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Pre‐ and postsynaptic modulation of monosynaptic reflex by GABA A receptors on turtle spinal cord
Author(s) -
Bautista Wendy,
Aguilar Justo,
LoezaAlcocer José Emanuel,
DelgadoLezama Rodolfo
Publication year - 2010
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 - 10.1113/jphysiol.2010.188979
Subject(s) - picrotoxin , spinal cord , gabaa receptor , bicuculline , gaba receptor antagonist , neuroscience , chemistry , tonic (physiology) , postsynaptic potential , receptor , biology , biochemistry
There is growing evidence that activation of high affinity extrasynaptic GABA A receptors in the brain, cerebellum and spinal cord substantia gelatinosa results in a tonic inhibition controlling postsynaptic excitability. The aim of the present study was to determine if GABA A receptors mediating tonic inhibition participate in the modulation of monosynaptic reflex (MSR) in the vertebrate spinal cord. Using an in vitro turtle lumbar spinal cord preparation, we show that conditioning stimulation of a dorsal root depressed the test monosynaptic reflex (MSR) at long condition–test intervals. This long duration inhibition is similar to the one seen in mammalian spinal cord and it is dependent on GABA A as it was completely blocked by 20 μ m picrotoxin (PTX) or bicuculline (BIC) or 1 μ m gabazine, simultaneously depressing the dorsal root potential (DRP) without MSR facilitation. Interestingly 100 μ m picrotoxin or BIC potentiated the MSR, depressed the DRP, and produced a long lasting motoneurone after‐discharge. Furosemide, a selective antagonist of extrasynaptic GABA A receptors, affects receptor subtypes with α 4/6 subunits, and in a similar way to higher concentrations of PTX or BIC, also potentiated the MSR but did not affect the DRP, suggesting the presence of α 4/6 GABA A receptors at motoneurones. Our results suggest that (1) the turtle spinal cord has a GABA A mediated long duration inhibition similar to presynaptic inhibition observed in mammals, (2) GABA A receptors located at the motoneurones and primary afferents might produce tonic inhibition of monosynaptic reflex, and (3) GABA A receptors modulate motoneurone excitability reducing the probability of spurious and inappropriate activation.