Abstract
Cardiovascular neurons in the Rostro-Ventrolateral Medulla (RVLM) have been shown to display a regular action potential discharge activity in vitro which has been proposed to result either from pacemaker conductances or from the activity of an oscillating network. Using intracellularly recordings in vitro from regularly-discharging RVLM neurons, we observed in young adult rats (>19 days) that the regular discharge activity in RVLM is labile, as many neurons were or spontaneously became quiescent during the recording. A regular discharge could be induced or restored in quiescent neurons by superfusing an external concentration of K + ions ([K +] ext) of 6 mM. In order to elucidate how neurotransmitters might influence this discharge activity, we studied the effects of a catecholamine, noradrenaline (present in this brain region). Noradrenaline depolarized or increased the spiking frequency of regularly-discharging neurons. This excitatory effect was sensitive to prazosin and propranolol. In the presence of these two blockers, noradrenaline induced a hyperpolarization sensitive to idazoxan and mimicked by α 2-adrenergic agonists. These effects persisted in the presence of tetrodotoxin. In spontaneously active neurons, prazosin plus propranolol abolished the discharge activity. At hyperpolarized potentials, the adrenoceptor blockers reduced the baseline synaptic/oscillatory activity. Our results demonstrate that the regular discharge activity of RVLM neurons is labile and depends on external ionic conditions, such as [K +] ext. This discharge activity can be modulated by catecholamines, acting at the 3 subtypes of adrenoceptors which co-exist on the same neuron. We propose that an endogenous release of catecholamines may condition the discharge activity of RVLM neurons.
Published Version
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