Separate metabolic pathways for Leu-enkephalin and Met-enkephalin-Arg6-Phe7 degradation by rat striatal synaptosomal membranes

@article{Benuck1982SeparateMP,
  title={Separate metabolic pathways for Leu-enkephalin and Met-enkephalin-Arg6-Phe7 degradation by rat striatal synaptosomal membranes},
  author={Myron Benuck and Martin J Berg and Neville Marks},
  journal={Neurochemistry International},
  year={1982},
  volume={4},
  pages={389-396}
}

Membrane-bound enzymes and their role in processing of the dynorphins and of the proenkephalin octapeptide Met-enkephalin-Arg-Gly-Leu

Dynorphins 1–13 and 1–17 may serve as precursors for the widely distributed CNS neuropeptide dynorphin 1–8 since they were cleaved by a separate SPM endopeptidase insensitive to phosphoramidon.

Formation of desTyr dynorphins 5–17 by a purified cytosolic aminopeptidase of rat brain

Rapid degradation of small peptides is consistent with a paracrine (neurotransmitter) role as compared to the postulated precursor or exocrine roles for the dynorphins with 13 residues or more.

The broad substrate specificity of human angiotensin I converting enzyme.

Recent, mostly in vitro studies with purified ACE indicate that ACE also cleaves peptides by other than peptidyldipeptidase action, and surprisingly cleaves the N-terminal tripeptide greater than Glu1-His2-Trp3 from LHRH.

5-Hydroxytryptamine2 and 5-hydroxytryptamine3 receptors mediate serotonin-induced short-circuit current in pig jejunum

The results suggest that 5-hydroxytryptamine elicits an increase in short-circuit current by activating epithelial and submucosal 5- Hydroxytryptamines2 and 5-Hydroxytiptamine3 receptor subtypes.

Angiotensin-converting enzyme governs endogenous opioid signaling and synaptic plasticity in nucleus accumbens

The results raise the enticing prospect that central ACE inhibition can boost endogenous opioid signaling for clinical benefit, while mitigating risk of addiction, and reduce the conditioned place preference caused by fentanyl administration.

Regulation of 5-HT Release in the CNS by Presynaptic 5-HT Autoreceptors and by 5-HT Heteroreceptors

The amount of serotonin (5-hydroxytryptamine; 5-HT) released from the varicosities of the serotoninergic axon terminals in response to invading action potentials at a given frequency is by no means

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