Dissociation in control of cardiovascular and behavioral responses to emotional stress by cholinergic neurotransmission in the bed nucleus of the stria terminalis in rats

s Selected For Presentation 23.5 Dissociation in control of cardiovascular and behavioral responses to emotional stress by cholinergic neurotransmission in the bed nucleus of the stria terminalis in rats C.C. Crestani, M.K. Gouveia, T.T. Miguel., C. Busnardo, A.A. Scopinho, F.M. Correa, R.L. Nunes-de-Souza Laboratory of Pharmacology, School of Pharmaceutical Sciences of Araraquara, Sao Paulo State UniversityUNESP, Araraquara, SP Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, MG Department of Pharmacology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto-SP, Brazil The bed nucleus of the stria terminalis (BNST) is a limbic forebrain structure implicated in physiological and behavioral responses to emotional stress. However, the local neurochemical mechanisms mediating the BNST control of stress responses are not fully known. Here, we investigated the involvement of BNST cholinergic neurotransmission in cardiovascular and neuroendocrine responses and behavioral consequences evoked by acute restraint stress in rats. For this, male Wistar rats had guide cannulas bilaterally implanted in the BST. A catheter was implanted in the femoral artery for cardiovascular recording and blood samples collection. The reduction in tail skin temperature was measured by a termovisor as an index of sympathetic-mediated vasoconstriction response. The restraint stress was realized by placing the animals in a plastic cylindrical tube during 30 minutes. Restraint-evoked anxiogenic-like effect was investigated by behavioral analysis in the elevated plus maze (EPM). Independent animals received bilateral microinjection into the BNST of the choline uptake inhibitor hemicholinium-3 (3 nmol/100 nl) or the muscarinic receptor antagonist methylatropine (3 nmol/100 nl) 10 minutes before the onset of restraint stress. BNST treatmentwith either hemicholinium3 or methylatropine enhanced the heart rate increase (hemicholinium3: P b 0.0001; methylatropine: P b 0.0001), without affecting blood pressure (hemicholinium-3: P N 0.05; methylatropine: P N 0.05), cutaneous temperature (hemicholinium-3: P N 0.05; methylatropine: P N 0.05), and plasma corticosterone (hemicholinium-3: P N 0.05; methylatropine: P N 0.05) responses. Restraint caused anxiogenic-like effect (P b 0.001), which was inhibited by BNST treatment with either hemicholinium-3 (P N 0.05) or methylatropine (P N 0.05). These findings indicate an opposite role of BNST cholinergic neurotransmission in control of cardiovascular responses (inhibitory influence) and emotional consequences (facilitatory influence) evoked by stress. Financial support: FAPESP, PADC/FCF-UNESP. doi:10.1016/j.autneu.2015.07.371 Symposium 24: Consciousness, The Autonomic Nervous System and Disorders of Orthostatic Tolerance 24.1 Interface between the Autonomic and Arousal Systems Eduardo E. Benarroch Department of Neurology, Mayo Clinic, Rochester, MN, USA There is anatomical and functional overlap and interconnections between the forebrain and brainstem areas involved in autonomic control and arousal. Central autonomic involved in control of both functions include the insular cortex, anterior and midcingulate cortex, amygdala, lateral hypothalamus, periaqueductal gray, parabrachial nucleus (PBN), nucleus of the solitary tract dorsal motor nucleus of the vagus, nucleus ambiguus, ventrolateral medulla (VLM), and medullary raphe. These areas receive direct or indirect input from wake-active cholinergic or monoaminergic neurons located in the basal forebrain, pedunculopontine nucleus, locus ceruleus (LC), rostral raphe, periaqueductal gray and tuberomammillary nucleus. All these nuclei also receive excitatory inputs from orexin neurons of the perifornical hypothalamus. Several examples illustrate the interactions of the autonomic systems with areas involved in arousal from sleep or behavioral/emotional arousal. For example, activation of the LC triggers sympathetic activation and inhibition of cardiovagal neurons, providing a functional link between arousal and increase in blood pressure and heart rate. Sympathoexcitatory C1 neurons respond to hypoxia and other stressors, and activate the LC; C1 neurons thereby promote arousal during non-REM sleep. The PBN is critical for arousal triggered by hypercapnia and promotes sympathetic activity. Orexin neurons maintain wakefulness and activate sympathetic output in response to chemoreflex and other stimuli. Neuroimaging studies show coactivation of area of the corticolimbic areas of the salience network and the sympathetic system; and that of the default mode network and the parasympathetic system. These multiple interactions may have relevance in the setting of sleep apnea, hypertension, fatal insomnia and limbic encephalitis. doi:10.1016/j.autneu.2015.07.372 24.2 Autonomic circadian regulation in post-traumatic vegetative state