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Effects of hypomagnesia on transmitter actions in neocortical slices
Author(s) -
ElBeheiry H.,
Puil E.
Publication year - 1990
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.1476-5381.1990.tb14197.x
Subject(s) - tetrodotoxin , acetylcholine , glutamate receptor , slice preparation , depolarization , neuroscience , chemistry , nmda receptor , extracellular , cortical spreading depression , hyperpolarization (physics) , biophysics , bursting , neurotransmitter , electrophysiology , medicine , endocrinology , biology , biochemistry , receptor , central nervous system , organic chemistry , migraine , nuclear magnetic resonance spectroscopy
1 The effects of hypomagnesia on the neuronal responses induced by iontophoretically applied acetylcholine, glutamate, N‐methylaspartate (NMDA) and γ‐aminobutyric acid (GABA) were investigated using intracellular recording techniques in in vitro slices of sensorimotor cortex (guinea‐pigs). 2 Perfusion with Mg‐free media, with or without tetrodotoxin (TTX), induced a small hyperpolarization (∼4mV) and a small decrease (∼10%) in the input resistance of neurones. During TTX‐blockade of Na‐spike genesis, spontaneous depolarizing waves of low frequencies were observed in neurones of slices under Mg‐free conditions. 3 The effects of acetylcholine and to a lesser extent, GABA actions, were depressed in a dose‐dependent, reversible manner by decreases in the [Mg 2+ ] of the perfusing media. In neurones of slices that had been incubated in Mg‐free artificial cerebrospinal fluid to ensure a maximal depletion, the responses to these transmitters were potentiated by each sequentially administered increase in extracellular [Mg 2+ ]. The actions of NMDA were potentiated during perfusion of Mg‐free media. However, the responses to glutamate, which may activate receptors for NMDA, were either depressed or unchanged under these conditions. 4 A regulatory role for external Mg cations in the responses of neocortical neurones to the transmitter substances, acetylcholine and GABA, can be inferred from these investigations which simulate hypomagnesemia. The dose‐dependent depression of GABA actions by low extracellular [Mg 2+ ] additionally provides a plausible mechanism that may contribute to the neuronal hyperexcitability that is observed during conditions of hypomagnesemia.