Neuropharmacological profile of V-9-M, a putative neuropeptide derived from procholecystokinin.

(1) The present review suggests that V-9-M, a putative neuromodulator derived from pro-CCK, possesses apparent sedative actions and prevents experimental amnesia in both passive and active avoidance paradigms in rats. (2) These properties are similar to CCK-8, but some differences were noticed; (i) CCK-8 is a potent appetite inhibitor, while V-9-M does not affect food intake in fasted rats, and (ii) small doses of apomorphine cause hypomotility which is abolished by CCK-8, while V-9-M decreases the motility further. (3) More important is the fact that peripheral administration of CCK-8 produces central actions, but that of V-9-M is ineffective. (4) Although CCK-8 and V-9-M are derived from the same pro-CCK, their chemical structures are quite different, and the receptors for these two peptides are not the same. (5) CCK-8 has both central and peripheral receptors, but the presence of a peripheral receptor for V-9-M is questionable. (6) The different properties may be partially explained by this. (7) However, immunochemical studies indicated the coexistence of CCK and GABA in the cortical neurons. (8) This suggests that V-9-M may be present in the GABA neurons together with other CCK fragments. (9) There might be close interaction between V-9-M and the GABAergic system.
AuthorsS Itoh, A Takashima
JournalProgress in neurobiology (Prog Neurobiol) Vol. 34 Issue 5 Pg. 429-36 ( 1990) ISSN: 0301-0082 [Print] ENGLAND
PMID2192395 (Publication Type: Journal Article, Review)
Chemical References
  • GABA Antagonists
  • Hypnotics and Sedatives
  • Peptide Fragments
  • Protein Precursors
  • procholecystokinin
  • Cholecystokinin
  • V-9-M cholecystokinin nonapeptide
  • Animals
  • Cholecystokinin (pharmacology, physiology)
  • Drug Interactions
  • GABA Antagonists
  • Hypnotics and Sedatives
  • Memory (drug effects)
  • Peptide Fragments (pharmacology, physiology)
  • Protein Precursors
  • Rats

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