Dopamine Receptor Inactivation in the Caudateputamen and Nucleus Accumbens Differentially Affects the Locomotor Activity of Young Rats
Presentation Type
Poster Presentation/Art Exihibt
College
College of Social and Behavioral Sciences
Major
Psychology
Location
Event Center A & B
Faculty Mentor
Dr. Sanders McDougall
Start Date
5-19-2016 1:00 PM
End Date
5-19-2016 2:30 PM
Abstract
Microinjecting the alkylating agent EEDQ into the caudate-putamen (CPu) of adult rats both inactivates DA receptors and blocks DA mediated behaviors. In contrast, DA receptor inactivation in the CPu of preweanling rats causes a paradoxical increase in DA agonist-induced locomotor activity. We have hypothesized that the heightened behavioral responsiveness exhibited by EEDQ-treated preweanling rats is due to elevated levels of high affinity D2 receptors. In other words, an EEDQ-induced increase in the percentage of D2(High) receptors is proposed to more than compensate for the overall loss of DA receptors, thus resulting in enhanced behavioral responsiveness when challenged with a DA agonist drug (cocaine or NPA). The purpose of the present study was threefold: (1) to replicate the finding that EEDQ potentiates the behavioral effects of NPA when microinjected into the CPu; (2) to determine whether administering EEDQ into the nucleus accumbens (NAcc) also potentiates the effects of NPA; and (3) to examine whether the ability to potentiate or attenuate DA agonist-induced locomotion is influenced by the amount of striatal and accumbal tissue affected by EEDQ.
Dopamine Receptor Inactivation in the Caudateputamen and Nucleus Accumbens Differentially Affects the Locomotor Activity of Young Rats
Event Center A & B
Microinjecting the alkylating agent EEDQ into the caudate-putamen (CPu) of adult rats both inactivates DA receptors and blocks DA mediated behaviors. In contrast, DA receptor inactivation in the CPu of preweanling rats causes a paradoxical increase in DA agonist-induced locomotor activity. We have hypothesized that the heightened behavioral responsiveness exhibited by EEDQ-treated preweanling rats is due to elevated levels of high affinity D2 receptors. In other words, an EEDQ-induced increase in the percentage of D2(High) receptors is proposed to more than compensate for the overall loss of DA receptors, thus resulting in enhanced behavioral responsiveness when challenged with a DA agonist drug (cocaine or NPA). The purpose of the present study was threefold: (1) to replicate the finding that EEDQ potentiates the behavioral effects of NPA when microinjected into the CPu; (2) to determine whether administering EEDQ into the nucleus accumbens (NAcc) also potentiates the effects of NPA; and (3) to examine whether the ability to potentiate or attenuate DA agonist-induced locomotion is influenced by the amount of striatal and accumbal tissue affected by EEDQ.
