Body weight and regulatory deficits following unilateral nigrostriatal lesions

Baez, Luis A.; Ahlskog, J. Eric; Randall, Patrick K.

doi:10.1016/0006-8993(77)90195-0

Cited by 37 publications

(10 citation statements)

References 25 publications

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“…This finding is in agreement with the report of Baez and his coworkers (Baez et al, 1977), and the observed depression of food intake in the lesioned animals confirms these authors' speculation that the lesion-induced depression of body weight was probably due to reduced food intake.…”

Section: Feeding Behavior and Body Weight Regulationsupporting

confidence: 93%

Feeding behavior and sensorimotor functioning in rats with unilateral medial forebrain bundle damage

Uguru-Okorie

1984

Psychobiology

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Section: Feeding Behavior and Body Weight Regulationsupporting

confidence: 93%

Feeding behavior and sensorimotor functioning in rats with unilateral medial forebrain bundle damage

Uguru-Okorie

1984

Psychobiology

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“…Animals with unilateral lesions of the substantia nigra also demonstrated persistent deficits in body weight [57], though with partial nigral dopamine neuron depletions, there appears to be no effect on free-feeding, but deficits in fine motor movement [30]. Interestingly, in tyrosine hydroxylase deficient mice [44], restoring tyrosine hydroxylase in the dorsal striatum (the major target of the substantia nigra) but not the ventral striatum (i.e., NAc) [58] corrects the feeding.…”

Section: Central Dopaminergic Pathwaysmentioning

confidence: 99%

Metabolic hormones, dopamine circuits, and feeding

Narayanan¹,

Guarnieri²,

DiLeone³

2010

Frontiers in Neuroendocrinology

152

121

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Recent evidence has emerged demonstrating that metabolic hormones such as ghrelin and leptin can act on ventral tegmental area (VTA) midbrain dopamine neurons to influence feeding. The VTA is the origin of mesolimbic dopamine neurons that project to the nucleus accumbens (NAc) to influence behavior. While blockade of dopamine via systemic antagonists or targeted gene delete can impair food intake, local NAc dopamine manipulations have little effect on food intake. Notably, non-dopaminergic manipulations in the VTA and NAc produce more consistent effects on feeding and food choice. More recent genetic evidence supports a role for the substantia nigra-striatal dopamine pathways in food intake, while the VTA-NAc circuit is more likely involved in higher-order aspects of food acquisition, such as motivation and cue associations. This rich and complex literature should be considered in models of how peripheral hormones influence feeding behavior via action on the midbrain circuits.

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“…In fact, when detailed histochemical analyses have been performed in subsequent studies Sandyk , 1992, 1993 ) a poor relationship between DA defi ciency and severity of behavioural defi cits was observed. In short, regardless of the nature of the dependant variable, many results do not acquiesce with the interpretation that DA defi ciency is related to the severity of behavioural defi cit (Fibiger et al , 1973 ;Marshall and Teitelbaum , 1973 ;Baez et al , 1977 ;Willis and Armstrong, 1998).…”

Section: Challenging Preclinical Concepts Da Defi Ciency-dependent Pdmentioning

confidence: 84%

“…Although it was originally suggested that the level of DA defi ciency required to produce permanent defi cits was 50 % (Oltmans and Harvey , 1972 ), others have estimated the cut-off point to be at 80 % (Hantraye et al , 1993 ), 85 % (Ungerstedt et al , 1977 ), 90 % (Ljungberg and Ungerstedt , 1976 ) and at 95 % or greater (Zigmond and Stricker , 1972 ). Although unilateral lesions were designed for the purpose of avoiding the severe bilateral defi cits, it is interesting to note that long-term defi cits have also been reported after unilateral lesions (Baez et al , 1977 ;Carey, 1982;Richards et al , 1990 ). In these instances, only half of the total NSD system is lesioned and resulting DA depletion could be no greater than 50 % (Kilpatrick et al , 1985 ), whereas behavioural impairment is severe.…”

Section: Percent Loss: the Unchangeable Dynamicmentioning

confidence: 99%

Breaking away from dopamine deficiency: an essential new direction for Parkinson’s disease

Willis¹,

Moore²,

Armstrong³

2012

Reviews in the Neurosciences

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For the past 40 years Parkinson's disease (PD) has been intrinsically associated with dopamine (DA) deficiency of the nigrostriatal DA system. One of the fundamental strengths of this theoretical approach is based on a presumed relationship between the degree of DA deficiency and the severity of motor impairment in the disease and its models. However, detailed examination of a substantial number of exemplary preclinical and clinical studies reveals that any such interpretation is overoptimistic and suggests that DA deficiency may be merely an epiphenomenon of a larger process underlying this disorder. Such a conclusion is based on numerous examples of miscarriage of basic principles of good scientific practice including (i) failure to thoroughly examine the adverse effects of DA replacement, (ii) drawing of statistical inference without recognising excessive spread of measure thereby lessening the importance of outliers, (iii) confounding independent and dependent variables within the scientific paradigm, (iv) overlooking fundamental principles of modern pharmacology, (v) confusing correlation with causation in linking cause and effect and (vi) disinclination to incorporate conflicting findings thereby infringing the quintessential scientific principle of tertium quid. This review demonstrates the inherent risks and dangers in the incontrovertible defence of DA deficiency theory and serves to address the ethical problems that emerge from the clinical application of scientific findings. There is increasing interest in new directions for PD research by dimming down the current emphasis on the importance of DA deficiency and its replacement. This would provide genuine hope and a new direction for the sufferers of a most debilitating disease.

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Body weight and regulatory deficits following unilateral nigrostriatal lesions

Cited by 37 publications

References 25 publications

Feeding behavior and sensorimotor functioning in rats with unilateral medial forebrain bundle damage

Feeding behavior and sensorimotor functioning in rats with unilateral medial forebrain bundle damage

Metabolic hormones, dopamine circuits, and feeding

Breaking away from dopamine deficiency: an essential new direction for Parkinson’s disease

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