- Title
- Attenuated glycine receptor function reduces excitability of mouse medial vestibular nucleus neurons
- Creator
- Camp, A. J.; Lim, R.; Anderson, W. B.; Schofield, P. R.; Callister, R. J.; Brichta, A. M.
- Relation
- Neuroscience Vol. 170, Issue 1, p. 348-360
- Publisher Link
- http://dx.doi.org/10.1016/j.neuroscience.2010.06.040
- Publisher
- Elsevier
- Resource Type
- journal article
- Date
- 2010
- Description
- Spontaneous activity in medial vestibular nucleus (MVN) neurons is modulated by synaptic inputs. These inputs are crucial for maintaining gaze and posture and contribute to vestibular compensation after lesions of peripheral vestibular organs. We investigated how chronically attenuated glycinergic input affects excitability of MVN neurons. To this end we used three mouse strains (spastic, spasmodic, and oscillator), with well-characterized naturally occurring mutations in the inhibitory glycine receptor (GlyR). First, using whole-cell patch-clamp recordings, we demonstrated that the amplitude of the response to rapidly applied glycine was dramatically reduced by 25 to 90% in MVN neurons from mutant mice. We next determined how reduced GlyR function affected MVN neuron output. Neurons were classified using two schemas: (1) the shape of their action potential afterhyperpolarization (AHP); and (2) responses to hyperpolarizing current injection. In the first schema, neurons were classified as types A, B and C. The prevalence of type C neurons in the mutant strains was significantly increased. In the second schema, the proportion of neurons lacking post inhibitory rebound firing (PRF-deficient) was increased. In both schemas an increase in AHP amplitude was a common feature of the augmented neuron group (type C, PRF-deficient) in the mutant strains. We suggest increased AHP amplitude reduces overall excitability in the MVN and thus maintains network function in an environment of reduced glycinergic input.
- Subject
- glycine; mouse; AHP; excitability
- Identifier
- http://hdl.handle.net/1959.13/932379
- Identifier
- uon:11329
- Identifier
- ISSN:0306-4522
- Language
- eng
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