GsAHP activation during STDP determines the direction of plasticity in hippocampal CA1 pyramidal neurons of adult rats

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2018-05

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Universidad de Valparaíso

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item.page.issne

item.page.doiurl

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Doctorado en Ciencias con Mención en Neurociencia

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The slow after-hyperpolarization (sAHP) is a Ca2+-dependent K+ current, which is implicated in the control of neuronal excitability as well as in the regulation of dendritic integration. In young rats (<p30), sAHP impairs LTP when is activated during plasticity induced by spike timing dependent plasticity (STDP) protocol and it is upregulated during development. However, the effect of the sAHP in synaptic plasticity of adult animals still has not been explored. Using whole-cell patch-clamp configuration in hippocampal CA1 pyramidal neurons of adult rats, we regulated the conductance of sAHP during causal STDP protocols to assess its effect on plasticity. To activate the sAHP we varied the spike frequency of STDP protocols and to attenuate sAHP we bath applied the noradrenergic (NA) agonist isoproterenol (ISOP). Our results demonstrate that the sAHP increment in membrane conductance (GsAHP) alone and not the spiking frequency determines the direction of plasticity using a single-AP pairing STDP protocol. Regenerative activation of GsAHP during a pre-post STDP protocol resulted in 3 outcomes: LTP, no change in EPSC efficacy (NON) and LTD. ISOP GsAHP-attenuation resulted exclusively in LTP. The corresponding GsAHP levels during STDP were: 2.39±0.53 nS for LTP, 4.40±0.66 nS for NON, 4.44±0.68 nS for LTD and 2.27±0.78 nS for ISOP. These results demonstrate the regulatory effect of GsAHP over the direction of plasticity and how the NA GsAHP regulation might subordinate hippocampal plasticity to attentional and emotional states.

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PLASTICIDAD NEURONAL, ISOPROTERENOL

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