Abstract
There is substantial pharmacological evidence that glutamate can modulate the effects of 5-hydroxytryptamine2A (5-HT2A) receptor activation through stimulation of metabotropic glutamate2/3 receptors (mGluR2/3) in the cerebral cortex. In this work, we show that deletion of mGluR2 profoundly attenuates the head twitch behavior elicited by 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) administration in mice. MGlu2 KO and age-matched ICR (CD-1) WT mice (N=8/dose) were administered DOI and observed for head twitch activity over 30 minutes. Additional CD-1 mice were administered the mGluR2/3 agonist LY379268 or the mGluR2 potentiator LY566332 followed by DOI, and observed for head twitches for 30 minutes. The results indicated that both LY379268 and LY566332 were able to reduce head twitches in a dose-dependent manner. More importantly, DOI (3mg/kg) failed to elicit head twitches in the mGlu2 KO mice where even a 30 mg/kg dose produced a head shake frequency only ~ 25% of that seen in WT mice. These results indicate that the mGluR2 receptor is intimately involved in modulating head twitches elicited by the 5-HT2A agonist DOI. This behavior, coupled with past electrophysiological, behavioral and biochemical results, suggests that mGluR2 functions as an autoreceptor in thalamocortical pathways impinging upon the principal output cells, layer V pyramidal cells, of the mPFC.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
