ISSN:
1471-4159
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Abstract: We sought to establish whether the endogenous opiate-receptor agonist Met-enkephalin (m-ENK) selectively modulates the release of endogenous tyrosine (Tyr) from brain slices prepared from the corpus striatum (CS). Amino acids (AAs) released from slices of CS and, for comparison, cerebral cortex (Cx) were measured by HPLC. Incubation of slices with m-ENK (1-10 μM) increased the basal release of Tyr (up to 293% of control) from CS, but not Cx, whereas other nonneurotransmitter AAs, phenylal-anine (Phe) and valine (Val), were unchanged. The release of the putative neurotransmitter AAs glutamate (Glu), tau-rine (Tau), and glycine (Gly) were similarly increased by 50–150% with m-ENK in slices of CS, but not Cx. The enhanced release of AAs by m-ENK was prevented by removal of extracellular Ca2+ or by preincubation with the opiate receptor antagonist naloxone. Neuronal depolarization by potassium (5–55 mM) in the presence of Ca2+ did not affect the release of Tyr, whereas release of neurotransmitter AAs such as γ-aminobutyric acid (GABA) were markedly increased. The increase in basal Tyr release by m-ENK was not the result of a decreased uptake of Tyr. Relative to slices, the basal release of Tyr, Phe, and Val from a synaptosomal (P2) preparation of CS was small (8–51%) compared to that of GABA, Gly, Glu, and Tau (49–123%). Nonetheless, m-ENK (10 μM) markedly increased the release of Tyr (to 833%), but not Glu, Gly, and Tau from the P2 fraction. Other neuropeptides including cholecystokinin octapeptide (CCK-8), thyrotropin-releasing hormone (TRH), and vaso-active intestinal peptide (VIP) facilitated the release of Tyr from brain slices in a regionally specific pattern. We conclude that: (1) Tyr is released from nerve terminal-enriched preparations of CS, but not Cx, by m-ENK via an opiate receptor-mediated, Ca2+-dependent process with regional selectivity; (2) neuronal depolarization alone, however, does not affect the release of Tyr; (3) CCK-8, TRH, and VIP also increase Tyr release with regional specificity, suggesting that receptors for other neuropeptides may also modulate Tyr release. The specific neuronal source and functional role of Tyr released from elements of CS via activation of opiate receptors remain to be elucidated.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1471-4159.1987.tb05705.x
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