PMID: 3924349Jun 1, 1985Paper

Amine accumulation in behavioural pathology

Brain Research
Gregory L Willis, G C Smith


When nigro-striatal and meso-cortical neurons degenerate there is a loss of dopamine in the terminal fields and an accumulation of amines in the axons of these systems as they traverse the hypothalamus through the medial forebrain bundle. Traditional lines of thought have attributed the occurrence of motor and consummatory deficits which occur after dopamine neuron degeneration to the loss of functional dopamine neurotransmitter in the terminal fields. However, we have hypothesized that hypothalamic amine accumulation represents an area of brain tissue where processes such as neurotransmitter release, ephaptic transmission or local axon swelling may be affecting adjacent neurons and may thereby participate in the production of behavioural deficits. There is a considerable amount of evidence from studies on both peripheral and central catecholamine-containing neurons indicating that when their axons degenerate a release of functional neurotransmitter can occur. Information from neuropharmacological studies indicates that several drugs which facilitate behavioural recovery from dopamine-depleting lesions may do so by affecting amine release or receptor sensitivity near areas of accumulation rather than depleted terminal fields. W...Continue Reading


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Jan 1, 1988·Progress in Neuro-psychopharmacology & Biological Psychiatry·G L WillisG A Donnan
Jul 1, 1987·Brain Research Bulletin·G L WillisG C Smith
Jul 15, 1999·Physiology & Behavior·G L Willis, S M Armstrong
Sep 5, 1998·Brain Research. Brain Research Reviews·G L Willis, S M Armstrong
Jan 1, 1987·Neuroscience and Biobehavioral Reviews·G L Willis
May 27, 2008·Brain Research·Gregory L Willis
Jul 1, 1993·The International Journal of Neuroscience·G L Willis, R Sandyk
Jul 1, 1992·The International Journal of Neuroscience·G L WillisR Sandyk
Sep 1, 1992·The International Journal of Neuroscience·R Sandyk, G L Willis
Jul 1, 1992·The International Journal of Neuroscience·G L Willis, R Sandyk
Jun 1, 1991·The Australian and New Zealand Journal of Psychiatry·G C Smith

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