A role for N-methyl-D-aspartate receptors in norepinephrine-induced long-lasting potentiation in the dentate gyrus.

摘要: Mechanisms of action norepinephrine (NE) on dentate gyrus granule cells were studied in rat hippocampal slices using extra- and intracellular recordings measurements stimulus amino acid-induced changes extracellular Ca2+ K+ concentration. Bath application NE (10–50 μM) induced long-lasting potentiation perforant path evoked potentials, markedly enhanced high-frequency stimulus-induced influx efflux, actions blocked by β-receptor antagonists mimicked β agonists. Enhanced was primarily postsynaptic, since presynaptic Δ [Ca2+]0 the stratum moleculare synaptic field not altered NE. Interestingly, both ionic fluxes population potentials antagonized N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonovalerate (APV). Furthermore, selectively Δ[Ca2+]0, Δ[K+]0 slow negative elicited iontophoretically applied NMDA, but those excitatory acid quisqualate. These results suggest that cell through NMDA ionophores is via activation. In recordings, depolarized (4.8±1.1 mV), increased input resistance (RN) 34±6.5%. also either β-antagonist propranolol or specific β1-blocker metoprolol. Moreover, depolarization RN increase persisted for long periods (93±12 min) after washout. contrast, while NE, presence APV, still RN, APV made these quickly reversible upon washout (16±9 min). This suggested induction long-term, short-term, plasticity requires may be enhancing firing some combination blockade late Ca2+-activated conductance cells, can bring into a voltage range where receptors are more easily activated. activity-independent increases, which required functional to persist.