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The proenkephalin A fragment, peptide E: central processing and CNS activity in vivo
European Journal of Pharmacology
|May 8, 1985
Summary
Peptide E, a proenkephalin A derivative, significantly impacts the central nervous system (CNS). It delays gastrointestinal transit and inhibits the micturition reflex, likely through mu-opioid receptor activation.
Area of Science:
- Neuroscience
- Gastroenterology
- Pharmacology
Background:
- Proenkephalin A is a precursor to various opioid peptides.
- Peptide E is a derivative of proenkephalin A with potential biological activity.
- The central nervous system (CNS) regulates gastrointestinal and urinary functions.
Purpose of the Study:
- To investigate the effects of peptide E and its potential metabolites on CNS-mediated functions.
- To compare the potency of peptide E and its fragments (BAM22P, BAM12P, [Met5]enkephalin).
- To elucidate the metabolic fate of peptide E in the brain.
Main Methods:
- Administration of peptides intracerebroventricularly (i.c.v.) in rodents.
- Assessment of gastrointestinal transit and micturition reflex.
- In vitro metabolism studies using mouse brain homogenates and High-Performance Liquid Chromatography (HPLC).
Main Results:
- Intracerebroventricular administration of peptide E delayed gastrointestinal transit in mice and inhibited the micturition reflex in rats.
- Peptide E and BAM22P exhibited the greatest potency among the tested peptides.
- In vitro studies showed peptide E binds avidly to brain homogenates, with minimal formation of known metabolites (only 8% over 40 min).
Conclusions:
- Peptide E, not its known metabolites, is primarily responsible for initiating CNS-mediated effects.
- The observed effects of peptide E are likely mediated through activation of mu-opioid receptors.
- Peptide E represents a significant endogenous modulator of gastrointestinal and urinary functions via CNS pathways.