title: κ-opioid receptors in the infralimbic cortex modulate the cardiovascular responses to acute stress.
abstract: What is the central question of this study? A brief experience of stress can cause structural remodelling in the infralimbic cortex. In the present study, we addressed the potential role played by opioidergic neurotransmission in the infralimbic cortex in the modulation of stress-evoked autonomic responses. What is the main finding and its importance? Using the restraint stress model, we showed that infralimbic cortex κ-opioid receptors, but not μ- and δ-opioid receptors, modulate stress-evoked cardiovascular responses. The infralimbic cortex (IL) is known to modulate behavioural and physiological responses during aversive situations. We investigated the hypothesis that opioid neurotransmission in the IL modulates the autonomic responses induced in rats subjected to restraint stress (RS). Male Wistar rats (250-280 g) were used. Guide cannulae were implanted bilaterally in the IL for the microinjection of either drugs or vehicle, and a polyethylene catheter was implanted into the femoral artery for recording of mean arterial pressure (MAP) and heart rate (HR) using a computerized acquisition system. Tail temperature was evaluated using a thermal camera. Rats were subjected to RS 10 min after the microinjection of drugs or vehicle into the IL. Exposure to RS evoked hypertension, tachycardia and a reduction in tail temperature. Bilateral microinjections of the non-selective opioid antagonist naloxone into the IL generated an inverted U-shaped dose-inhibition curve on RS-evoked MAP and HR responses. Microinjection of nor-BNI (κ-selective antagonist) reduced the increases in MAP and HR evoked by RS. In contrast, pretreatment of the IL with CTAP (μ-selective antagonist) or naltrindole (δ-selective antagonist) had no effect on the restraint-evoked increases in MAP and HR. None of these treatments altered the reduction in the tail temperature evoked by RS. In conclusion, κ-opioid receptors in the IL modulate pressor and tachycardiac responses caused by RS, suggesting a facilitatory role of this structure in this aversive situation.
authors: Department of Pharmacology of the School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors: Aline
authors: A
authors: Fassini
authors: América A
authors: AA
authors: Scopinho
authors: Leonardo B M
authors: LB
authors: Resstel
authors: Fernando M A
authors: FM
authors: Corrêa
mesh_terms: D000818:Animals; D062186:Arterial Pressure / Q000502:physiology*; D001341:Autonomic Nervous System / Q000502:physiology*; D025461:Feedback, Physiological / Q000502:physiology; D006321:Heart / Q000502:physiology; D006339:Heart Rate / Q000502:physiology*; D065726:Limbic Lobe / Q000502:physiology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D017473:Receptors, Opioid, kappa / Q000378:metabolism*; D013312:Stress, Physiological / Q000502:physiology*
chemical_list: D017473:Receptors, Opioid, kappa