Elsevier

Brain Research Reviews

Volume 16, Issue 3, September–December 1991, Pages 223-244
Brain Research Reviews

Dopamine transmission in the initiation and expression of drug- and stress-induced sensitization of motor activity

https://doi.org/10.1016/0165-0173(91)90007-UGet rights and content

Abstract

Progress has been made over the last 10 years in determining the neural mechanisms of sensitization induced by amphetamine-like psychostimulants, opioids and stressors. Changes in dopamine transmission in axon terminal fields such as the nucleus accumbens appear to underlie the expression of sensitization, but the actions of drugs and stressors in the somatodendritic regions of the A10/A9 dopamine neurons seem critical for the initiation of sensitization. Manipulations that increase somatodendritic dopamine release and permit the stimulation of D1 dopamine receptors in this region induce changes in the dopamine system that lead to the development of long-term sensitization. However, it is not known exactly how the changes in the A10/A9 region are encoded to permit augmented dopamine transmission in the terminal field. One possibility is that the dopamine neurons of sensitized animals have become increasingly sensitive to excitatory pharmacological and environmental stimuli or desensitized to inhibitory regulation. Alternatively, changes in cellular activity or protein synthesis may result in a change in the presynaptic regulation of axon terminal dopamine release.

References (301)

  • S. Browder et al.

    Midbrain dopamine neurons: differential responses to amphetamine isomers

    Brain Research

    (1981)
  • M.J. Brownstein et al.

    On the origin of substance P and glutamic acid decarboxylase (GAD) in the substantia nigra

    Brain Research

    (1977)
  • J.M. Burgunder et al.

    Distribution, projection and dopaminergic regulation of the neurokinin B mRNA-containing neurons of the rat caudate-putamen

    Neuroscience

    (1989)
  • M. Cador et al.

    Substance P, neurotensin and enkephalin injections into the ventral tegmental area: comparative study on dopamine turn-over in several forebrain structures

    Brain Research

    (1989)
  • E. Carboni et al.

    Amphetamine, cocaine, phencyclidine and nomifensine increase extracellular dopamine concentrations preferentially in the nucleus accumbens of freely moving rats

    Neuroscience

    (1989)
  • C.J. Carter

    Topographical distribution of possible glutamatergic pathways from the frontal cortex to the striatum and substantia nigra in rats

    Neuropharmacology

    (1982)
  • E. Castaneda et al.

    The long-term effects of repeated amphetamine treatment in vivo on amphetamine, KG and electrical stimulation evoked striatal dopamine release in vitro

    Life Sci.

    (1988)
  • N.A. Castle et al.

    Toxins in the characterization of potassium channels

    Trends Neurosci.

    (1989)
  • H.T. Chang

    Substance P-dopamine relationship in the rat substantia nigra: a light and electron microscopy study of double immunocytochemically labeled materials

    Brain Research

    (1988)
  • A. Cheramy et al.

    In vivo presynaptic control of dopamine release in the cat caudate nucleus. Facilitatory or inhibitory influence of glutamate

    Neuroscience

    (1986)
  • C.E. Connor et al.

    Evidence that amphetamine and Na+ gradient reversal increase striatal synaptosomal dopamine synthesis through carrier-mediated efflux of dopamine

    Biochem. Pharmacol.

    (1986)
  • H.E. Criswell et al.

    Long-term D1-dopamine receptor sensitization in neonatal 6-OHDA-lesioned rats is blocked by an NMDA antagonist

    Brain Research

    (1990)
  • C.J. Cruz et al.

    Quantitative radioimmuno-cytochemical evidence that haloperidol and SCH 23390 induce opposite changes in substance P levels of rat substantia nigra

    Brain Research

    (1988)
  • C.J. Cruz et al.

    Nigrostriatal dopamine neurons are required to maintain basal levels of substance P in the rat substantia nigra

    Neuroscience

    (1989)
  • A.Y. Deutch et al.

    Substance K and substance P differentially modulate mesolimbic and mesocortical systems

    Peptides

    (1985)
  • A.Y. Deutch et al.

    Footshock and conditioned stress increase in 3,4-dihydroxyphenylacetic acid (DOPAC) in the ventral tegmental area but not substantia nigra

    Brain Research

    (1985)
  • G. Di Chiara et al.

    Evidence for a GABAergic projection from the substantia nigra to the ventromedial thalamus and to the superior colliculus of the rat

    Brain Research

    (1979)
  • G.G. Dougherty et al.

    Chronic d-amphetamine in nucleus accumbens: lack of tolerance or reverse tolerance of locomotor activity

    Life Sci.

    (1981)
  • L.P. Dwoskin et al.

    Repeated cocaine administration results in super-sensitivity of striatal D2 dopamine autoreceptors to pergolide

    Life Sci.

    (1988)
  • A.S. Eison et al.

    The behavioral effects of a novel substance P analogue following infusion into the ventral tegmental area or substantia nigra of the rat brain

    Brain Research

    (1982)
  • J.L. Fitzgerald et al.

    Chronic cocaine treatment does not alter rat striatal D2 autoreceptor sensitivity to pergolide

    Brain Research

    (1991)
  • K. Fuxe et al.

    Studies on neurotensin-catecholamine interactions in the hypothalamus and in the forebrain of the male rat

    Neurochem. Int.

    (1984)
  • K. Gale et al.

    Presence of substance P and GABA in separate striatonigral neurons

    Brain Research

    (1977)
  • R.F. Gariano et al.

    Burst firing induced in mid-brain dopamine neurons by stimulation of the medial prefrontal and anterior cingulate cortices

    Brain Research

    (1988)
  • F.G. Gonon

    Non-linear relationship between impulse flow and dopamine released by rat midbrain dopaminergic neurons as studied by in vivo electrochemistry

    Neuroscience

    (1988)
  • A.A. Grace et al.

    Paradoxical GABA excitation of nigral dopaminergic cells: indirect mediation through reticulata inhibitory neurons

    Eur. J. Pharmacol.

    (1979)
  • A.A. Grace et al.

    Opposing effects of striatonigral feedback pathways on midbrain dopamine cell activity

    Brain Research

    (1985)
  • H.J. Groenewegen et al.

    Neuroscience

    (1987)
  • K. Gysling et al.

    Morphine-induced activation of A10 dopamine neurons in the rat brain

    Brain Research

    (1983)
  • K. Gysling et al.

    Morphine-induced activation of A10 dopamine neurons in the rat brain

    Brain Research

    (1983)
  • B. Hahn et al.

    Alterations of amphetamine elicited perserveration and locomotor excitation following acute and repeated Stressor application

    Pharmacol. Biochem. Behav.

    (1986)
  • G. Halliday et al.

    Substance P-like immunoreactive fibres in the ventromedial mesencephalic tegmentum of rat

    Brain Res. Bull.

    (1988)
  • G.R. Hanson et al.

    Response by the neurotensin systems of the basal ganglia to cocaine treatment

    Eur. J. Pharmacol.

    (1989)
  • N.C. Harris et al.

    A possible pacemaker mechanism in pars compacta neurons of the guinea-pig substantia nigra revealed by various ion channel blocking agents

    Neuroscience

    (1989)
  • E.D. Abercrombie et al.

    Differential effect of stress on in vivo dopamine release in striatum, nucleus accumbens, and medial frontal cortex

    J. Neurochem.

    (1989)
  • J. Aceves et al.

    l-DOPA facilitates GABA release activating D1 dopamine receptors in the basal ganglia of the rat brain

    Soc. Neurosci. Abstr.

    (1989)
  • D.K. Adachi et al.

    Neurotensin binds to dopamine

    J. Neurochem.

    (1990)
  • L.F. Agnati et al.

    Further evidence for the existence of interactions between receptors for dopamine and neurotensin. Dopamine reduces the affinity and increases the number of [3H]neurotensin binding sites in the subcortical limbic forebrain of the rat

    Acta Physiol. Scand.

    (1985)
  • L.F. Agnati et al.

    Neurotensin in vitro markedly reduces the affinity in subcortical limbic 3H-N-propylapomorphine binding sites

    Acta Physiol. Scand.

    (1983)
  • R.F. Akers et al.

    Translocation of protein kinase C activity may mediate hippocampal long-term potentiation

    Science

    (1986)
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