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Inhibition of spontaneous EPSCs and IPSCs by presynaptic GABA B receptors on rat supraoptic magnocellular neurons
Author(s) -
Kabashima Narutoshi,
Shibuya Izumi,
Ibrahim Nurhadi,
Ueta Yoichi,
Yamashita Hiroshi
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.113bf.x
Subject(s) - picrotoxin , neuroscience , muscimol , chemistry , supraoptic nucleus , excitatory postsynaptic potential , gabaa receptor , glutamatergic , agonist , magnocellular cell , glutamate receptor , gaba receptor antagonist , bicuculline , receptor , biology , inhibitory postsynaptic potential , oxytocin , biochemistry
1 The function of presynaptic GABA receptors in the regulation of transmitter release in supraoptic nucleus (SON) magnocellular neurons was investigated by recording spontaneous postsynaptic currents from rat magnocellular SON neurons in a slice preparation (150μM thick, 1.8 mm in diameter) using the whole‐cell patch‐clamp technique. 2 Both the spontaneous EPSCs and IPSCs were TTX resistant. The EPSCs were abolished by 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX), whereas the IPSCs were abolished by picrotoxin, suggesting that the EPSCs and IPSCs are synaptic inputs from glutamatergic and GABAergic neurons, respectively. 3 The selective GABA B agonist, baclofen, reduced the frequency of both the EPSCs and IPSCs without affecting the amplitude. The time constant of the decay phase of both the EPSCs and IPSCs remained unchanged after baclofen application. 4 The reduction of the frequency of the synaptic currents by baclofen was dose dependent (10 nM to 100 μ m ) and the EC 50 values were 5.8 and 8.5 μ m for the EPSCs and IPSCs, respectively. 5 The effect of baclofen (10μM) was antagonized by the selective GABA B antagonist, 2‐hydroxy‐saclofen (2OH‐saclofen), at 300 μ m . 6 When given alone, 2OH‐saclofen (100 μ m ) increased the frequency of both the EPSCs and IPSCs without affecting their amplitude, suggesting that endogenously released GABA in the slice acts on presynaptic GABA B receptors. 7 The GABA A agonist, muscimol, reduced the frequency of EPSCs, and picrotoxin increased the frequency of the EPSCs, suggesting that GABA A receptors also participate in the presynaptic inhibition of glutamate release. 8 Taken together, these data suggest that GABA B receptors are present on the presynaptic terminals of both GABA and glutamate neurons in the SON, and that these presynaptic GABA B receptors play an important role in the regulation of the neuronal activity in SON magnocellular neurons.