Exer 5c

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Exer 5c

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A major interest in our lab has been to investigate how exercise modulates basal ganglia function and modifies disease progression.

Dopamine DA depletion leads to loss of dendritic spines within the caudate nucleus and putamen striatum in PD and its animal models and contributes to motor impairments.

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There is evidence to suggest that the DA-D2R-indirect pathway MSNs may be preferentially affected after DA-depletion with a predominate loss of dendritic spine density when compared to MSNs of the DA-D1R-direct pathway in rodents; however, others have reported that Exer 5c pathways may be affected in primates.

The purpose of this study was to investigate the effects of intensive exercise on Exer 5c spine density and arborization in MSNs of these two pathways in the MPTP mouse model of PD.

In addition, exercise increased the expression of synaptic proteins PSD and synaptophysin. Taken together these findings support the potential effect of exercise in modifying synaptic connectivity within the DA-depleted striatum and in modifying disease progression in individuals with PD. Individuals with PD Exer 5c both cognitive and motor deficits including balance instability, gait dysfunction, slowness, tremor, and rigidity.

While DA replacement therapy remains a cornerstone of treatment, its efficacy diminishes over time. Currently, there is no known cure for PD. A major interest of research in PD is to find treatments that have the capacity to modify disease progression or better prevent disease onset.

For example, epidemiological studies have suggested that intensive exercise, especially in males, over a lifetime can influence the occurrence of PD Chen et al. Over the last decade a number of investigators have demonstrated exercise to the beneficial for the treatment of PD especially for the treatment of gait and balance Petzinger et al.

In animal models of PD, exercise has been shown to have the capacity to be both neuroprotective, by preventing the loss of DA in lesion models Gerecke et al. These observations, along with ongoing basic and clinical research, are beginning to investigate the potential role of exercise in modifying disease progression in individuals with PD as well as in animal models of DA-depletion.

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Towards this goal, a major focus of our lab has been to elucidate the underlying molecular mechanisms by which exercise affects neuroplasticity including synaptic structure and function within the injured basal ganglia in neurotoxin animal models of PD. In PD and in neurotoxin animal models, the depletion of striatal DA leads to alterations in basal ganglia neurotransmission that manifest in a number of different ways.

For example, the striatopallidal indirect projection medium spiny neurons MSNs become hyperactive and are thought to underlie the onset of akinesia slowness of movement Calabresi et al. In addition, corticostriatal projections targeting striatal MSNs also display aberrant glutamatergic neurotransmission as demonstrated through electrophysiological techniques Cepeda et al.

Therefore, it is not surprising that striatal MSNs manifest these changes in neurotransmission by alterations in the dendritic spine number and dendritic arborization, the primary morphological correlates of synaptic neurotransmission.

For example, studies using Golgi staining have shown a reduction in dendritic arborization and spine density in the caudate nucleus and putamen in tissues from patients with PD McNeill et al.

Similar findings have been made in both the 6-hydroxydopamine 6-OHDA rat and the 1-methylphenyl-1,2,3,6-tetrahydropyridine MPTP nonhuman primate models of DA-depletion where spine density changes have been reported Ingham et al. The purpose of this study was to determine if intensive exercise in the form of treadmill running leads to a reversal of both dendritic spine loss and the reduction in dendritic arborization in a mouse model of DA-depletion.

This speculation is largely based on the fact that we observe exercise enhanced alterations in both glutamate and DA neurotransmission in the MPTP-lesioned mouse model Kintz et al.

Since dendritic spine density and branching are influenced by experience including environmental enrichment and exercise in several regions of the mammalian brain we were interested in knowing if exercise leads to a similar outcome Comery et al. Utilizing the MPTP mouse model of DA-depletion with either Golgi staining or biocytin labeling we examined the effects of 6 weeks of intensive treadmill running on dendritic spine density and arborization of MSNs within the dorsolateral striatum, a region responsible for motor control and a site where we have documented neuroplastic changes in response to exercise Petzinger et al.

Mice were group housed with a reverse light cycle lights off 7 a. All efforts were made to minimize animal suffering and the number of animals used to achieve statistical significance. Louis, MO at 2-hour intervals.

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Remaining mice received intraperitoneal injections of saline. HPLC analysis was conducted 5 days after lesioning, corresponding to the start of the treadmill exercise regimen, and at 42 days after lesioning, corresponding to the completion of the treadmill exercise regimen.The IL Assembler generates a portable executable (PE) file from intermediate language (IL).

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Exer 5c

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