Cysteamine effects on somatostatin, catecholamines, pineal NAT and melatonin in rats

Susan M. Webb; Thomas H. Champney; Richard W. Steger; Mary K. Vaughan; Russel J. Reiter

doi:10.1016/0361-9230(86)90051-1

Cysteamine effects on somatostatin, catecholamines, pineal NAT and melatonin in rats

Susan M. Webb, Thomas H. Champney, Richard W. Steger, Mary K. Vaughan, Russel J. Reiter

Cell Systems & Anatomy

Research output: Contribution to journal › Article

6 Scopus citations

Abstract

The thiol reagent cysteamine was administered to adult male rats with the aim of investigating its effect on different neural and pineal components. As expected, immunoreactive somatostatin decreased in the median eminence (ME) (p < 0.05) and gastric antrum (p < 0.05) after cysteamine; however, no significant change was observed in the pineal IRS content after drug treatment. A decrease in norepinephrine was observed in the ME (p < 0.001), hypothalamus (p < 0.001) and pineal gland (p < 0.05), together with a rise in ME (p < 0.005) and hypothalamic dopamine (p < 0.005) content; these results are consistent with a dopamine-beta-hydroxylase inhibiting effect of cysteamine. No effect was observed on hypothalamic serotonin and 5-hydroxyindole-acetic acid content. Pineal N-acetyltransferase (NAT) activity was significantly higher (p < 0.05) after cysteamine than after saline, but no statistically significant effect was observed on pineal melatonin content. The mechanism involved in the NAT rise is presumably not related to the known stimulatory effect of norepinephrine, which fell after cysteamine. It is suggested that cysteamine may act at an intracellular level, inhibiting NAT degradation, an effect demonstrated in vitro and thought to be related to a thiol:disulfide exchange mechanism.

Original language	English (US)
Pages (from-to)	315-320
Number of pages	6
Journal	Brain Research Bulletin
Volume	16
Issue number	3
DOIs	https://doi.org/10.1016/0361-9230(86)90051-1
State	Published - Mar 1986

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Keywords

Catecholamines
Cysteamine
Melatonin
Pineal NAT
Rats
Somatostatin
Thiol:disulfide exchange

ASJC Scopus subject areas

Neuroscience(all)

Cite this

Webb, S. M., Champney, T. H., Steger, R. W., Vaughan, M. K., & Reiter, R. J. (1986). Cysteamine effects on somatostatin, catecholamines, pineal NAT and melatonin in rats. Brain Research Bulletin, 16(3), 315-320. https://doi.org/10.1016/0361-9230(86)90051-1

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abstract = "The thiol reagent cysteamine was administered to adult male rats with the aim of investigating its effect on different neural and pineal components. As expected, immunoreactive somatostatin decreased in the median eminence (ME) (p < 0.05) and gastric antrum (p < 0.05) after cysteamine; however, no significant change was observed in the pineal IRS content after drug treatment. A decrease in norepinephrine was observed in the ME (p < 0.001), hypothalamus (p < 0.001) and pineal gland (p < 0.05), together with a rise in ME (p < 0.005) and hypothalamic dopamine (p < 0.005) content; these results are consistent with a dopamine-beta-hydroxylase inhibiting effect of cysteamine. No effect was observed on hypothalamic serotonin and 5-hydroxyindole-acetic acid content. Pineal N-acetyltransferase (NAT) activity was significantly higher (p < 0.05) after cysteamine than after saline, but no statistically significant effect was observed on pineal melatonin content. The mechanism involved in the NAT rise is presumably not related to the known stimulatory effect of norepinephrine, which fell after cysteamine. It is suggested that cysteamine may act at an intracellular level, inhibiting NAT degradation, an effect demonstrated in vitro and thought to be related to a thiol:disulfide exchange mechanism.",

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AB - The thiol reagent cysteamine was administered to adult male rats with the aim of investigating its effect on different neural and pineal components. As expected, immunoreactive somatostatin decreased in the median eminence (ME) (p < 0.05) and gastric antrum (p < 0.05) after cysteamine; however, no significant change was observed in the pineal IRS content after drug treatment. A decrease in norepinephrine was observed in the ME (p < 0.001), hypothalamus (p < 0.001) and pineal gland (p < 0.05), together with a rise in ME (p < 0.005) and hypothalamic dopamine (p < 0.005) content; these results are consistent with a dopamine-beta-hydroxylase inhibiting effect of cysteamine. No effect was observed on hypothalamic serotonin and 5-hydroxyindole-acetic acid content. Pineal N-acetyltransferase (NAT) activity was significantly higher (p < 0.05) after cysteamine than after saline, but no statistically significant effect was observed on pineal melatonin content. The mechanism involved in the NAT rise is presumably not related to the known stimulatory effect of norepinephrine, which fell after cysteamine. It is suggested that cysteamine may act at an intracellular level, inhibiting NAT degradation, an effect demonstrated in vitro and thought to be related to a thiol:disulfide exchange mechanism.

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10.1016/0361-9230(86)90051-1