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Abstract
<p class="first" id="P2">Dopamine signaling encodes reward learning and motivated
behavior through modulation
of synaptic signaling in the nucleus accumbens, and aberrations in these processes
are thought to underlie obsessive behaviors associated with alcohol abuse. The nucleus
accumbens is divided into core and shell sub-regions with overlapping but also divergent
contributions to behavior. Here we optogenetically targeted dopamine projections to
the accumbens allowing us to isolate stimulation of dopamine terminals
<i>ex vivo</i>. We applied 5 pulse (phasic) light stimulations to probe intrinsic
differences in
dopamine release parameters across regions. Also, we exposed animals to 4 weeks of
chronic intermittent ethanol vapor and measured phasic release. We found that initial
release probability, uptake rate and autoreceptor inhibition were greater in the accumbens
core compared to the shell, yet the shell showed greater phasic release ratios. Following
chronic ethanol, uptake rates were increased in the core but not the shell, suggesting
region-specific neuronal adaptations. Conversely, kappa opioid receptor function was
upregulated in both regions to a similar extent, suggesting a local mechanism of kappa
opioid receptor regulation that is generalized across the nucleus accumbens. These
data suggest that dopamine axons in the nucleus accumbens core and shell display differences
in intrinsic release parameters, and that ethanol-induced adaptations to dopamine
neuron terminal fields may not be homogeneous. Also, chronic ethanol exposure induces
an upregulation in kappa opioid receptor function, providing a mechanism for potential
over-inhibition of accumbens dopamine signaling which may negatively impact downstream
synaptic function and ultimately bias choice towards previously reinforced alcohol
use behaviors.
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