Activation of dopaminergic neurons modulates ventral pallidal responses evoked by amygdala stimulation.
The ventral pallidum is a basal forebrain region that is thought to integrate cognitive processes with motoric behaviors. These functions are influenced by ventral pallidal inputs, which include projections from the amygdala and the ventral tegmental area/substantia nigra zona compacta. By examining the consequences of this convergence at the neuronal level, the present study indicates that electrical activation of ventral tegmental regions releases dopamine in the ventral pallidum which subsequently modulates pallidal electrophysiological responses evoked by stimulating the amygdala. Stimulation-evoked responses were characterized for extracellular single unit recordings of spontaneously active ventral pallidal neurons from chloral hydrate anesthetized rats. Stimulation of the amygdala evoked short latency (< or = 12 ms; possibly monosynaptic) and/or long latency (> 12 ms; polysynaptic) responses in all ventral pallidal neurons tested. Fifty-nine per cent of the tested neurons responded to ventral tegmental stimulation with short latency inhibition, and these neurons were often sensitive to microiontophoretically applied dopamine. Iontophoresis of dopamine antagonists SCH23390 (a D1 antagonist) or sulpiride (a D2 antagonist) attenuated the ventral tegmental-induced inhibitions. These observations indicate that the evoked responding was the result of endogenously released dopamine, and that D1 and D2 receptors were involved in this effect. Ninety-two per cent of the ventral pallidal neurons that demonstrated short latency responses to amygdala stimulation also exhibited short latency responses to activation of the ventral tegmentum. This suggests that these inputs often converge onto the same pallidal neurons. Amygdala-evoked responses were consistently attenuated by prior stimulation of the ventral tegmentum. Similarly, microiontophoretic ejection of dopamine attenuated amygdala-evoked effects. These results indicate that dopamine modulates amygdala-evoked pallidal responses. Such modulation may contribute to the integrative functions of the ventral pallidum.
Maslowski-Cobuzzi
R J
RJ
Neurosience Program, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153.
Napier
T C
TC
D000679:Amygdala / Q000502:physiology*; D000818:Animals; D004298:Dopamine / Q000494:pharmacology / Q000502:physiology*; D004558:Electric Stimulation; D005917:Globus Pallidus / Q000166:cytology / Q000502:physiology*; D007478:Iontophoresis; D008297:Male; D008636:Mesencephalon / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011954:Receptors, Dopamine / Q000145:classification / Q000502:physiology; D013378:Substantia Nigra / Q000502:physiology
D011954:Receptors, Dopamine; D004298:Dopamine