The neurological basis of motor asymmetry following unilateral nigrostriatal lesions in the rat: the effect of secondary superior colliculus lesions.
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Biomedical subjects
Publications and source records attributed to A R Crossman.
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The efferent projections of the nucleus accumbens have been examined in the rat. This has been achieved by mapping the distribution of degenerating axons and terminals following the placement of small electrolytic lesions within the accumbens. Quantitatively, the majority of accumbens efferent fibres appear to terminate in the diencephalon, while there are also projections to cortical and brain stem structures. The evidence suggests that the nucleus accumbens sends efferent fibres to the cingulum, lateral hypothalamus, globus pallidus, thalamus (including the reuniens, gelatinosus, parataenial, medial and anteromedial nuclei) and the substantia nigra.
The role of the motor cortex in the mediation of asymmetric movement after unilateral 6-hydroxydopamine (6-OHDA) brain lesions has been examined in the rat. The effect of unilateral and bilateral sensorimotor decortication upon spontaneous and drug (apomorphine and amphetamine)-induced motor asymmetry has been studied following unilateral injection of 6-OHDA into the lateral hypothalamus. Both bilateral decortication and unilateral decortication on the side of the 6-OHDA lesion caused a transient reversal of the spontaneous motor asymmetry normally seen in 6-OHDA lesioned animals. Neither unilateral nor bilateral sensorimotor decortication abolished drug-induced turning behaviour. It is postulated that subcortical basal ganglia efferent pathways may be involved in the mediation of motor asymmetry after unilateral 6-OHDA lesions of the nigrostriatal dopaminergic projection.
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Neurones in the substantia nigra of the rat, anaesthetized with urethane, are inhibited both by electrical stimulation of the ipsilateral caudate nucleus and by iontophoretically applied gamma-aminobutyric acid (GABA). Iontophoretically applied picrotoxin reversibly blocks both of these inhibitory responses. These results are consistent with the hypothesis that GABA is the transmitter released by the inhibitory striato-nigral pathway.
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Post-mortem tissue was obtained from subjects with Parkinson's disease (PD), Alzheimer's disease (AD) and age-matched controls. Iron levels were measured from various sites of the basal ganglia and neocortex using atomic absorption spectrophotometry. The results indicate that iron levels are increased in the substantia nigra and the lateral segment of the globus pallidus of parkinsonian tissue. In contrast, the medial segment of the globus pallidus shows reduced iron levels in AD when compared to age-matched controls. No significant alterations of iron concentration were detected in AD in any region. These results are discussed in terms of the role of iron in the basal ganglia, mechanisms of abnormal deposition and possible neurotoxicity in PD.