Slow synchronized bursts of inhibitory postsynaptic currents (0.1–0.3 Hz) by cholinergic stimulation in the rat frontal cortex in vitro

Neuroscience ◽  
2001 ◽  
Vol 107 (4) ◽  
pp. 551-560 ◽  
Author(s):  
S Kondo ◽  
Y Kawaguchi
1998 ◽  
Vol 80 (2) ◽  
pp. 621-627 ◽  
Author(s):  
Zhiguo Chu ◽  
John J. Hablitz

Chu, Zhiguo and John J. Hablitz. Activation of group I mGluRs increases spontaneous IPSC frequency in rat frontal cortex. J. Neurophysiol. 80: 621–627, 1998. The effect of metabotropic glutamate receptor (mGluR) activation on inhibitory synaptic transmission was examined by using whole cell patch-clamp recordings. Spontaneous (s) and miniature (m) inhibitory postsynaptic currents (IPSCs) were recorded from visually identified layer II/III pyramidal neurons in rat neocortex in vitro. Excitatory postsynaptic currents (EPSCs) were blocked by using bath application of 20 μM d(−)2-amino-5-phosphonovaleric acid and 10 μM 6-cyano-7-nitroquinoxaline-2,3-dione. In the presence of 1 S,3 R-1-aminocyclopentane-1,3-dicarboxylic acid (30–100 μM), l-quisqualate (5 μM), and the group I selective mGluR agonist ( S)-3,5-dihydroxyphenylglycine (100 μM), the frequency of sIPSCs was increased. Decay kinetics of sIPSCs were unaffected. No enhancement of mIPSCs was observed. Bath application of group II (2 S,3 S,4 S-α-carboxycyclopropyl-glycine; 5 μM) and group III selective mGluR agonists (l-2-amino-4-phosphonobutyric acid; 100 μM) had no detectable effects on the frequency or amplitude of sIPSCs. These findings indicate that activation of group I mGluRs (mGluR1 and/or mGluR5) enhances γ-aminobutyric acid–mediated synaptic inhibition in layer II/III pyramidal neurons in neocortex. The lack of effect on mIPSCs suggests a presynaptic action via excitation of inhibitory interneurons.


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