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Brain histamine turnover enhanced by footshock
Abstract:
When footshock was given to mice at 15-s intervals for 30-120 min, there was a significant increase in the brain level of tele-methyl-histamine (t-MH), a predominant metabolite of brain histamine (HA). This footshock-induced elevation of the t-MH level also occurred in mice pretreated with pargyline but not in mice pretreated with metoprine. The footshock facilitated the HA depletion induced by a-fluoromethylhistidine. These results suggest that footshock increases the brain HA turnover.
Insights
Footshock stress significantly elevates tele-methyl-histamine (t-MH) levels in the brain, indicating increased histamine (HA) turnover. This effect is modulated by specific enzyme inhibitors, suggesting a complex regulatory mechanism.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Histamine (HA) is a neurotransmitter involved in various brain functions.
- Tele-methyl-histamine (t-MH) is a primary metabolite of histamine in the brain.
- Stress can influence neurotransmitter systems, including the histaminergic system.
Purpose of the Study:
- To investigate the effect of acute footshock stress on brain histamine turnover.
- To explore the role of specific enzymes in mediating stress-induced changes in histamine metabolism.
Main Methods:
- Mice were subjected to footshock stress at 15-s intervals for 30-120 minutes.
- Brain levels of tele-methyl-histamine (t-MH) were measured.
- Mice were pretreated with pargyline or metoprine.
- Histamine (HA) depletion was assessed after pretreatment with a-fluoromethylhistidine.
Main Results:
- Footshock significantly increased brain t-MH levels.
- Pretreatment with pargyline did not block the footshock-induced elevation of t-MH.
- Pretreatment with metoprine blocked the footshock-induced elevation of t-MH.
- Footshock enhanced histamine (HA) depletion induced by a-fluoromethylhistidine.
Conclusions:
- Footshock stress increases brain histamine turnover.
- The results suggest that MAO B may be involved in the regulation of histamine metabolism during stress.
- These findings contribute to understanding the neurochemical underpinnings of stress responses.