Characterization of delta-sleep-inducing peptide-evoked release of Met-enkephalin from brain synaptosomes in rats.
Nakamura. A A; Sakai. K K; Takahashi. Y Y; Shiomi. H H
Key Findings
- DSIP (10â»Âčâ°â10â»âčâŻM) triggers calciumâdependent release of Metâenkephalin from medullary synaptosomes.
- The release is TTXâinsensitive, indicating a direct action on nerve endings.
- Regionâspecific effects: significant release in cortex, hypothalamus, midbrain, hippocampus, and thalamus, but not in striatum.
- DSIP also increases calcium uptake in these synaptosomes, supporting the influx mechanism.
Practical Outcomes
- The study hints that DSIP might boost the brain's own opioid peptides, which could affect pain perception or mood. However, the work is limited to rat brain slices and does not provide dosing guidance or human data, so it isnât ready for direct use in selfâexperiment protocols.
Summary
In rat brain tissue, the peptide DSIP caused nerve endings to let in calcium and release the natural opioid Metâenkephalin, but only in certain brain regions. This effect was seen at very low concentrations and did not happen in the striatum.
Abstract
Delta-sleep-inducing peptide (DSIP) stimulates the release of Met-enkephalin (Met-ENK) from superfused slices of the rodent lower brainstem in vitro. In our present study, DSIP (10(-10)-10(-9) M) induced a significant release of Met-ENK from medullary synaptosomes of rats. This DSIP-evoked release of Met-ENK was Ca2+ dependent and tetrodotoxin (TTX) insensitive. Furthermore, DSIP (10(-11)-10(-9) M) significantly increased 45Ca2+ uptake in medullary synaptosomes. These results demonstrate that DSIP acts directly on the nerve endings of Met-ENK-containing neurons to release this pentapeptide by generating a Ca2+ influx into these neurons. Effects of DSIP on Met-ENK release in other discrete brain regions were also studied. Significant DSIP-evoked Met-ENK release from synaptosomes was observed in the cortex, hypothalamus, and midbrain (at concentrations of 10(-10) and 10(-9) M) and in the hippocampus and thalamus (only at 10(-9) M), but not in the striatum. In the hypothalamus, the release of Leu-enkephalin from its synaptosomes was slightly, but not significantly, enhanced by DSIP (10(-10)-10(-8) M). Our findings demonstrate that DSIP triggered a Ca2+ influx in nerve endings to induce a subsequent release of Met-ENK from neurons in only certain brain regions.
Study Information
pubmed
1991
1991-09-01T00:00:00.000Z
10.1111/j.1471-4159.1991.tb08251.x
4
58