NMDA and dopamine D2 receptors in the caudate-putamen are not involved in control of motor readiness in rats.
RATIONALE: In reaction time (RT) paradigms, in which a variable preparation interval preceded the imperative stimulus, RT become shorter as a function of increasing time from the start of a trial until presentation of the imperative stimulus. The shortening of RT as the preparatory foreperiod elapses reflects increasing motor readiness; however, the underlying neurochemical mechanisms are still poorly defined. OBJECTIVE: The present study investigated in rats whether signals transmitted via the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors and via dopamine D2 receptors in the caudate-putamen (CPu) are involved in motor readiness. METHODS: A simple RT task demanding conditioned lever release was used, in which the upcoming reward magnitude (5 pellets or 1 pellet) was signalled in advance by discriminative stimuli and the imperative stimulus was subsequently presented after a variable foreperiod (200, 500 or 800 ms). RESULTS: In intact rats, RT of conditioned responses was shortened with foreperiod lengthening and with expectancy of the high reward magnitude, but there was no interaction between both factors. Bilateral infusion of the competitive NMDA antagonist DL-2-amino-5-phosphonovaleric acid (APV) (2, 10 micrograms in 0.5 microliter/side), of the preferential dopamine D2 antagonist haloperidol (5, 12.5 micrograms in 0.5 microliter/side) or infusion of vehicle (0.5 microliter/side) into the central subregion of the CPu had no effect on progressive RT shortening with increasing foreperiod. CONCLUSION: The present data provide no clues to suggest that motor readiness relies on stimulation of dopamine D2 and NMDA receptors in the central CPu.[1]References
- NMDA and dopamine D2 receptors in the caudate-putamen are not involved in control of motor readiness in rats. Hauber, W., Giertler, C., Bohn, I. Psychopharmacology (Berl.) (2001) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
