Abstract
Since the demonstration of dopamine-containing nerve terminals within cortical regions1,2, studies have confirmed the existence of a dopaminergic projection to the medial prefrontal cortex3,4. Cortical dopamine (DA) may be a functional neurotransmitter, as there are selective high-affinity receptor binding5,6 and uptake sites7,8 within this area, a DA-selective adenylate cyclase system8,9, cells responsive to iontophoretically applied DA10, and a pool of DA amenable to release in vivo11 or in vitro12,13. Lesions of either midbrain cell bodies in the ventral tegmental area14,15 or of frontal cortical areas directly16, with subsequent loss of DA terminals from the medial prefrontal cortex, induce hyperactivity in rats16, and enhanced behavioural responses to amphetamine16,17. Lesion of subcortical DA pathways results in the opposite effects, suggesting that frontal cortical DA systems may have an inhibitory role in motor behaviour15,16. Dopamine-dependent hyperactivity and stereotypy is believed to be mediated from extrapyramidal and mesolimbic DA-innervated sites18. We previously noted that loss of catecholamine terminals within the frontal cortex of the rat results in increased DA turnover and utilization in subcortical striatal and limbic regions after one week19. We now show evidence of both enhanced pre-synaptic and post-synaptic mechanisms in the terminal regions of the ascending nigrostriatal and mesolimbic DA pathways one month after destruction of DA terminals within the medial prefrontal cortex of the rat. The increased 3H-ADTN and 3H-spiperone binding, enhanced DA-induced stimulation of adenylate cyclase and potentiated uptake capacity for DA within striatum and nucleus accumbens may demonstrate a functional basis for the observed potentiated behavioural responses.
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Pycock, C., Kerwin, R. & Carter, C. Effect of lesion of cortical dopamine terminals on subcortical dopamine receptors in rats. Nature 286, 74–77 (1980). https://doi.org/10.1038/286074a0
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DOI: https://doi.org/10.1038/286074a0
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