Presentation Details
Chemogenetic activation of amygdalar prodynorphin neurons modulates taste-guided licking behavior in mice

Jinrong Li, Christian Lemon.

University of Oklahoma, Norman, OK, USA

Abstract


The central nucleus of the amygdala (CeA) is a critical hub for processing the hedonic value (appetitive & aversive) of tastes. Recent work identified a population of prodynorphin-expressing (Pdyn+) neurons in this area that selectively encodes sweet attraction, yet their role in orosensory preferences for taste is unknown. Here we investigated how chemogenetic activation of CeA Pdyn+ neurons affected mouse taste-guided licking behavior in brief-access fluid exposure tests, which capture oral sensory/tongue control of licking behavior. Intracranial delivery of Cre-dependent viruses in female and male Pdyn_Cre mice induced expression of the excitatory designer receptor hM3Dq:mCherry (hM3Dq mice, n = 13) or fluorophore mCherry alone (mCherry control mice, n = 8) in CeA Pdyn+ neurons. Several weeks later, hM3Dq and mCherry mice entered brief-access tests where they could lick solutions during discrete, seconds-long trials. Stimuli included concentration series of the behaviorally appetitive sugar sucrose (0, 0.1, 0.3, 0.5, 1 M) and the innately avoided bitter taste stimulus quinine (0, 0.1, 0.3, 1 mM). A blinded experimenter administered intraperitoneal injection of saline before daily sucrose tests for 4 days followed by daily injection of the hM3Dq ligand deschloroclozapine (DCZ, 0.1 mg/kg) before sucrose tests 4 days in both hM3Dq and mCherry mice. With DCZ, hM3Dq mice displayed greater average licking of sucrose (i.e., enhanced appetitive responding) with concentrations lower than 0.5 M, in comparison to mCherry mice and to saline injection in hM3Dq mice (group x sucrose x injection interaction, F(4,68) = 2.7, p = 0.035). Quinine analyses are on-going. Current available data suggest that CeA Pdyn+ neurons participate in appetitive taste-guided licking behaviors.  Support: NIH DC011579

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