α2 and β-adrenoceptor agonists modulate [3H]dopamine release from rat nucleus accumbens slices: Implications for research into depression
Date
1984
Authors
Nurse B.
Russell V.A.
Taljaard J.J.F.
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Abstract
The modulatory effects of noradrenergic agonists on the 25 mM K+-induced release of [3H]dopamine (3H-DA) from rat brain nucleus accumbens slices was investigated, using a superfusion technique. The K+-induced release of 3H-DA was Ca2+ dependent, significantly enhanced (25-32%; p < 0.02) by the β-adrenoceptor agonist isoproterenol (10 μM), and significantly decreased (13-25%; p < 0.05) by the α2-adrenoceptor agonist clonidine (10 μM). At these concentrations neither drug affected basal release of 3H-DA. Clonidine (100 μM) increased the basal release of 3H-DA, while decreasing the K+-induced release by 19% (p < 0.01). The inclusion of desipramine in the incubation medium, to prevent accumulation of 3H-DA into noradrenergic neurons, did not alter the inhibitory effect of clonidine (10 μM) on 3H-DA release. This study provides direct evidence that noradrenergic neurons can modulate dopaminergic neurotransmission in the mesolimbic system.
Description
Keywords
alpha adrenergic receptor stimulating agent, beta adrenergic receptor stimulating agent, calcium, clonidine, desipramine, isoprenaline, potassium, radioisotope, animal cell, brain, central nervous system, dopamine h 3, dopamine release, dose response, drug antagonism, drug comparison, drug elimination, drug interaction, drug potentiation, drug response, eighth nerve nucleus, nonhuman, rat, Animal, Calcium, Clonidine, Comparative Study, Depressive Disorder, Dopamine, Human, In Vitro, Isoproterenol, Male, Norepinephrine, Nucleus Accumbens, Rats, Rats, Inbred Strains, Septal Nuclei, Support, Non-U.S. Gov't, Synaptic Transmission
Citation
Neurochemical Research
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