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α 2 ‐Adrenoreceptor activation inhibits LTP and LTD in the basolateral amygdala: involvement of G i/o ‐protein‐mediated modulation of Ca 2+ ‐channels and inwardly rectifying K + ‐channels in LTD
Author(s) -
DeBock F.,
Kurz J.,
Azad S. C.,
Parsons C. G.,
Hapfelmeier G.,
Zieglgänsberger W.,
Rammes G.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02544.x
Subject(s) - basolateral amygdala , long term potentiation , chemistry , excitatory postsynaptic potential , neurotransmission , postsynaptic potential , amygdala , long term depression , yohimbine , endocrinology , medicine , clonidine , neuroscience , antagonist , glutamate receptor , receptor , biology , biochemistry , ampa receptor
Activation of adrenoreceptors modulates synaptic transmission in the basolateral amygdala. Here, we investigated the effects of α 2 ‐adrenoreceptor activation on long‐term depression and long‐term potentiation in an in vitro slice preparation of the mouse basolateral amygdala. Field potentials and excitatory postsynaptic currents were evoked in the basolateral amygdala by stimulating the lateral amygdala. Norepinephrine (20 µ m ) reduced synaptic transmission and completely blocked the induction of long‐term potentiation and long‐term depression. The α 2 ‐adrenoreceptor antagonist yohimbine (2 µ m ) reversed this effect. The α 2 ‐adrenoreceptor agonist clonidine (10 µ m ) mimicked the effects of norepinephrine. The G i/o ‐protein inhibitor pertussis toxin (5 µg/mL) reversed the effect of clonidine. Long‐term depression was blocked in the presence of ω‐conotoxin GVIA, but not ω‐agatoxin IVA. Clonidine inhibited voltage‐activated Ca 2+ currents mediated via N‐ or P/Q‐type Ca 2+ ‐channels. The inhibitory action of clonidine on long‐term depression was reversed when inwardly rectifying K + ‐channels were blocked by Ba 2+ (300 µ m ). The present data suggest that α 2 ‐adrenoreceptor activation impairs the induction of long‐term depression in the basolateral amygdala by a G i/o ‐protein‐mediated inhibition of presynaptic N‐type Ca 2+ ‐channels and activation of inwardly‐rectifying K + ‐channels.