2009
DOI: 10.1016/j.brainres.2009.07.084
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Alpha-methyltyrosine inhibits formation of reactive oxygen species and diminishes apoptosis in PC12 cells

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Cited by 7 publications
(6 citation statements)
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“…Because central, presynaptic alpha-2 adrenergic receptors inhibit catecholamine secretion, we first reasoned that there would be a TBI-induced downregulation of the Adra2c gene, which regulates basal sympathetic norepinephrine release, 17 and ongoing catecholamine secretion necessitates an increase in catecholamine synthesis which is toxic to neurons. 18 We also postulated that similar to what was reported following other types of physiological or psychological stress, there would be a TBI-induced upregulation of the sodium chloride cotransporter gene 1 (Nkcc1) and downregulation of the potassium chloride cotransporter gene (Kcc2). A shift in the balance of intraneuronal chloride concentrations mediated by dysregulation of Nkcc1 and Kcc2 transport following injury has been found to shift hyperpolarizing inhibitory γ-amino butyric acid (GABA A ) neurons to depolarizing excitatory neurons.…”
mentioning
confidence: 68%
See 1 more Smart Citation
“…Because central, presynaptic alpha-2 adrenergic receptors inhibit catecholamine secretion, we first reasoned that there would be a TBI-induced downregulation of the Adra2c gene, which regulates basal sympathetic norepinephrine release, 17 and ongoing catecholamine secretion necessitates an increase in catecholamine synthesis which is toxic to neurons. 18 We also postulated that similar to what was reported following other types of physiological or psychological stress, there would be a TBI-induced upregulation of the sodium chloride cotransporter gene 1 (Nkcc1) and downregulation of the potassium chloride cotransporter gene (Kcc2). A shift in the balance of intraneuronal chloride concentrations mediated by dysregulation of Nkcc1 and Kcc2 transport following injury has been found to shift hyperpolarizing inhibitory γ-amino butyric acid (GABA A ) neurons to depolarizing excitatory neurons.…”
mentioning
confidence: 68%
“…We also investigated the cellular mechanisms by which αMT-dependent inhibition of catecholamine synthesis may prove salutary following TBI. Because central, presynaptic alpha-2 adrenergic receptors inhibit catecholamine secretion, we first reasoned that there would be a TBI-induced downregulation of the Adra2c gene, which regulates basal sympathetic norepinephrine release, 17 and ongoing catecholamine secretion necessitates an increase in catecholamine synthesis which is toxic to neurons 18 . We also postulated that similar to what was reported following other types of physiological or psychological stress, there would be a TBI-induced upregulation of the sodium chloride cotransporter gene 1 (Nkcc1) and downregulation of the potassium chloride cotransporter gene (Kcc2).…”
mentioning
confidence: 99%
“…Elevated levels of circulating corticosteriods found to mediate the critical role of IL-1β in chronic stress-induced depression and suppressed neurogenesis in mice [10]. The hypercortisolism and excessive inflammatory responses have been also reported to contribute to neuronal apoptosis and death [11,12].…”
Section: Introductionmentioning
confidence: 99%
“…Oxidative stress is probably one of the mechanisms involved in neuronal damage induced by I/R. The brain contains many antioxidant molecules that prevent and/or inhibit harmful free radical reactions (Woodman et al, 2009). Kidney I/R injury often cause damage to remote organs.…”
Section: Introductionmentioning
confidence: 99%