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

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Date
2016-09-06
Author
Brenes García, Oscar Gerardo
Caravelli, Valentina
Gosso, Sara
Romero Vásquez, Adarli
Carbone, Emilio
Montarolo, Pier Giorgio
Ghirardi, Mirella
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Abstract
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.
URI
http://hdl.handle.net/10669/73461
External link to the item
10.1016/j.eplepsyres.2016.09.008
http://www.sciencedirect.com/science/article/pii/S0920121116301693
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  • Medicina, ciencias biomédicas y salud pública [1401]



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  • Repositorios universitarios

  • Repositorio del SIBDI-UCR
  • Biblioteca Digital del CIICLA
  • Repositorio Documental Rafael Obregón Loría (CIHAC)
  • Biblioteca Digital Carlos Melendez (CIHAC)
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  • Scientific Electronic Library Online (SciELO)
  • Directory of Open Access Journals (DOAJ)
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Contact Us | Send Feedback
Repositorio Institucional de la Universidad de Costa Rica. Algunos derechos reservados. Este repositorio funciona con DSpace.
Universidad de Costa Rica