Inhibitory control of rat lateral amygdaloid projection cells

The amygdaloid complex has long been implicated in seizure disorders. Yet, projection cells of the lateral amygdaloid nucleus (LA) display little spontaneous activity suggesting that this seizure prone structure is normally controlled by strong inhibitory mechanisms. This control is achieved in part by local interneurons; however, a synaptically activated, Ca(2+)-dependent K(+) (K(Ca)) conductance has recently been identified as a second major inhibitory mechanism. In the present study, we investigated which K(Ca) channels underlie this conductance, and their roles in the generation of the synaptic responses and spike adaptation of LA projection cells. Intracellular recordings were obtained from LA projection cells in barbiturate-anesthetized rats. In recordings with K-acetate pipettes, perirhinal stimulation evoked an initial excitatory postsynaptic potential (EPSP) followed by a prolonged monophasic hyperpolarization, similar to what was observed in cats under in vivo conditions, and distinct from the multiphasic hyperpolarization observed previously in rodents with in vitro recordings. This indicates that differences in the cellular environment, not interspecies differences, are responsible for the differing response profiles previously reported. In recordings with pipettes containing 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid or Cs-acetate the reversal potentials were significantly more positive than those recorded with K-acetate, consistent with a K(Ca) conductance contribution to the response. To investigate the K(Ca) channels underlying this conductance, intracellular recordings were obtained while perfusing the LA with Ringer's solution and then switching to a solution containing charybdotoxin, isoproterenol, or apamin. Charybdotoxin and isoproterenol produced positive shifts in the reversal potential, whereas apamin did not. By contrast, all three substances decreased adaptation during spike trains elicited by depolarizing current injections. These results suggest that intermediate (IK) and small (SK) conductance K(Ca) channels limit LA projection cell excitability, with IK channels involved in controlling both the synaptic response and intrinsic excitability of these neurons, and SK channels being involved only in the latter.