Both Prelimbic and Infralimbic Noradrenergic Neurotransmissions Modulate Cardiovascular Responses to Restraint Stress in Rats

The prelimbic (PL) and infralimbic (IL) subareas of the medial prefrontal cortex (mPFC) have been implicated in physiological and behavioral responses during aversive threats. The previous studies reported the noradrenaline release within the mPFC during stressful events, and the lesions of catecholaminergic terminals in this cortical structure affected stress-evoked local neuronal activation. Nevertheless, the role of mPFC adrenoceptors on cardiovascular responses during emotional stress is unknown. Thus, we investigated the role of adrenoceptors present within the PL and IL on the increase in both arterial pressure and heart rate (HR) and on the sympathetically mediated cutaneous vasoconstriction evoked by acute restraint stress. For this, bilateral guide cannulas were implanted into either the PL or IL of male rats. All animals were also subjected to catheter implantation into the femoral artery for cardiovascular recording. The increase in both arterial pressure and HR and the decrease in the tail skin temperature as an indirect measurement of sympathetically mediated cutaneous vasoconstriction were recorded during the restraint session. We observed that the microinjection of the selective α2-adrenoceptor antagonist RX821002 into either the PL or IL decreased the pressor response during restraint stress. Treatment of the PL or IL with either the α1-adrenoceptor antagonist WB4101 or the α2-adrenoceptor antagonist reduced the restraint-evoked tachycardia. The drop in the tail skin temperature was decreased by PL treatment with the β-adrenoceptor antagonist propranolol and with the α1- or α2-adrenoceptor antagonists. The α2-adrenoceptor antagonist into the IL also decreased the skin temperature response. Our results suggest that the noradrenergic neurotransmission in both PL and IL mediates the cardiovascular responses to aversive threats.

Vestibular modulation of skin sympathetic nerve activity in sopite syndrome induced by low-frequency sinusoidal motion

Little is known about the autonomic consequences of sopite syndrome—the drowsiness that can be induced by low-amplitude cyclic motion. We recorded skin sympathetic nerve activity (SSNA) in seated participants exposed to slow sinusoidal linear acceleration (0.03–0.2 Hz), which preferentially activates hair cells in the utricular part of the otolithic organs, at amplitudes that generated no sensations of motion. At all frequencies, there was a clear vestibular modulation of SSNA and cutaneous vasoconstriction.

Contribution of nucleus raphe magnus to thermoregulation

Thermoregulation is the maintenance of the core body temperature. The regulation of body temperature is one of the most important functions of the nervous system. Nucleus raphe magnus, as a central circuit coordinates the homeostatic response and maintains body temperature during environmental temperature challenges and adjusts body temperature during the inflammatory response and behavioral states and in response to decreasing energy homeostasis. Our aim in this review is the understanding of thermoregulation by raphe magnus in mammals. This review summarizes the basic concepts of thermoregulation and subsequently assesses the physiological responses to cold stress, including skin blood flow control, sweating, sympathetic-derived cutaneous vasoconstriction and peripheral thermoregulatory control in brown adipose tissue.

Cooling-induced dilatation of cutaneous arteries is mediated by increased myoendothelial communication

Cold causes cutaneous vasoconstriction to restrict heat loss. Although cold also initiates cutaneous dilatation, the mechanisms and role of this dilatation have not been clearly defined. This study demonstrates that cooling increases myoendothelial coupling between smooth muscle and endothelial cells in cutaneous arteries, which is associated with increased endothelium-derived hyperpolarization (EDH)-type dilatation. Dysfunction in this process may contribute to excessive cold-induced constriction and tissue injury

Short-term menthol treatment promotes persistent thermogenesis without induction of compensatory food consumption in Wistar rats: implications for obesity control

In this study, we aimed to evaluate the influence of daily repeated menthol treatments on body mass and thermoregulatory effectors in Wistar rats, considering that menthol is a transient receptor potential melastatin 8 channel agonist that mimics cold sensation and activates thermoregulatory cold-defense mechanisms in mammals, promoting hyperthermia and increasing energy expenditure, and has been suggested as an anti-obesity drug. Male Wistar rats were topically treated with 5% menthol for 3 or 9 consecutive days while body mass, food intake, abdominal temperature, metabolism, cutaneous vasoconstriction, and thermal preference were measured. Menthol promoted hyperthermia on all days of treatment, due to an increase in metabolism and cutaneous vasoconstriction, without affecting food intake, resulting in less mass gain in menthol-hyperthermic animals. As the treatment progressed, the menthol-induced increases in metabolism and hyperthermia were attenuated but not abolished. Moreover, cutaneous vasoconstriction was potentiated, and an increase in the warmth-seeking behavior was induced. Taken together, the results suggest that, although changes occur in thermoeffector recruitment during the course of short-term treatment, menthol is a promising drug to prevent body mass gain. NEW & NOTEWORTHY Menthol produces a persistent increase in energy expenditure, with limited compensatory thermoregulatory adaptations and, most unexpectedly, without affecting food intake. Thus short-term treatment with menthol results in less mass gain in treated animals compared with controls. Our results suggest that menthol is a promising drug for the prevention of obesity.