Calcitriol protects against reductions in striatal serotonin in rats treated with neurotoxic doses of methamphetamine.

The present experiments were designed to examine the ability of calcitriol to protect against methamphetamine (METH)-induced reductions in striatal serotonin (5-HT) release and content. Male Fischer-344 rats were administered vehicle or calcitriol (0.3, 1.

Reduced ability of calcitriol to promote augmented dopamine release in the lesioned striatum of aged rats.

Parkinson's disease (PD) is a progressive and debilitating neurodegenerative disorder that affects over one million people in the United States. Previous studies, carried out in young adult rats, have shown that calcitriol, the active metabolite of vitamin D, can be neuroprotective in 6-hydroxydopamine (6-OHDA) models of PD. However, as PD usually affects older individuals, the ability of calcitriol to promote dopaminergic recovery was examined in lesioned young adult (4 month old), middle-aged (14 month old) and aged (22 month old) rats.

Calcitriol promotes augmented dopamine release in the lesioned striatum of 6-hydroxydopamine treated rats.

Current therapies for Parkinson's disease (PD) offer symptomatic relief but do not provide a cure or slow the disease process. Treatments that could halt progression of the disease or help restore function to damaged neurons would be of substantial benefit. Calcitriol, the active metabolite of vitamin D, has been shown to have significant effects on the brain.

Evoked dopamine overflow is augmented in the striatum of calcitriol treated rats.

Calcitriol, the active metabolite of vitamin D, has been shown to have significant effects on the brain. These actions include reducing the severity of some central nervous system lesions, possibly by upregulating trophic factors such as glial cell line-derived neurotrophic factor (GDNF). GDNF has substantial effects on the nigrostriatal dopamine (DA) system of young adult, aged and lesioned animals.

Neurturin protects against 6-hydroxydopamine-induced reductions in evoked dopamine overflow in rat striatum.

Neurturin (NTN), a member of the glial cell line-derived neurotrophic factor (GDNF) family, has substantial effects on normal and lesioned nigrostriatal dopamine systems. However, its ability to protect against toxin-induced loss of striatal dopamine release has not been previously reported. The goal of the present study was to determine if NTN could protect against 6-hydroxydopamine (6-OHDA)-induced reductions in striatal dopamine overflow and tissue levels of dopamine and to compare the effects of NTN with those of GDNF.

Neurturin effects on nigrostriatal dopamine release and content: comparison with GDNF.

Neurturin (NTN) is a member of the glial cell line-derived neurotrophic factor (GDNF) family; and, while GDNF has been shown to increase dopamine (DA) release in normal animals, the ability of NTN to alter DA release has not been previously reported. The purpose of the present study was to determine if NTN could alter striatal DA release, and to compare the effects of NTN to GDNF. Male Fischer-344 rats were given a single injection of vehicle or 5 microg NTN or GDNF into the right substantia nigra.

Strain difference in the up-regulation of FGF-2 protein following a neurotoxic lesion of the nigrostriatal pathway.

Lesions of the nigrostriatal pathway are known to induce a compensatory up-regulation of various neurotrophic factors. In this study we examined protein content of basic fibroblast growth factor (FGF-2) in tissue samples taken from the ventral midbrain and striatum at two different time points following a neurotoxic lesion of the nigrostriatal pathway in two different rat strains, the outbred Sprague-Dawley (SD) and inbred F344 9 Brown Norway F1 hybrid (F344BNF1). Despite both rat strains having comparable lesions of the nigrostriatal pathway, we observed a difference in the temporal up-regulation of FGF-2 in ventral midbrain samples taken from the side ipsilateral to the lesion.

Protection by GDNF and other trophic factors against the dopamine-depleting effects of neurotoxic doses of methamphetamine.

Repeated methamphetamine (METH) administration to animals can result in long-lasting decreases in striatal dopamine (DA) content. It has previously been shown that glial cell line-derived neurotrophic factor (GDNF) can reduce the DA-depleting effects of neurotoxic doses of METH. However, there are several other trophic factors that are protective against dopaminergic toxins.

Calcitriol protects against the dopamine- and serotonin-depleting effects of neurotoxic doses of methamphetamine.

Repeated methamphetamine (METH) administration to animals can result in long-lasting decreases in brain dopamine (DA) and serotonin (5-HT) content. Calcitriol, the active metabolite of vitamin D, has potent effects on brain cells, both in vitro and in vivo, including the ability to upregulate trophic factors and protect against various lesions. The present experiments were designed to examine the ability of calcitriol to protect against METH-induced reductions in striatal and nucleus accumbens levels of DA and 5-HT.

Reductions in spontaneous locomotor activity in aged male, but not female, rats in a model of early Parkinson's disease.

The excessive loss of dopamine (DA) neurons that occurs with Parkinson's disease is usually confined to older individuals. While 6-hydroxydopamine (6-OHDA) is often used in animal models of DA neuron degeneration, there have been relatively few studies that have examined the effects of 6-OHDA in older animals. In the present study, we compared the effects of a bilateral, partial lesion with 6-OHDA in young (4 months), middle-aged (14 months), and aged (24 months) Fischer-344 rats of both sexes.

HIV-1 protein Tat potentiation of methamphetamine-induced decreases in evoked overflow of dopamine in the striatum of the rat.

HIV-1 infection of the brain can lead to the development of clinical syndromes reminiscent of Parkinson's disease, suggesting that HIV infection may damage nigrostriatal dopamine (DA) neurons. Although the responsible mechanisms have not been well defined, neurotoxic viral proteins, such as Tat, released from infected cells may be involved. Drug abuse is a major risk factor for contracting HIV infection.