Autoreceptor-mediated changes in dopaminergic terminal excitability: effects of striatal drug infusions.
The neurophysiological correlates of autoinhibition at the terminals of nigrostriatal dopaminergic neurons were studied by measuring the changes in antidromic excitability of nigrostriatal neurons following local infusions of various catecholamine agonists and antagonists into the neostriatum. Infusions of apomorphine or amphetamine reduced terminal excitability whereas the dopamine antagonists, haloperidol, fluphenazine or sulpiride, led to increases in terminal excitability. Alterations in antidromic excitability were constrained to the terminal regions and were not observed when infusions and excitability testing were performed in the medial forebrain bundle. The alpha-2 agonist, clonidine, did not alter dopaminergic terminal excitability. Our results indicate that pharmacological manipulations which have been shown to reduce the amount of stimulation-induced transmitter release from dopaminergic terminals are associated with a dopamine autoreceptor-mediated hyperpolarization and/or alteration in ionic conductance of the terminal membranes. These results are discussed with respect to mechanisms of autoinhibition in the central nervous system.
D000818:Animals; D003342:Corpus Striatum / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects; D008297:Male; D008474:Medial Forebrain Bundle / Q000502:physiology; D009431:Neural Conduction; D009433:Neural Inhibition / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000502:physiology*; D013378:Substantia Nigra / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects
D011954:Receptors, Dopamine; D004298:Dopamine