Membrane dysfunction induced by in vitro XXXX in immature @entity35 hippocampal @entity1249 neurons.

@entity7504 @entity1249 @entity63 @entity26 @entity19241 @entity35 @entity413
We investigated differences between immature and mature hippocampal neurons in their response to deprivation of @entity26 and @entity413 (in vitro @entity63 ), using intracellular recording techniques from @entity1249 pyramidal neurons in @entity35 brain slices. The membrane was more depolarized in immature hippocampal @entity1249 neurons (postnatal day 7, P7) compared with the adult neurons (P140), and the apparent input resistance in immature neurons was higher than that in adult neurons. In immature neurons, the threshold for action potential generation was high, and the peak amplitude of the action potential was low in comparison with adult neurons. A time-dependent inward rectification, at potentials negative than the resting potential, was prominent in neurons of @entity19241 and @entity7504 . After @entity7504 , the resting membrane potential, the apparent input resistance, and the threshold and the peak amplitude of the action potential did not significantly change with increasing age. In adult neurons, application of @entity63 -simulating medium caused irreversible changes in membrane potential consisting of an initial hyperpolarization followed by a slow depolarization and a rapid depolarization. Once the rapid depolarization occurred, reintroduction of @entity26 and @entity413 failed to restore the membrane potential, a state referred to as irreversible membrane dysfunction. In neurons of ages P7 or @entity19241 , the initial hyperpolarization was not apparent, whereas a slow depolarization followed by a rapid depolarization was observed. With development of the neurons, the latency for onset of the rapid depolarization became shorter and its maximal slope increased. Moreover, neurons of ages @entity19241 or @entity7504 showed a partial or complete recovery after reintroduction of @entity26 and @entity413 , unlike mature neurons. In summary, the present study has demonstrated that the initial hyperpolarization and rapid depolarization induced by in vitro @entity63 is age dependent. The rapid depolarization is not readily produced in the neurons in age less than @entity7504 during ischemic exposure.
