Biology subjects

Hillard, C. J.

Publications and source records attributed to Hillard, C. J..

2 recordsLinked to original sources

bioRxiv2023

Endocannabinoid and psychological responses to acute resistance exercise in trained and untrained adults

ObjectiveThis study examined the effects of acute resistance exercise on circulating endocannabinoid (eCB) and mood responses in trained and untrained healthy adults. Methods: Thirty-two healthy adults (22.1 {+/-} 2.9 years) were recruited from trained (reporting resistance exercise at least twice per week for [≥] previous three months) and untrained (performing no resistance exercise for [≥] previous three months) groups. Participants completed three sets of resistance exercise (16 repetitions at 50% 1-repetition max, 12 repetitions at 70% 1-repetition max, 8 repetitions at 80% 1-repetition max). Mood states, affect, and circulating eCB concentrations were evaluated before and after resistance exercise. ResultsThere were significant decreases in AEA, PEA, and OEA levels following acute resistance exercise (p <0.05), with no significant group differences or group by time interactions. 2-AG did not change significantly. Positive affect increased significantly following resistance exercise (p =0.009), while negative affect decreased (p <0.001). Depression, anger, confusion, and total mood disturbance decreased significantly (p <0.05), while vigor increased significantly following resistance exercise (p =0.005). There were no significant group differences or group by time interactions for any psychological outcomes. ConclusionThese results indicate that acute resistance exercise may reduce eCB and related lipid concentrations, which is opposite to the increase in lipids typically observed with acute aerobic exercise. Furthermore, psychological improvements occur after resistance exercise regardless of decreases in eCBs, supporting the notion that psychological changes with exercise likely occur through a wide variety of biological and environmental mechanisms.

physiology↗

bioRxiv2022

Role of mesolimbic endocannabinoid signaling in stress-driven cocaine use in rats

Stress is prevalent in the lives of those with substance use disorders (SUDs) and influences SUD outcomes. Understanding the neurobiological mechanisms through which stress promotes drug use is important for the development of effective SUD interventions. We have developed a model wherein exposure to a stressor, uncontrollable electric footshock, daily at the time of cocaine self-administration (SA) escalates intake in male rats. Here we test the hypothesis that stress-induced escalation of cocaine SA requires CB1 cannabinoid receptor signaling. Male Sprague-Dawley rats self-administered cocaine (0.5 mg/kg/inf, i.v.) during 2-h sessions comprised of four 30-min SA components separated by 5-min shock sequences or 5-min shock-free periods for 14 days. Footshock produced an escalation of cocaine SA that persisted following shock removal. Systemic administration of the cannabinoid receptor type 1 (CB1R) antagonist, AM251, attenuated cocaine intake only in rats with a history of stress. This effect was localized to the mesolimbic system, as intra-nucleus accumbens (NAc) shell and intra-ventral tegmental area (VTA) micro-infusions of AM251 attenuated cocaine intake only in stress-escalated rats. Cocaine SA, regardless of stress history, increases CB1R binding site density in the VTA, but not NAc shell. Following extinction, cocaine-primed reinstatement (10 mg/kg, ip) was increased in rats with prior footshock during SA. AM251 attenuated reinstatement only in rats with a stress history. Altogether, these data demonstrate that mesolimbic CB1R signaling is required to escalate intake and heighten relapse susceptibility and suggest that repeated stress at the time of cocaine use enhances mesolimbic CB1R signaling through a currently unknown mechanism.

neuroscience↗