Desai M A, McBain C J, Kauer J A, Conn P J
Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322.
Neurosci Lett. 1994 Nov 7;181(1-2):78-82. doi: 10.1016/0304-3940(94)90564-9.
Previous studies suggest that activation of metabotropic glutamate receptors (mGluRs) reduces GABA-mediated synaptic inhibition in area CA1 of the hippocampus. However, the mechanisms involved in this disinhibition are not known. We report that mGluR activation reduces both the GABAA and GABAB receptor-mediated components of evoked inhibitory postsynaptic potentials (IPSPs) by reducing transmission at excitatory synapses onto inhibitory interneurons and inhibitory synapses onto CA1 pyramidal cells.
先前的研究表明，代谢型谷氨酸受体（mGluRs）的激活会降低海马体CA1区中GABA介导的突触抑制。然而，这种去抑制所涉及的机制尚不清楚。我们报告称，mGluR激活通过减少兴奋性突触到抑制性中间神经元的传递以及抑制性突触到CA1锥体细胞的传递，降低了诱发抑制性突触后电位（IPSPs）中GABAA和GABAB受体介导的成分。
