Speaker:Â Dr. Lauren Faget, Assistant Professor of Biological Sciences at Boise State University
Host:Â Dr. Allan Albig, Biological Sciences
Title:Â GABAergic and glutamatergic projections from the Ventral Pallidum: two parallel pathways with opponent roles in motivated behaviors
Abstract:Â The ventral pallidum (VP) is a structure centrally located in the brain that controls reward and motivated behaviors. The VP is predominantly composed of GABAergic neurons but also includes neurons expressing the glutamatergic marker vesicular glutamate transporter (VGLUT2). Using cell-type-specific tracing we found that VP glutamate and GABA neurons share similar main projections to the ventral tegmental area (VTA) and the lateral habenula (LHb). And preliminary data show that the two main neuronal populations of the nucleus accumbens (NAc), structure providing the main inhibitory input to the VP, functionally connect onto both VP cell types. However, using optogenetic manipulation, we observed that activation of VP GABA and glutamate cell bodies elicit opposite appetitive behaviors, reinforcement and avoidance respectively. To better understand how VP neurons differentially drive behavior, we recorded calcium transients in VP GABA and glutamate neurons in freely behaving animals during rewarding or aversive events. Also, to shine light on how VP neurons modulate VTA cell population activity, we measured VTA Dopamine, GABA, and glutamate neuron calcium transients in response to VP GABA or glutamate neuron optogenetic activation. These data surprisingly suggest a role for both VP GABA and glutamate neurons in encoding the salience of appetitive events, either rewarding or aversive. However, we observed that their activation had differential consequences on the dopamine system and VTA neuronal population activity, in line with their ability to drive opponent motivated behaviors. These findings highlight a potent role for bidirectional control of motivated behaviors by collaborative VP inhibitory and excitatory neurons, dysregulation of which could contribute to the emergence of deficits in reward functions associated with drug addiction and other neuropsychiatric diseases.
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