Amphetamine-induced Release Research Articles

Uptake and release of noradrenaline in rat cerebral cortex in vitro: No effect of benzodiazepines and barbiturates

The effects of two barbiturates (phenobarbitone and pentobarbitone) and one benzodiazepine (chlordiazepoxide) were studied on uptake, retention and spontaneous and stimulation-induced release of 3H-noradrenaline in rat cerebral cortex slices in vitro. The drugs, in a wide range of concentrations, did not interfere with the uptake and retention of 3H-noradrenaIine nor did they change the spontaneous release when slices, preincubated with 3H-noradrenaline, were rinsed together with the drug. The field stimulation-induced release of 3H-noradrenaline was also unaffected by these drugs. Pentobarbitone did not affect the amphetamine-induced release of 3H-noradrenaline from the slices. Previous findings show that barbiturates and benzodiazepines decrease the turnover of noradrenaline in the cerebral cortex. The present results make it improbable that this turnover effect is mediated via a direct effect of the drugs on the noradrenaline nerve terminals.

Release of dopamine from central noradrenaline nerves after treatment with reserpine plus amphetamine.

The dexamphetamine-induced release of dopamine and noradrenaline was studied in regions of the rat central nervous system rich in dopamine or noradrenaline nerve terminals by analyzing the accumulation of the 3-O-methylated catecholamines after inhibition of the monoamine oxidase. Reserpine pretreatment almost completely inhibited the amphetamine-induced release of noradrenaline from the noradrenaline nerves and reduced the dopamine release from the dopamine nerves by about one third. Amphetamine caused a release of dopamine, instead of noradrenaline, from the noradrenaline nerves after pretreatment with reserpine, and this replacement accounted for about two thirds of the missing noradrenaline. This dopamine was found to be of small functional significance due to a weak stimulating action on the noradrenaline receptors of the effector cells.

Differential sensitivity of amygdala and hypothalamus to amphetamine-induced release of norepinephrine.

Differential sensitivity of amygdala and hypothalamus to amphetamine-induced release of norepinephrine.