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  • Title: Adrenergic receptor activation hyperpolarizes the caudal neurosecretory cells of the flounder, Platichthys flesus.
    Author: Hubbard PC, Balment RJ, McCrohan CR.
    Journal: J Neuroendocrinol; 1996 Feb; 8(2):153-9. PubMed ID: 8868263.
    Abstract:
    The physiological factors that govern activity of the caudal neurosecretory system in teleost fish are poorly understood. Immunocytochemical evidence indicates that the neurosecretory Dahlgren cells are innervated by descending monoaminergic fibres. Using intracellular recording techniques in an isolated preparation of the posterior spinal cord of the flounder (Platichthys flesus) we have demonstrated that superfusion of adrenaline or noradrenaline (10(-7) - 10(-3) M) causes hyperpolarization of Dahlgren cells (up to -30 mV). This hyperpolarization is likely to reflect an inhibitory effect of noradrenergic nerves on the neurosecretory system in vivo, reducing the rate of hormone release. Fluctuations in the input resistance and membrane time constant suggest involvement of a multiplicity of cellular mechanisms, including the opening and closing of populations of ion-selective channels. Superfusion with dopamine (10(-7) - 10(-3) M) had no effect. Superfusion with the beta-adrenoreceptor agonist, isoprenaline, caused hyperpolarization but to a markedly lesser extent than the maximum effect of adrenaline or noradrenaline, suggesting that their effects are mediated, only in part, by a beta-adrenoreceptor subtype. Superfusion of the preparation with a membrane permeable, non-hydrolysable cyclic AMP analogue (8-[4-chlorophenylthio]-cAMP) resulted in a slight hyperpolarization which was accompanied by a small, but significant, increase in input resistance. These data are consistent with at least part of the beta-adrenoreceptor mediated effect involving closure of cAMP-sensitive ion channels. Superfusion with the alpha 1-adrenoreceptor agonist, phenylephrine, had no effect on any electrophysiological parameter studied. However, the alpha 2-adrenoreceptor agonist, clonidine, caused hyperpolarization which again failed to reach the maximum level produced by adrenaline or noradrenaline. Together, these data suggest that the adrenergic inhibition of Dahlgren cell activity is mediated by both alpha 2- and beta-adrenoreceptor subtypes.
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