The proposed study is the continuation of a long-term investigation of the neuronal and synaptic organization of the basolateral amygdala (ABL). It will focus on the regulation of ABL interneurons by transmitter-specific neuromodulator systems.
Aim #1 will identify subpopulations of interneurons in the primate ABL on the basis of their content of peptides and calcium-binding proteins. These markers will be used to identify each subpopulation in Aims #2 and 3.
Aim #2 will use integrated anatomical/physiological experiments to determine if different interneuronal subpopulations exhibit distinct electrophysiological characteristics. In addition, ion channels responsible for some of these electrophysiological features will be localized using immunohistochemical techniques.
Aim #3 will analyze the innervation of ABL neuronal subpopulations by dopaminergic, noradrenergic, and serotonergic afferents. It will also be determined using integrated anatomical-physiological/pharmacological methods if particular interneuronal subpopulations exhibit specific serotonin receptors.
Aim #4 will analyze the innervation of ABL intemeuronal subpopulations by cholinergic axons and determine which interneurons express nicotinic versus muscarinic cholinergic receptors. ? Additional anatomical studies in rodents will test the hypothesis that the ABL, like the neocortex and hippocampus, contains subsets of GABAergic neurons that receive inputs from, and provide outputs to, the GABAergic projection neurons of the basal forebrain. These proposed studies include the first comprehensive analysis of the electrophysiological properties of identified ABL interneuronal subpopulations in both rodent and primate brain slices. In addition, the modulation of key electrophysiological properties in these neurons by serotonin and serotonergic drugs will be investigated. These studies will contribute to an understanding of inhibitory mechanisms in the ABL and should be critical for the development of novel pharmacological treatments to modulate the activity of the ABL in epilepsy and psychiatric disorders. ? ?
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