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pubmed:abstractText |
In thalamocortical relay (TC) neurons, G-protein-coupled receptors play an important part in the control of activity modes. A conditional G?(q) knockout on the background of a constitutive G?(11) knockout (G?(q)/G?(11) (-/-)) was used to determine the contribution of Gq/G11 family G-proteins to metabotropic serotonin (5-HT) and glutamate (Glu) function in the dorsal part of the lateral geniculate nucleus (dLGN). In control mice, current clamp recordings showed that ?-m-5-HT induced a depolarization of V(rest) which was sufficient to suppress burst firing. This depolarization was concentration-dependent (100 ?M: +6 ± 1?mV, n = 10; 200 ?M: +10 ± 1?mV, n = 7) and had a conditioning effect on the activation of other G?(q)-mediated pathways. The depolarization was significantly reduced in G?(q)/G?(11) (-/-) (100 ?M: 3 ± 1?mV, n = 11; 200 ?M: 5 ± 1?mV, n = 6) and was apparently insufficient to suppress burst firing. Activating G?(q)-coupled muscarinic receptors affected the magnitude of ?-m-5-HT-induced effects in a reciprocal manner. Furthermore, the depolarizing effect of mGluR1 agonists was significantly reduced in G?(q)/G?(11) (-/-) mice. Immunohistochemical stainings revealed binding of 5-HT(2C)R- and mGluR1?-, but not of 5-HT(2A)R-specific antibodies in the dLGN of G?(q)/G?(11) (-/-) mice. In conclusion, these findings demonstrate that transmitters of ascending brainstem fibers and corticofugal fibers both signal via a central element in the form of Gq/G11-mediated pathways to control activity modes in the TC system.
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