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ANTAGONISM BY SOME ANTIHISTAMINES OF THE AMINO ACID‐EVOKED RESPONSES RECORDED FROM THE LOBSTER MUSCLE FIBRE AND THE FROG SPINAL CORD
Author(s) -
CONSTANTI A.,
NISTRI A.
Publication year - 1976
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.1476-5381.1976.tb08627.x
Subject(s) - glutamate receptor , chemistry , tetrodotoxin , hyperpolarization (physics) , biophysics , histamine , pharmacology , membrane potential , reversal potential , biology , biochemistry , patch clamp , receptor , stereochemistry , nuclear magnetic resonance spectroscopy
1 The effects of some antihistamines on the lobster muscle fibre and the frog spinal cord were investigated using intracellular and extracellular recordings, respectively. 2 On lobster muscle, histamine H 1 ‐blockers reversibly antagonized responses to bath‐applied glutamate, aspartate and quisqualate but not responses to γ‐aminobutyric acid (GABA). Iontophoretic glutamate potentials were also reduced. Histamine (up to 1 m m ) had no effect on this preparation. 3 The H 1 ‐antagonists produced a small increase in muscle membrane conductance and a slight hyperpolarization. These effects were largely unchanged in a low Cl − bathing solution. Procaine (1 m m ) decreased membrane conductance and did not affect responses to GABA or glutamate. 4 The H 2 ‐antagonist burimamide blocked both glutamate and GABA‐evoked responses on the lobster muscle without affecting resting potential or conductance. 5 In the frog cord, bath‐applied histamine produced ventral root depolarizations and dorsal root hyperpolarizations (sometimes biphasic responses). These effects were reduced by tetrodotoxin (TTX) but not by antazoline (H 1 ‐blocker) or burimamide; the latter reversibly antagonized responses to both glutamate and GABA on TTX‐treated cords while antazoline was ineffective. 6 It is suggested that antihistamines can act as non‐specific amino acid antagonists by interacting at the level of the receptor‐coupled ionophores.

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