Social buffering is the phenomenon in which the presence of an
affiliative conspecific mitigates stress responses. We previously
demonstrated that social buffering completely ameliorates conditioned
fear responses in rats. The present study explored the neurochemical
background of this social buffering. In Experiment 1, fear-conditioned
subjects first received an intraperitoneal injection of either naloxone
(non-selective opioid receptor antagonist), haloperidol (dopamine D2
receptor antagonist), SR49059 (vasopressin V1A receptor antagonist),
atosiban (oxytocin receptor antagonist), or saline. The subjects were
then exposed to a conditioned stimulus with an unfamiliar
non-conditioned rat. Naloxone, but not the other three antagonists,
blocked social buffering. In Experiment 2, we assessed the effect of
naloxone on locomotor activity during an open-field test. Naloxone did
not affect walking steps during the test. Therefore, it is unlikely that
the results of Experiment 1 were due to decreased activity by naloxone.
In Experiment 3, we assessed Fos expression in 16 brain regions
accompanied by the blockade of social buffering by naloxone. Consistent
with the results of Experiment 1, Fos expression was increased in the
paraventricular nucleus of the hypothalamus. In addition, Fos expression
was decreased in the nucleus accumbens shell, anterior cingulate cortex,
and insular cortex and tended to be decreased in the nucleus accumbens
core. Naloxone thus appears to affect these four regions and/or act
upstream of these regions during blockade of social buffering. Based on
these results, we conclude that naloxone blocks social buffering of
conditioned fear responses in rats.