AI Article Synopsis

  • Propofol has been shown to have addictive properties in both humans and rats, and the communication between the basolateral amygdala (BLA) and the nucleus accumbens shell (NAsh) plays a key role in modulating reward-seeking behaviors.
  • Research involved training male rats to self-administer propofol and analyzing changes in neural activity and signaling pathways related to addiction, particularly focusing on AMPA receptors and dopamine receptors.
  • Results indicated that propofol self-administration increases action potentials and excitatory postsynaptic currents in the NAsh, while interfering with the BLA-to-NAsh circuitry significantly affects propofol-seeking behavior, highlighting the importance of AMPARs and dopamine interactions in propofol

Article Abstract

Propofol addictive properties have been demonstrated in humans and rats. The glutamatergic transmission from basolateral nucleus of amygdala (BLA) to the nucleus accumbens (NAc) modulates reward-seeking behaviour; especially, NAc shell (NAsh) is implicated in reward-seeking response. Previous studies indicated the interactions between AMPA receptors (AMPARs) and dopamine D1 receptor (D1R) in NAc mediated drug addiction, but whether the circuit of BLA-to-NAsh and AMPARs regulate propofol addiction remains unclear. We trained adult male Sprague-Dawley rats for propofol self-administration to examine the changes of action potentials (APs) and spontaneous excitatory postsynaptic currents (sEPSCs) in the NAsh. Thereafter, optogenetic stimulation with adeno-associated viral vectors microinjections in BLA was used to explore the effect of BLA-to-NAsh on propofol self-administration behaviour (1.7 mg/kg/injection). The pretreatment effects with NBQX (0.25-1.0 μg/0.3 μl/site) or vehicle in the NAsh on propofol self-administration behaviour, the expressions of AMPARs subunits and D1R/ERK/CREB signalling pathway in the NAc were detected. The results showed that the number of APs, amplitude and frequency of sEPSCs were enhanced in propofol self-administrated rats. Propofol self-administration was inhibited in the NpHR3.0-EYFP group, but in the ChR2-EYFP group, there was a promoting effect, which could be weakened by NBQX pretreatment. NBQX pretreatment also significantly decreased the expressions of GluA2 subunit and D1R in the NAc but did not change the expressions of GluA1 and ERK/CREB signalling pathway. The evidence supports a vital role of BLA-to-NAsh circuit in regulating propofol self-administration and suggests this central reward processing may function through the interaction between AMPARs and D1R in the NAsh.

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Source
http://dx.doi.org/10.1111/adb.13310DOI Listing

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