Altered inhibitory synaptic transmission in superficial dorsal horn neurones in spastic and oscillator mice

Graham, BA, Schofield, PR, Sah, P and Callister, RJ (2003) Altered inhibitory synaptic transmission in superficial dorsal horn neurones in spastic and oscillator mice. Journal of Physiology-london, 551 3: 905-916. doi:10.1113/jphysiol.2003.049064


Author Graham, BA
Schofield, PR
Sah, P
Callister, RJ
Title Altered inhibitory synaptic transmission in superficial dorsal horn neurones in spastic and oscillator mice
Journal name Journal of Physiology-london   Check publisher's open access policy
ISSN 0022-3751
Publication date 2003-01-01
Sub-type Article (original research)
DOI 10.1113/jphysiol.2003.049064
Volume 551
Issue 3
Start page 905
End page 916
Total pages 12
Place of publication New York
Publisher Cambridge Univ Press
Language eng
Abstract The spastic (spa) and oscillator (ot) mouse have naturally occurring mutations in the inhibitory glycine receptor (GlyR) and exhibit severe motor disturbances when exposed to unexpected sensory stimuli. We examined the effects of the spa and ot mutations on GlyR- and GABA(A)R-mediated synaptic transmission in the superficial dorsal horn (SFDH), a spinal cord region where inhibition is important for nociceptive processing. Spontaneous mIPSCs were recorded from visually identified neurones in parasagittal spinal cord slices. Neurones received exclusively GABA(A)R-mediated mIPSCs, exclusively GlyR-mediated mIPSCs or both types of mIPSCs. In control mice (wild-type and spa/+) over 40 % of neurones received both types of mIPSCs, over 30 % received solely GABA(A)R-mediated mIPSCs and the remainder received solely GlyR-mediated mIPSCs. In spa/spa animals, 97 % of the neurones received exclusively GABA(A)ergic or both types of mIPSCs. In ot/ot animals, over 80 % of the neurones received exclusively GABA(A)R-mediated mIPSCs. GlyR-mediated mIPSC amplitude and charge were reduced in spa/spa and ot/ot animals. GABA,Rmediated mIPSC amplitude and charge were elevated in spa/spa but unaltered in ot/ot animals. GlyR- and GABA(A)R-mediated mIPSC decay times were similar for all genotypes, consistent with the mutations altering receptor numbers but not kinetics. These findings suggest the spastic and oscillator mutations, traditionally considered motor disturbances, also disrupt inhibition in a sensory region associated with nociceptive transmission. Furthermore, the spastic mutation results in a compensatory increase in GABA(A)ergic transmission in SFDH neurones, a form of inhibitory synaptic plasticity absent in the oscillator mouse.
Keyword Physiology
Rat Spinal-cord
Receptor Alpha-1 Subunit
Brain-stem Motoneurons
Central-nervous-system
Glycine-receptor
Gaba(a) Receptors
Frameshift Mutation
Gabaergic Synapses
Slice Preparation
Evoked Allodynia
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
Queensland Brain Institute Publications
 
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Created: Mon, 13 Aug 2007, 23:50:57 EST