We conducted ex-vivo whole-cell electrophysiological recordings from mice expressing channelrhodopsin-2 in nucleus accumbens afferents, including the ventral hippocampus and amygdala. Thus far, our preliminary results indicate a dissociation in the modulation of nucleus accumbens afferents by kappa-opioid and mu-opioid receptors. Kappa-opioid receptor activation inhibits synaptic transmission in the amygdala to nucleus accumbens, but not hippocampus to nucleus accumbens, pathway. Conversely, mu-opioid receptor activation inhibits hippocampal inputs to a subset of nucleus accumbens neurons, an effect not observed on the amygdala to nucleus accumbens pathway. Future studies are aimed at understanding the cell-types (D1 vs D2) modulated by mu- and kappa-opioid receptors, how different NAcc afferents can drive post-synaptic nucleus accumbens neurons to release opioid peptides, and the contribution of opioid receptors on nucleus accumbens afferent terminals to motivated behavior.
| Tejeda, Hugo A; Wu, Jocelyn; Kornspun, Alana R et al. (2017) Pathway- and Cell-Specific Kappa-Opioid Receptor Modulation of Excitation-Inhibition Balance Differentially Gates D1 and D2 Accumbens Neuron Activity. Neuron 93:147-163 |
| Tejeda, Hugo A; Bonci, Antonello (2014) Shedding ""UV"" light on endogenous opioid dependence. Cell 157:1500-1 |
