CaV channel blockade in the extended amygdala has a delayed effect on the reward efficacy of medial forebrain bundle stimulation.

Previous work in our laboratory has shown that stimulating D2 dopamine receptors in the central sublenticular extended amygdala (SLEAc) can render medial forebrain bundle (MFB) stimulation less rewarding. One of the many ways in which D2 stimulation could affect the activity status of SLEAc neurons is by indirectly blocking calcium ion (Ca) influx through CaV channels. He we directly investigate the effects of blocking CaV channels on the rewarding effect of MFB stimulation.

Toward a systems-oriented approach to the role of the extended amygdala in adaptive responding.

Research into the structure and function of the basal forebrain macrostructure called the extended amygdala (EA) has recently seen considerable growth. This paper reviews that work, with the objectives of identifying underlying themes and developing a common goal towards which investigators of EA function might work. The paper begins with a brief review of the structure and the ontological and phylogenetic origins of the EA.

Comparison of the effects on brain stimulation reward of D1 blockade or D2 stimulation combined with AMPA blockade in the extended amygdala and nucleus accumbens.

This report compares the effects on medial forebrain bundle self-stimulation of injecting into either the sublenticular central extended amygdala (SLEAc) or nucleus accumbens shell (NAcS) the D1 dopamine receptor blocker SCH23390 or the D2 dopamine receptor agonist quinpirole alone or in combination with the AMPA glutamate receptor blocker NBQX. These manipulations all render affected neurons less excitable and therefore are expected to increase the stimulation pulse frequency required to maintain half-maximal response rate (required frequency, or RF). Injections were made ipsilateral and contralateral to the stimulation site but not bilaterally.

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

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.

Brain stimulation reward is affected by D2 dopamine receptor manipulations in the extended amygdala but not the nucleus accumbens.

This work examines the effects on brain stimulation reward (BSR) of D1 and D2 dopamine receptor manipulations in the sublenticular central extended amygdala (SLEAc) and the nucleus accumbens shell (NAc). Fifty-three male Long Evans rats received medial forebrain bundle stimulation electrodes and bilateral injection guide cannulae aimed at either the SLEAc or the NAc. The rate-frequency paradigm was used to assess drug-induced changes in stimulation reward effectiveness and in response rate following 0.