Abstract
Huntington’s disease (HD) is an inherited, neurodegenerative disorder that results from the degeneration of striatal neurons, mainly GABAergic neurons. The study of neurochemical activity has provided reliable markers to explain motor disorders. To treat neurodegenerative diseases, stem cell transplants with bone marrow (BM) have been performed for several decades. In this work we determine the effect of mononuclear bone marrow cell (mBMC) transplantation on the rotational behavior and neurochemical activity in a model of Huntington’s disease in rats. Four experimental groups were organized: Group I: Control animals (n = 5); Group II: Lesion with quinolinic acid (QA) in the striatum (n = 5); Group III: Lesion with QA and transplant with mBMC (n = 5); Group IV: Lesion with QA and transplant with culture medium (Dulbecco’s modified Eagle’s medium (DMEM) injection) (n = 5). The rotational activity induced by D-amphetamine was evaluated and the concentration of the neurotransmitter amino acids (glutamate and GABA) was studied. The striatal cell transplantation decreases the rotations induced by D-amphetamine (p < 0.04, Wilcoxon matched pairs test) and improves the changes produced in the levels of neurotransmitters studied. This work suggests that the loss of GABAergic neurons in the brain of rats lesioned with AQ produces behavioral and neurochemical alterations that can be reversed with the use of bone marrow mononuclear cell transplants.
Highlights
Huntington’s disease (HD) has been associated with a degeneration of striatal cells, mainly death of medium spiny GABAergic projection neurons within the caudate nucleus and putamen. the most pronounced pathology is observed in the basal ganglia, cell death occurs early in the cerebral cortex [1]
The most pronounced pathology is observed in the basal ganglia, cell death occurs early in the cerebral cortex [1]
The injection of quinolinic acid into the striatum is used as a theoretical model of HD [2]
Summary
Huntington’s disease (HD) has been associated with a degeneration of striatal cells, mainly death of medium spiny GABAergic projection neurons within the caudate nucleus and putamen. The most pronounced pathology is observed in the basal ganglia, cell death occurs early in the cerebral cortex [1]. The experimental models play essential roles in the understanding of disease. Sci. 2018, 8, 87 mechanisms, progression, and drug efficacy testing. The injection of quinolinic acid into the striatum is used as a theoretical model of HD [2]. Quinolinic acid (QA) produces loss of GABAergic neurons; in this way there is an imbalance between the healthy and damaged striatum in response to the action of an intact dopaminergic system, which produces an asymmetric motor response to the action of a dopaminergic agonist, D-amphetamine
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