Intracellular recordings were made from locus coeruleus neurons in slices taken from rats 8-26 d of age. Neurons from these animals exhibited spontaneous action potentials, which were superimposed on slow (0.3-3 Hz) rhythmic depolarizations. The frequency of these potentials was closely related to the age of the animals from which the slice was taken, the slowest frequencies being observed in tissues from the youngest animals. In adult animals, such rhythmic activity was only rarely observed under normal recording conditions. The rhythmic depolarizations had a slow rate of rise and fall, were 3-15 mV in amplitude, were not affected by tetrodotoxin, and were abolished in solutions that contained elevated magnesium content. When the membrane potential was hyperpolarized by passing current through the recording electrode, the depolarizing rhythmic activity persisted even at very negative potentials (-120 mV). These depolarizations appear to be generated by the inward movement of calcium ions, probably in dendritic regions of the neuron. Superfusion of phenylephrine caused membrane depolarizations, increased the frequency of action potentials and of the slow, rhythmic depolarizations in about 80% of the cells from young rats, whereas it had no effect or a depressant action on cells from adults. Noradrenaline hyperpolarized the cells through an alpha2-adrenoceptor and abolished the slow depolarizations. In cells from young rats, the hyperpolarization produced by noradrenaline reached a maximum and then declined, such that there was a 'sag' in the membrane potential toward the resting potential following the peak of the hyperpolarization. Following the washout of noradrenaline, the membrane potential repolarized before moving toward the resting level. The decline of the membrane potential during the application of noradrenaline and the repolarization following the wash of noradrenaline were antagonized by prazosin. The results indicate that locus coeruleus neurons exhibit alpha1-adrenoceptor responsiveness during early stages of development, which is almost absent in adult animals. This might cause an enhanced responsiveness of these neurons during early postnatal periods.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Neuroscience|
|State||Published - 1987|
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