Involvement of CDC25Mm/Ras-GRF1-dependent signaling in the control of neuronal excitability

Tonini, Raffaella, Fanceschetti, Silvana, Parolaro, Daniela, Sala, Mariaelvina, Mancinelli, Enzo, Tininini, Silvia, Brusetti, Ronny, Sancini, Giulio, Brambilla, Riccardo ORCID: https://orcid.org/0000-0003-3569-5706, Martegani, Enzo, Sturani, Emmapaola and Zippel, Renata 2001. Involvement of CDC25Mm/Ras-GRF1-dependent signaling in the control of neuronal excitability. Molecular and Cellular Neuroscience 18 (6) , pp. 691-701. 10.1006/mcne.2001.1050

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Abstract

Ras-GRF1 is a neuron-specific guanine nucleotide exchange factor for Ras proteins. Mice lacking Ras-GRF1 (−/−) are severely impaired in amygdala-dependent long-term synaptic plasticity and show higher basal synaptic activity at both amygdala and hippocampal synapses (Brambilla et al.,1997). In the present study we investigated the effects of Ras-GRF1 deletion on hippocampal neuronal excitability. Electrophysiological analysis of both primary cultured neurons and adult hippocampal slices indicated that Ras-GRF1−/− mice displayed neuronal hyperexcitability. Ras-GRF1−/− hippocampal neurons showed increased spontaneous activity and depolarized resting membrane potential, together with a higher firing rate in response to injected current. Changes in the intrinsic excitability of Ras-GRF1−/− neurons can entail these phenomena, suggesting that Ras-GRF1 deficiency might alter the balance between ionic conductances. In addition, we showed that mice lacking Ras-GRF1 displayed a higher seizure susceptibility following acute administration of convulsant drugs. Taken together, these results demonstrated a role for Ras-GRF1 in neuronal excitability.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Schools > Biosciences
Subjects:	Q Science > Q Science (General)
Publisher:	Elsevier
ISSN:	1044-7431
Last Modified:	27 Oct 2022 08:26
URI:	https://orca.cardiff.ac.uk/id/eprint/62315

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