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Biomedical subjects

I Mody

Publications and source records attributed to I Mody.

95 records · Page 6Linked to original sources
PubMed1983

Role of norepinephrine in seizurelike activity of hippocampal pyramidal cells maintained in vitro: alteration by 6-hydroxydopamine lesions of norepinephrine-containing systems.

Perfusion of 50 microM norepinephrine (NE) produced a marked, reversible decrease (range 20-28%) of the extracellular population spike and excitatory postsynaptic potential (EPSP) responses of the CA1 region evoked by stratum radiatum stimulation in the rat hippocampal slice preparation. The effects of NE were dramatically altered in slices obtained from animals which were previously treated with intracerebral or intraventricular injections of 6-hydroxydopamine (6-OHDA) to destroy forebrain catecholamine systems. In the latter preparations NE produced a reduction in the inhibition of the EPSP (50%), enhancement of the population spike amplitude, and multiple spike discharges characteristic of ongoing epileptiform activity. The reversal of NE-induced inhibition and the generation of seizurelike activity in 6-OHDA-treated animals suggests that NE may, in part, act upon interneurons to produce a disinhibition of CA1 pyramidal cells.

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PubMedDate not supplied

NMDA receptors of dentate gyrus granule cells participate in synaptic transmission following kindling.

In the mammalian central nervous system, receptors for the excitatory amino-acid neurotransmitters are divided into three subtypes depending on their sensitivity to three specific agonists: kainate, quisqualate and N-methyl-D-aspartate (NMDA). The ionophores operated by NMDA are gated by Mg2+ in a voltage-dependent manner and allow passage of several cations, including Ca2+ which may be important in plastic alterations of neuronal excitability. Indeed, specific antagonists of NMDA receptors effectively block spatial learning, long-term potentiation and some animal models of chronic epilepsy. Despite their abundance on central neurons, NMDA receptors, with a few noteworthy exceptions, do not generally seem to be involved in low-frequency synaptic transmission. Here we report for the first time that NMDA receptors of the dentate gyrus, where they do not normally contribute to the generation of synaptic potentials, become actively involved in synaptic transmission following long-lasting neuronal changes induced by daily electrical stimulation (kindling) of the amygdala or hippocampal commissures. In contrast to controls, the excitatory postsynaptic potentials (e.p.s.ps) of granule cells in hippocampal slices obtained from kindled animals displayed characteristics typical of an NMDA-receptor-mediated component. The involvement of NMDA receptors in synaptic transmission may underlie the long-lasting changes in neuronal function induced by kindling.

Animals↗
PubMedDate not supplied

Reduction of rat hippocampal calcium-binding protein following commissural, amygdala, septal, perforant path, and olfactory bulb kindling.

The calcium-binding protein (CaBP) content of the hippocampal formation was determined by radioimmunoassay in control and kindled rats. Kindling of a number of different sites resulted in a reduction in the CaBP content of the hippocampal formation, which was shown immunohistochemically to be restricted to the dentate granule cells and their processes. The maximum decline in CaBP varied with the different kindling sites: perforant path, 33%; commissural path, 32%; septum, 30%; amygdala, 18%; and olfactory bulbs, 15%. There were no changes in the CaBP content of the stimulated areas themselves. In cases where the kindling stimulus was delivered unilaterally (perforant path and amygdala), the maximum decrease in hippocampal CaBP was observed ipsilateral to the site of stimulation when the criterion for full kindling was established (six consecutive stage 5 motor seizures). Further kindling trials were required to produce a similar magnitude decrease in the CaBP content of the contralateral hippocampus. These observations are discussed both in relation to the possible role of CaBP in the establishment of a seizure response to kindling and also as a potential compensatory mechanism that may serve to overcome the epileptogenic effects of kindling.

Amygdala↗