of the dentate gyrus, prepiriform, lateral piriform and perirhinal cortices, and scattered locations throughout temporal neocortex. Our results suggest that status epiiepticus induction may lead to a long-lasting state of Fos down-regulation.
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    Loss of NADPH diaphorase-positive neurons in the hippocampal formation of chronic pilocarpine-epileptic rats
    (Wiley-Blackwell, 1999-01-01) Hamani, C.; Tenorio, F.; Mendez-Otero, R.; Mello, LEAM; Universidade Federal de São Paulo (UNIFESP); Universidade Federal do Rio de Janeiro (UFRJ)
    Recent evidence suggests an important role for NO in cholinergic models of epilepsy. Nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd), a marker of NO containing neurons, was shown to intensely colocalize with GABA in double-labeling studies performed in the hippocampal formation (exception made for the pyramidal cell layer) (Valtschanoff et al., J Comp Neurol 1993:331:111-121). in this sense, it further characterizes an extremely important cell category due to the relevant involvement of inhibitory systems in the mechanisms of genesis and propagation of seizures. Here, we assessed the histochemistry for NADPHd in the hippocampal complex: of chronic pilocarpine-epileptic animals. NADPHd-positive cells were lost in almost every hippocampal subfield in pilocarpine-treated rats. the central portion of the polymorphic layer of the dentate gyrus (hilus) presented one of the highest losses of NADPHd-positive cells (55-79%) in the hippocampus. A significant loss of NADPHd-positive cells was seen in strata oriens, pyramidale, and radiatum CA1, CA2, and CA3 subfields. NADPHd staining in the subicular pyramidal cell layer was not different from that observed in controls. A significant loss of NADPHd-stained cells was observed in entorhinal cortex layers II and III in the epileptic group. for entorhinal cortex layers V and VI, however, results varied from an almost complete tissue destruction to an overexpression of NADPHd-positive cells, as well as an increase in neuropil staining.In summary, loss of NADPHd staining was not uniform throughout the hippocampal formation. There has been a growing support for the notion that GABAergic neurons in the hippocampal formation are not equally sensitive to insults. Our results suggest that, as a marker for a subpopulation of GABAergic neurons, NADPHd helps in further refining the characterization of the different neuronal populations sensitive to epileptic activity. (C) 1999 Wiley-Liss, Inc.