Abstract
Mianserin increased stimulation-induced release of noradrenaline from guinea-pig atria and brain cortex slices. The increase still occured when neuronal reuptake of noradrenaline was blocked by cocaine. Mianserin blocked the neuronal uptake of 3H-noradrenaline only in high concentrations (1 μ M in atria produced 40% block; 10 μ M in cortex produced 57% block). Lower concentrations (0.01 μ M in atria; 1 μ M in cortex) significantly increased stimulation-induced release of noradrenaline. It is concluded that increases in transmitter release from noradrenergic nerves produced by mianserin can be attributed to blockade of the α 2-adrenoceptors involved in autoinhibitory feedback mechanism at nerve terminals, rather than to blockade of neuronal reuptake of noradrenaline. This effect on noradrenergic transmission in the central nervous system could explain the antidepressant actions of mainserin in accordance with the hypothesis of Schildkraut.
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