Rapid induction of neurotrophin mRNAs in rat glial cell cultures by Semax, an adrenocorticotropic hormone analog

Шадрина, М. И.; Долотов, О. В.; Гривенников, И. А.; Slominsky, Petr; Andreeva, L. A.; Иноземцева, Л. С.; Limborska, Svetlana A.; Myasoedov, N. F.

doi:10.1016/s0304-3940(01)01994-2

Cited by 41 publications

(18 citation statements)

References 11 publications

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“…ACTH was observed to downregulate ciliary neurotropic factor mRNA levels without modifying other neurotrophins in cultured astrocytes (Kokubo et al 2002). By contrast, an analog of ACTH increased Bdnf mRNA levels in rat glial cell cultures (Shadrina et al 2001) and after cerebral ischemia (Dmitrieva et al 2010). Concordantly, we showed that MC4R activation induces expression of BDNF in cultured rat astrocytes (Caruso et al 2012), suggesting that neuroprotection by MC4R can involve neurotropic factor release.…”

Section: Mc4r and Neuroprotectionsupporting

confidence: 52%

Astrocytes: new targets of melanocortin 4 receptor actions

Caruso¹,

Carniglia²,

Durand³

et al. 2013

Journal of Molecular Endocrinology

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Astrocytes exert a wide variety of functions with paramount importance in brain physiology. After injury or infection, astrocytes become reactive and they respond by producing a variety of inflammatory mediators that help maintain brain homeostasis. Loss of astrocyte functions as well as their excessive activation can contribute to disease processes; thus, it is important to modulate reactive astrocyte response. Melanocortins are peptides with well-recognized anti-inflammatory and neuroprotective activity. Although melanocortin efficacy was shown in systemic models of inflammatory disease, mechanisms involved in their effects have not yet been fully elucidated. Central anti-inflammatory effects of melanocortins and their mechanisms are even less well known, and, in particular, the effects of melanocortins in glial cells are poorly understood. Of the five known melanocortin receptors (MCRs), only subtype 4 is present in astrocytes. MC4R has been shown to mediate melanocortin effects on energy homeostasis, reproduction, inflammation, and neuroprotection and, recently, to modulate astrocyte functions. In this review, we will describe MC4R involvement in anti-inflammatory, anorexigenic, and anti-apoptotic effects of melanocortins in the brain. We will highlight MC4R action in astrocytes and discuss their possible mechanisms of action. Melanocortin effects on astrocytes provide a new means of treating inflammation, obesity, and neurodegeneration, making them attractive targets for therapeutic interventions in the CNS.

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Section: Mc4r and Neuroprotectionsupporting

confidence: 52%

Astrocytes: new targets of melanocortin 4 receptor actions

Caruso¹,

Carniglia²,

Durand³

et al. 2013

Journal of Molecular Endocrinology

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“…Semax stimulates the synthesis of neurotrophins, e.g. NGF and BDNF [13], and hence, its neuroprotective effect can be explained by enhanced expression of antioxidant defense proteins and increased resistance of mitochondria to oxidative and "calcium" stress [11]. Further studies of the effects of semax and its analogs can include measurements of the production of free-radical compounds in neurons exposed to glutamate in parallel with these peptides.…”

Section: Resultsmentioning

confidence: 99%

“…It was shown that semax specifically binds with membranes of rat brain cells [2], but no sites binding its Pro-Gly-Pro (PGP) fragment were detected on the plasma membrane. Semax in a concentration of 100 µM 5-7-fold increased the expression of mRNA of trophic factors BDNF and NGF in primary culture of glial cells [13]. We studied the mechanisms of the neuroprotective action of semax and PGP on the cell model of glutamate neurotoxicity.…”

mentioning

confidence: 99%

Effects of semax and its Pro-Gly-Pro fragment on calcium homeostasis of neurons and their survival under conditions of glutamate toxicity

Storozhevykh¹,

Tukhbatova²,

Senilova³

et al. 2007

Bull Exp Biol Med

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Semax (100 microM) and its Pro-Gly-Pro fragment (20 and 100 microM) delayed the development of calcium dysregulation and reduction of the mitochondrial potential in cultured cerebellar granule cells under conditions of glutamate neurotoxicity. Incubation with these peptides improved neuronal survival by on average 30%. The neuroprotective effect of semax in cerebral ischemia/hypoxia can be due to improvement of mitochondrial resistance to "calcium" stress.

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“…It can be hypothesized that the normalizing effects of semax in animals with haloperidolor neurotoxin-induced damage to the cerebral dopaminergic system are mediated by different mechanisms. The effects of semax in neurotoxin-treated animals can result from its neuroprotective action [2,8], which moderates damages and restores the function of reversibly damaged dopamine-producing neurons. By contrast, the normalizing action of semax on acquisition of the conditioned reflex, which is disturbed by haloperidol, can be explained by the compensatory influences of other neurotransmitter systems.…”

Section: Resultsmentioning

confidence: 99%

“…This effect can result from the modulating effect of semax and stimulation of neurotransmitter release or can be determined by the neurotrophic effect of semax, because it increases the content of neurotrophic factors in CNS [2,8].…”

mentioning

confidence: 99%

Effects of semax against the background of dopaminergic receptor blockade with haloperidol

et al. 2006

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We studied the neurotropic effects of ACTH(4-10) analog semax against the background of dopaminergic receptors blockade with haloperidol. Intranasal administration of semax (0.05, 0.2, and 0.6 mg/kg) produced virtually no effect on disturbances of orientation and exploratory reactions and motor activity caused by intraperitoneal injection of 0.2 mg/kg haloperidol. By contrast, preliminary administration of 0.05 mg/kg semax prevented haloperidol-induced disturbances in active avoidance conditioning.

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Rapid induction of neurotrophin mRNAs in rat glial cell cultures by Semax, an adrenocorticotropic hormone analog

Cited by 41 publications

References 11 publications

Astrocytes: new targets of melanocortin 4 receptor actions

Astrocytes: new targets of melanocortin 4 receptor actions

Effects of semax and its Pro-Gly-Pro fragment on calcium homeostasis of neurons and their survival under conditions of glutamate toxicity

Effects of semax against the background of dopaminergic receptor blockade with haloperidol

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