The application proposes to investigate the hypothesis that noradrenaline containing neurons in the caudal ventrolateral medulla (VLM) of the cat are excited by acute increases in arterial blood pressure and that adrenaline containing neurons in the rostral VLM are inhibited by acute increases in arterial blood pressure. Further it is proposed that caudal VLM neurons influence the activity of rostral VLM neurons either through monosynaptic connections or through indirect pathways. Thus, interactions between caudal and rostral VLM neurons constitute neuronal mechanisms in the VLM of the cat that are part of baroreflex control of sympathetic nerve activity. The concept that VLM neurons are part of the baroreflex will be investigated in anesthetized cats prepared with a single innervated isolated carotid sinus (other baroreceptor regions denervated) and prepared for the recording of single unit activity of caudal and rostral VLM neurons. The behavior of VLM neurons to baroreceptor input will be examined by systematically forcing carotid sinus pressure and recording neuronal activity in response to this baroreceptor input. After completion of each experiment the brain stem of these cats will be processed for immunocytochemical identification of noradrenaline and adrenaline containing neurons. Noradrenaline containing neurons will be identified as those neurons that stain only with dopamine-beta-hydroxylase antibodies (rabbit) and adrenaline containing neurons as those that stain with phenylethanolamine-N-methyltransferase antibodies (rabbit). The response properties of individual neurons will be correlated to their location within populations of noradrenaline and adrenaline containing neurons in the VLM. Additional experiments are proposed to investigate the probable neural pathways through which caudal VLM neurons can influence the activity of rostral VLM neurons. First, the projection of caudal VLM neurons to the ipsilateral rostral VLM will be determined through the use of antidromic microstimulation and/or spike-triggered averaging of recorded field potentials. Second, monosynaptic connections between caudal and rostral VLM neurons will be investigated by recording simultaneous activity from pairs of these neurons and application of cross correlation analysis. Third, the possibility of an indirect pathway from the caudal VLM to rostral VLM neurons via neurons in the NTS will be investigated by electrophysiologic determination of axonal projections from the caudal VLM to the ipsilateral NTS in combination with the electrophysiologic determination of axonal projections from the NTS to the ipsilateral rostral VLM. The proposed experiments should contribute to the understanding of the role of VLM in baroreflex control of the circulation.
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