Pyramidal neurons in immature rat hippocampus are sensitive to β-adrenergic agents

Abstract

The development of hippocampal neuronal sensitivities to the β-noradrenergic agent, isoproterenol, was examined in tissue from immature rats. The in vitro hippocampal slice preparation was used to assess intracellularly recorded responses from hippocampal neurons to pressure-pulse and bath application of noradrenergic drugs. Effects of the drug on individual hippocampal CA3 pyramidal neurons were compared across several stages of development, ranging from postnatal day 4–5 (P4–5) to maturity. Isoproterenol, pressure-pulse applied to CA3c pyramidal cells, produced a depolarization of membrane potential and an increase in cell input resistance in tissue as young as P7. Spike frequency adaptation (in trains of action potentials triggered by depolarizing pulses) was reduced, as were the slow after-hyperpolarizations following the spike trains. All agonist effects were blocked by timolol, a β-antagonist. Drug-induced changes in cell membrane and firing properties in immature tissue were qualitatively similar to β-receptor-mediated noradrenergic effects in adult tissue. These results indicate that the β-receptor-mediated component of the noradrenergic effect in rat hippocampus is physiologically functional by the seventh day of postnatal life; at earlier times (P4–5) these β-receptor-mediated noradrenergic actions are, at best, equivocal.