Subconvulsant doses of pentylenetetrazol uncover the epileptic phenotype of cultured synapsin-deficient Helix serotonergic neurons in the absence of excitatory and inhibitory inputs

 

Guardado en:
Detalles Bibliográficos
Autores: Brenes García, Oscar Gerardo, Caravelli, Valentina, Gosso, Sara, Romero Vásquez, Adarli, Carbone, Emilio, Montarolo, Pier Giorgio, Ghirardi, Mirella
Formato: artículo original
Fecha de Publicación:2016
Descripción:Synapsins are a family of presynaptic proteins related to several processes of synaptic functioning. A variety of reports have linked mutations in synapsin genes with the development of epilepsy. Among the proposed mechanisms, a main one is based on the synapsin-mediated imbalance towards network hyperexcitability due to differential effects on neurotransmitter release in GABAergic and glutamatergic synapses. Along this line, a non-synaptic effect of synapsin depletion increasing neuronal excitability has recently been described in Helix neurons. To further investigate this issue, we examined the effect of synapsin knock-down on the development of pentylenetetrazol (PTZ)-induced epileptic-like activity using single neurons or isolated monosynaptic circuits reconstructed on microelectrode arrays (MEAs). Compared to control neurons, synapsin-silenced neurons showed a lower threshold for the development of epileptic-like activity and prolonged periods of activity, together with the occurrence of spontaneous firing after recurrent PTZ-induced epileptic-like activity. These findings highlight the crucial role of synapsin on neuronal excitability regulation in the absence of inhibitory or excitatory inputs.
País:Kérwá
Institución:Universidad de Costa Rica
Repositorio:Kérwá
OAI Identifier:oai:kerwa.ucr.ac.cr:10669/73461
Acceso en línea:http://www.sciencedirect.com/science/article/pii/S0920121116301693
https://hdl.handle.net/10669/73461
Palabra clave:Synapsin
Pentylenetetrazol (PTZ)
Invertebrate neurons
Convulsants
Helix snail