The biochemistry and pharmacology of mesoamygdaloid dopamine neurons.
Populations of DA neurons innervating the component nuclei of the amygdaloid complex differ in their inferred density of innervation, estimated rate of impulse activity, and adaptive response to the prolonged administration of antipsychotic drugs. Mesoamygdaloid DA neurons have in common the absence of tonically inhibitory, nerve terminal autoreceptors regulating DA synthesis, the nonassociation with a DA-stimulated adenylate cyclase, and the regulation of DA synthesis by receptor-mediated neuronal feedback mechanisms and end-product inhibition. The output of the amygdaloid complex appears to be organized into distinct functions subserved by component nuclei. The present findings suggest a differing role for DA afferents in modulating the functional output of discrete nuclei. The significance of this focal influence will be speculative pending a more complete understanding of the physiology of DA neurotransmission in the amygdaloid complex. Populations of DA neurons innervating discrete amygdaloid nuclei exhibit a composite of mechanisms of regulation and signal transduction and pharmacology that differ from that of other mesotelencephalic DA systems. These comparisons highlight the fact that the nucleus accumbens and olfactory tubercle do not represent or reflect DA neurotransmission in the limbic system. The study of the physiology, pharmacology, and pathology of mesolimbic DA neurons can and should extend beyond the nucleus accumbens and olfactory tubercle to the amygdala and other brain structures central to the organization of the limbic system. It is our opinion that the term "mesolimbic" DA system has purely anatomical connotations and that a more specific terminology (e.g., meso-central amygdaloid nuclear) would express the functional organization of this system more accurately.
Kilts
C D
CD
Department of Psychiatry and Pharmacology, Duke University Medical Center, Durham, North Carolina 27710.
Anderson
C M
CM
Ely
T D
TD
Mailman
R B
RB
D000262:Adenylyl Cyclases / Q000378:metabolism; D000679:Amygdala / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D004298:Dopamine / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D008636:Mesencephalon / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology; D015398:Signal Transduction
D011954:Receptors, Dopamine; D000262:Adenylyl Cyclases; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine