PubMed 22906479

Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Kir2.3

Title: Brain stimulation reward is altered by affecting dopamine-glutamate interactions in the central extended amygdala.

Authors: M Waraczynski, W Zwifelhofer, L Kuehn

Journal, date & volume: Neuroscience, 2012 Nov 8 , 224, 1-14

PubMed link:

This work compares the effects on brain stimulation reward (BSR) when combining D2 dopamine receptor and AMPA glutamate receptor manipulations in the sublenticular central extended amygdala (SLEAc) and the nucleus accumbens shell (NAc shell). Thirty-seven male Long Evans rats received medial forebrain bundle (MFB) stimulation electrodes and bilateral injection guide cannulae aimed at either the SLEAc or the NAc shell. The rate-frequency paradigm was used to assess drug-induced changes in stimulation reward effectiveness and in response rate following 0.5 μl infusions of 0.50 μg of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide (NBQX) (AMPA receptor antagonist), 10.0 μg of quinpirole (D2 receptor agonist), 0.25 μg of AMPA (AMPA receptor agonist), 3.0 μg of eticlopride (D2 receptor antagonist), 0.50 μg of NBQX with 10.0 μg of quinpirole, and 0.25 μg of AMPA with 3.0 μg of eticlopride. The drugs were injected both ipsi- and contralateral to the stimulation site. AMPA blockade and D2 stimulation synergized to reduce BSR's reward efficacy when directed at the SLEAc contralateral to the stimulation site whereas changes in reward efficacy were primarily D2-dependent following injections into the ipsilateral SLEAc. When injected into the NAc shell the drugs had only one significant effect on the frequency required to maintain half-maximal responding: injections of NBQX with quinpirole ipsilateral to the stimulation site increased required frequency significantly more than did injections of saline. Contrary to expectations, stimulating AMPA receptors with and without co-blockade of D2 receptors also decreased the stimulation's reward efficacy, although these effects may reflect general behavioral disruption more than effects on reward per se. These results indicate a role for the SLEAc in BSR and also suggest that SLEAc neurons ipsi- and contralateral to the stimulated MFB play their roles in BSR through different mechanisms.