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The Neurobiological Substrates of Depression in Parkinson’s Disease: A Hypothesis

Published online by Cambridge University Press:  18 September 2015

H.C. Fibiger
H.C. Fibiger*
Affiliation:
Division of Neurological Sciences, Department of Psychiatry, University of British Columbia, Vancouver, B.C
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Abstract

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Evidence from a variety of sources indicates that the mesolimbic-mesocortical dopamine projections may play an important role in some types of reward or reinforcement processes in animals. There is circumstantial evidence that this is also true in humans. Since a reduced ability to experience pleasure or reward (i.e. anhedonia) is a cardinal feature of clinical depression, and since the mesolimbic and mesocortical dopamine projections have been shown to degenerate in Parkinson’s disease, it is suggested that damage to these reward-related systems may contribute directly to the high incidence of depression that has been reported in this disease.

Type
1. Neurotransmitters and the Pharmacology of the Basal Ganglia
Information
Canadian Journal of Neurological Sciences , Volume 11 , Issue S1: Current Concepts and Controversies in Parkinson’s Disease , February 1984 , pp. 105 - 107
Copyright
Copyright © Canadian Neurological Sciences Federation 1984

References

Barbeau, A (1969) L-dopa therapy in Parkinson’s disease: a critical review of nine years’ experience. Can. Med. Assoc. J. 101: 791–800.Google ScholarPubMed
Bergstrom, DA, Kellar, KJ (1979) Adrenergic and serotonergic receptor binding in rat brain after chronic desmethylimipramine treatment. J. Pharmac. Exp. Ther. 209:256–261.Google ScholarPubMed
Brown, GL, Wilson, WP (1972) Parkinsonism and depression. South Med. J. 65:540–545.CrossRefGoogle ScholarPubMed
Celesia, GC, Wanamaker, WM (1972) Psychiatric disturbances in Parkinson’s disease. Dis. Nerv. Syst. 33:577–583.Google ScholarPubMed
Clavier, RM, Fibiger, HC (1977) On the role of ascending catecholaminergic projections in self-stimulation of the substantia nigra. Brain Research 131:271–286.CrossRefGoogle ScholarPubMed
Fibiger, HC (1978) Drugs and reinforcement: A critical review of the catecholamine theory. Ann. Rev. Pharmacol. Toxicol. 18:37–56.CrossRefGoogle ScholarPubMed
Goeders, NE, Smith, JE (1983) Critical dopaminergic involvement in cocaine reinforcement. Science 221:773–775.CrossRefGoogle Scholar
Gunne, LM, Anggard, E, Jonsson, LE (1972) Clinical trials with amphetamine-blocking drugs. Psychiatr. Neurol. Neurochir. 75:225–226.Google ScholarPubMed
Hokfelt, T, Rehfeld, JR.Skirboll, L, Ivemark, B, Goldstein, M.Markey, M & , K (1980) Evidence for coexistence of dopamine and CCK in mesolimbic neurons. Nature 285:476–478.CrossRefGoogle Scholar
Hokfelt, T, Skirboll, L, Rehfeld, JF, Goldstein, M, Markey, K, Dann, O (1980) A subpopulation of mesencephalic dopamine neurons projecting to limbic areas contains a cholecystokinin-like peptide: Evidence from immunohistochemistry combined with retrograde tracing. Neuroscience 5:2093–2124.CrossRefGoogle ScholarPubMed
Horn, S (1974) Some psychological factors in parkinsonism. Neurol. Neurosurg. Psychiatry 37:27–31.CrossRefGoogle ScholarPubMed
Huang, YH, Maas, JW, Hu, GH (1980) The time course of noradrenergic pre- and postsynaptic activity during chronic desipramine treatment. Eur. J. Pharm. 68:41–47.CrossRefGoogle ScholarPubMed
Javoy-Agid, F, Ploska, A, Agid, Y (1981) Microtopography of tyrosine hydroxylase, glutamic acid decarboxylase, and choline acetyltransferase in the substantia nigra and ventral tegmental area of control and parkinsonian brains. J. Neurochem. 37:1218–1227.CrossRefGoogle ScholarPubMed
Jonsson, L, Anggard, E, Gunne, L (1971) Blockade of intravenous amphetamine euphoria in man. Clin. Pharmacol. Ther. 12:889–896.CrossRefGoogle ScholarPubMed
Lyness, WH, Friedle, NM, Moore, KE (1979) Destruction of dopaminergic nerve terminals in nucleus accumbens: Effect on d-amphetamine self-adminstration. Pharmac. Biochem. Behav. 11:553–556.CrossRefGoogle Scholar
Mayeux, R, Stern, Y, Rosen, J, Leventhal, J (1981) Depression, intellectual impairment, and Parkinson disease. Neurology 31:645–650.CrossRefGoogle ScholarPubMed
Mindham, RHS (1970) Psychiatric symptoms in parkinsonism. J. Neurol. Neurosurg. Psychiatry 33:188–189.CrossRefGoogle ScholarPubMed
Mindham, RHS, Marsden, CD, Parkes, JD (1976) Psychiatric symptoms during l-dopa therapy for Parkinson’s disease and their relationship to physical disability. Psychol. Med. 6:23–33.CrossRefGoogle ScholarPubMed
Parkinson, J (1938) An essay of the shaking palsy, 1817. Med. Class 2:964–997.Google Scholar
Phillips, AG, Fibiger, HC (1978) The role of dopamine in maintaining intracranial self-stimulation in the ventral tegmentum, nucleus accumbens, and prefrontal cortex. Canadian J. Psychol. 32:58–66.CrossRefGoogle ScholarPubMed
Price, KS, Farley, IJ, Hornykiewicz, O (1979) Neurochemistry of Parkinson’s disease: relation between striatal and limbic dopamine. In: Advances in biochemical Psychopharmacology, Vol. 19: Dopamine, (Eds.) Roberts, PJ, Woodruff, GN, New York: Raven Press, pp. 208–217.Google Scholar
Riederer, P, Birkmayer, W, Seemann, D, Wuketich, St (1977) Brain-noradrenaline and 3-methoxy-4-hydroxyphenylglycol in Parkinson’s syndrome. J. Neural. Trans. 41:241–251.Google ScholarPubMed
Roberts, DCS, Corcoran, ME, Fibiger, HC (1977) On the role of ascending catecholaminergic systems in intravenous self-administration of cocaine. Pharmac. Biochem. Behav. 6:615–620.CrossRefGoogle ScholarPubMed
Roberts, DCS, Koob, GF, Klonoff, P, Fibiger, HC (1980) Extinction and recovery of cocaine self-administration following 6-hydroxydopamine lesions of the nucleus accumbens. Pharmac. Biochem. Behav. 12:781–787.CrossRefGoogle ScholarPubMed
Robins, AH (1976) Depression in patients with parkinsonism. Br. J. Psychiatry 128:141–145.CrossRefGoogle ScholarPubMed
Sourkes, TL (1976) Parkinson’s disease and other disorders of the basal ganglia. In: Basic Neurochemistry (Eds) Siegel, GJ, Albers, RW, Katzman, R, Agranoff, BW, Boston: Little, Brown and Company, pp. 668–684.Google Scholar
Spyraki, C, Fibiger, HC, Phillips, AG (1982a) Cocaine-induced place preference conditioning: Lack of effects of neuroleptics and 6-hydroxydopamine lesions. Brain Research 253:195–203.CrossRefGoogle ScholarPubMed
Spyraki, C, Fibiger, HC.Phillips, AG (1982b) Dopaminergic substrates of amphetamine-induced place preference conditioning. Brain Research 253:185–193.CrossRefGoogle ScholarPubMed
Sulser, F (1978) Functional aspects of the norepinephrine receptor coupled adenylate cyclase system in the limbic forebrain and its modification by drugs which precipitate or alleviate depression: molecular approaches to an understanding of affective disorders. Pharmakopsychiat 11:43–52.CrossRefGoogle ScholarPubMed
Warburton, JW (1967) Depressive symptoms in Parkinson patient referred for thalamotomy. J. Neurol. Neurosurg. Psychiatry 30:368–370.CrossRefGoogle ScholarPubMed
Wise, RA (1978) Catecholamine theories of reward: A critical review. Brain Research 152:215–247.CrossRefGoogle ScholarPubMed
Yahr, MD, Duvoisin, RS, Schear, MJ, Barrett, RE, Hoehn, MM (1969). Treatment of parkinsonism with levodopa. Arch. Neurol. 21:343–54.CrossRefGoogle ScholarPubMed
Yokel, RA, Wise, RA (1976) Attenuation of intravenous amphetamine reinforcement by central dopamine blockade in rats. Psycho-pharmacology 48:311–318.CrossRefGoogle ScholarPubMed