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Presynaptic α 2 Adrenoceptors Inhibit Glutamate Release from Rat Spinal Cord Synaptosomes
Author(s) -
Kamisaki Yoshinori,
Hamada Toshihiro,
Maeda Kazuhisa,
Ishimura Masahiko,
Itoh Tadao
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03180.x
Subject(s) - rauwolscine , idazoxan , yohimbine , glutamate receptor , chemistry , medicine , endocrinology , neurotransmitter , spinal cord , synaptosome , nociception , veratridine , biology , central nervous system , neuroscience , biochemistry , antagonist , receptor , prazosin , sodium , organic chemistry , sodium channel
The presynaptic regulation of amino acid release from nerve terminals was investigated using synaptosomes prepared from the rat spinal cord. The basal releases of endogenous glutamate (Glu), aspartate (Asp), and γ‐amino‐butyric acid (GABA) were 34.6, 21.5, and 10.0 pmol/min/mg of protein, respectively. Exposure to a depolarizing concentration of KCl (30 m M ) evoked 2.7‐, 1.5‐, and 2.9‐fold increases in Glu, Asp, and GABA release, respectively. Clonidine reduced the K + ‐evoked overflow of Glu to 56% of the control overflow with a potency (IC 50 ) of 17 n M , but it did not affect K + ‐evoked overflow of Asp, GABA, and their basal releases. Similarly, noradrenaline inhibited the K + ‐evoked overflow of Glu, although phenylephrine and isoproterenol showed no effect. The inhibitory effect of clonidine was counteracted by α 2 ‐adrenoceptor antagonists, rauwolscine, yohimbine, and idazoxan, regardless of the imidazoline structures. Because Glu is considered a neurotransmitter of primary afferents that transmit both nociceptive and nonnociceptive stimuli in the spinal cord, these data suggest that part of Glu release may be regulated by the noradrenergic system through α 2 adrenoceptors localized on the primary afferent terminals.