Naloxone disrupts the development of a conditioned ejaculatory preference based on a somatosensory cue in male rats.

Male rats develop a conditioned ejaculatory preference (CEP) toward females bearing an odor or somatosensory cue (rodent jacket) when those stimuli are paired with the postejaculatory reward state. As with a copulatory conditioned place preference, CEP for an odor depends on endogenous opioid transmission after ejaculation. The nonselective opioid receptor antagonist naloxone (NAL) disrupts CEP for an odor cue on female rats when injected systemically to males prior to each conditioning trial. Here, we evaluated whether NAL would disrupt the development of a CEP for the somatosensory cue. Long-Evans males were assigned randomly to two groups and underwent 14 copulatory conditioning trials for 30 min each, spaced every 4 days, and consisting of sequential pairing of a jacket on a sexually receptive female and no jacket on a sexually nonreceptive female. The control group was injected with saline (SAL) in both conditions throughout training, whereas the experimental group was injected with NAL when females were receptive and wore a jacket, and with SAL when they were not receptive and did not wear a jacket. On the final test, all males were injected with SAL and placed into an open field with two sexually receptive females, one with the jacket and the other without the jacket. Control males displayed a significant CEP for females with the jacket on, whereas males injected with NAL during sexually receptive jacket conditions displayed a significant CEP for the nonjacketed female. This study confirms that opioid transmission is necessary for the establishment of a somatosensory CEP. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Inhibition of lysine-specific demethylase enzyme disrupts sexually conditioned mate guarding in the female rat.

Although female rats are typically described as having a promiscuous mating strategy, if sexually naïve females have their formative sexually rewarding experiences paired with the same male, they will recognize that male and display mate-guarding behavior towards him in the presence of a female competitor. Female rats that display mate guarding behavior also show enhanced activation of oxytocin and vasopressin neurons in the supraoptic and paraventricular hypothalamic nucleus. Here, we examined the potential role that histone demethylation might have in establishing this pair-bonded behavior, and whether the corresponding changes in oxytocin and vasopressin neuronal activation depended on demethylation. To accomplish this, we examined the effect of a lysine-specific demethylase-1 inhibitor to block the action of demethylase enzymes and maintain the methylation state of corresponding genes. Female rats treated with the demethylase inhibitor failed to show any measure of mate guarding, whereas females treated with vehicle displayed mate guarding behavior. Demethylase inhibitor treatment also blocked the ability of familiar male cues to activate oxytocin and vasopressin neurons, whereas vehicle-treated females showed this enhanced activation. These data indicate that histone demethylation is a crucial component in the epigenetic modification of neural circuitry that underlies conditioned mate guarding in female rats. These results are the first to demonstrate the role of histone demethylation underlying changes in mating strategy.