The medial preoptic area modulates autonomic function under resting and stress conditions

- Inhibition of the mPOA neurotransmission caused tachycardia, without affecting blood pressure.
- Treatment of mPOA with CoCl2 caused hyperthermia (increased Tbody) and a Ttail decrease.
- The pharmacological inhibition of the mPOA with CoCl2 increased the sympathetic component of the cardiac baroreflex.
- Pretreatment of the mPOA with CoCl2 increased tachycardiac without affecting the RS-evoked pressor response.
- CoCl2 administration into mPOA increased hyperthermic responses and reduced the fall in Ttail evoked by RS.

The medial preoptic area (mPOA) participates in the temperature and cardiovascular control. The mPOA receives inputs from limbic structures and sends projections to hypothalamus and brainstem. Moreover, stress elicits pronounced neuronal activation in mPOA, suggesting its involvement in central neural pathway mediating stress responses. In the present study, we report the effect of acute mPOA neurotransmission inhibition using cobalt chloride (CoCl2-nonselective synapse blocker) on the mean arterial pressure (MAP), heart rate (HR), body and tail temperature (Tbody and Ttail, respectively), as well as on the HR component of baroreflex. We also verified the participation of mPOA in the autonomic changes evoked by acute restraint stress (RS). Our results demonstrated that microinjection of CoCl2 into mPOA caused tachycardia, hyperthermia and a Ttail decrease, without altering MAP. The inhibition of mPOA with CoCl2 increased the sympathetic component of cardiac baroreflex when assessed 10 min after its administration. In addition, pretreatment of mPOA with CoCl2 increased RS-evoked tachycardic and hyperthermic responses evoked by RS when compared with aCSF-treated animals, without affecting the RS-evoked pressor response and the fall in Ttail. In summary, our results suggest that mPOA exerts a tonic inhibitory influence on the sympathetic cardiac tone under both rest and stress conditions, modulating negatively the sympathetic component of baroreflex. Results also confirm the mPOA involvement in the control of body temperature because its inhibition was followed by a sustained increase in body temperature and vasoconstriction in the tail artery territory.