Premium
Inhibitory actions of opioid compounds on calcium fluxes and neurotransmitter release from mammalian cerebral cortical slices
Author(s) -
Bradford H.F.,
Crowder J.M.,
White E.J.
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb09474.x
Subject(s) - (+) naloxone , chemistry , opioid , glutamate receptor , pharmacology , inhibitory postsynaptic potential , neurotransmitter , opioid receptor , receptor , agonist , enkephalin , medicine , endocrinology , biochemistry , biology
1 The effects of opioid agonists on veratrine‐stimulated Ca 2+ influx and amino acid neurotransmitter release in rat cerebrocortical brain slices were studied. Inhibitory effects were seen on both of these parameters with all of the opioid agonists used. 2 None of the drugs used affected basal 45 Ca 2+ uptake, basal K + content or basal amino acid release from the slices. 3 At high concentrations (100 μM) fentanyl, tifluadom, U50,488H, butorphanol and bremazocine greatly inhibited the depolarization of the slices by veratrine as determined by the reduced release of K + . 4 The opioid receptor subtypes at which the drugs were acting were characterized by the antagonistic effects of naloxone and WIN44441‐3. 5 The opioid‐induced inhibition of stimulated Ca 2+ uptake and amino acid release were not antagonized by WIN44441‐2, the inactive enantiomer of WIN44441‐3. 6 It is concluded that opioid agonists acting through μ‐ and k‐receptors and probably through δ‐ and s̀‐receptors, have an inhibitory effect on Ca 2+ uptake into cerebrocortical brain slices and the subsequent release of aspartate, glutamate and γ‐aminobutyric acid (GABA).