Tags

Type your tag names separated by a space and hit enter

Striatal neuronal activity and responsiveness to dopamine and glutamate after selective blockade of D1 and D2 dopamine receptors in freely moving rats.
J Neurosci. 1999 May 01; 19(9):3594-609.JN

Abstract

Although striatal neurons receive continuous dopamine (DA) input, little information is available on the role of such input in regulating normal striatal functions. To clarify this issue, we assessed how systemic administration of selective D1 and D2 receptor blockers or their combination alters striatal neuronal processing in freely moving rats. Single-unit recording was combined with iontophoresis to monitor basal impulse activity of dorsal and ventral striatal neurons and their responses to glutamate (GLU), a major source of excitatory striatal drive, and DA. SCH-23390 (0.2 mg/kg), a D1 antagonist, strongly elevated basal activity and attenuated neuronal responses to DA compared with control conditions, but GLU-induced excitations were enhanced relative to control as indicated by a reduction in response threshold, an increase in response magnitude, and a more frequent appearance of apparent depolarization inactivation. In contrast, the D2 antagonist eticlopride (0.2 mg/kg) had a weak depressing effect on basal activity and was completely ineffective in blocking the neuronal response to DA. Although eticlopride reduced the magnitude of the GLU response, the response threshold was lower, and depolarization inactivation occurred more often relative to control. The combined administration of these drugs resembled the effects of SCH-23390, but whereas the change in basal activity and the GLU response was weaker, the DA blocking effect was stronger than SCH-23390 alone. Our data support evidence for DA as a modulator of striatal function and suggest that under behaviorally relevant conditions tonically released DA acts mainly via D1 receptors to provide a continuous inhibiting or restraining effect on both basal activity and responsiveness of striatal neurons to GLU-mediated excitatory input.

Authors+Show Affiliations

Program in Neural Science, Department of Psychology, Indiana University, Bloomington, Indiana 47405, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10212318

Citation

Kiyatkin, E A., and G V. Rebec. "Striatal Neuronal Activity and Responsiveness to Dopamine and Glutamate After Selective Blockade of D1 and D2 Dopamine Receptors in Freely Moving Rats." The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, vol. 19, no. 9, 1999, pp. 3594-609.
Kiyatkin EA, Rebec GV. Striatal neuronal activity and responsiveness to dopamine and glutamate after selective blockade of D1 and D2 dopamine receptors in freely moving rats. J Neurosci. 1999;19(9):3594-609.
Kiyatkin, E. A., & Rebec, G. V. (1999). Striatal neuronal activity and responsiveness to dopamine and glutamate after selective blockade of D1 and D2 dopamine receptors in freely moving rats. The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 19(9), 3594-609.
Kiyatkin EA, Rebec GV. Striatal Neuronal Activity and Responsiveness to Dopamine and Glutamate After Selective Blockade of D1 and D2 Dopamine Receptors in Freely Moving Rats. J Neurosci. 1999 May 1;19(9):3594-609. PubMed PMID: 10212318.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Striatal neuronal activity and responsiveness to dopamine and glutamate after selective blockade of D1 and D2 dopamine receptors in freely moving rats. AU - Kiyatkin,E A, AU - Rebec,G V, PY - 1999/4/23/pubmed PY - 1999/4/23/medline PY - 1999/4/23/entrez SP - 3594 EP - 609 JF - The Journal of neuroscience : the official journal of the Society for Neuroscience JO - J Neurosci VL - 19 IS - 9 N2 - Although striatal neurons receive continuous dopamine (DA) input, little information is available on the role of such input in regulating normal striatal functions. To clarify this issue, we assessed how systemic administration of selective D1 and D2 receptor blockers or their combination alters striatal neuronal processing in freely moving rats. Single-unit recording was combined with iontophoresis to monitor basal impulse activity of dorsal and ventral striatal neurons and their responses to glutamate (GLU), a major source of excitatory striatal drive, and DA. SCH-23390 (0.2 mg/kg), a D1 antagonist, strongly elevated basal activity and attenuated neuronal responses to DA compared with control conditions, but GLU-induced excitations were enhanced relative to control as indicated by a reduction in response threshold, an increase in response magnitude, and a more frequent appearance of apparent depolarization inactivation. In contrast, the D2 antagonist eticlopride (0.2 mg/kg) had a weak depressing effect on basal activity and was completely ineffective in blocking the neuronal response to DA. Although eticlopride reduced the magnitude of the GLU response, the response threshold was lower, and depolarization inactivation occurred more often relative to control. The combined administration of these drugs resembled the effects of SCH-23390, but whereas the change in basal activity and the GLU response was weaker, the DA blocking effect was stronger than SCH-23390 alone. Our data support evidence for DA as a modulator of striatal function and suggest that under behaviorally relevant conditions tonically released DA acts mainly via D1 receptors to provide a continuous inhibiting or restraining effect on both basal activity and responsiveness of striatal neurons to GLU-mediated excitatory input. SN - 0270-6474 UR - https://www.unboundmedicine.com/medline/citation/10212318/Striatal_neuronal_activity_and_responsiveness_to_dopamine_and_glutamate_after_selective_blockade_of_D1_and_D2_dopamine_receptors_in_freely_moving_rats_ L2 - http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=10212318 DB - PRIME DP - Unbound Medicine ER -