Proceedings of The Physiological Society
Cardiff University (2009) Proc Physiol Soc 17, PC05
The role of GluR1 in experience dependent depression in the visual cortex
A. Ranson1, K. D. Fox1, F. Sengpiel1
1. School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Primary sensory cortex is capable of adapting to altered sensory input, a process termed experience dependent plasticity. One form of adaptation is depression at the synaptic level of an input that no longer provides coherent sensory information. In a recent study we found complementary in vivo and in vitro evidence that this type of depression (as induced by whisker removal) in L2/3 of the mouse somatosensory cortex (S1) is dependent upon the presence of the GluR1 AMPA-R subunit (Wright, Glazewski et al., 2008). We have now examined whether an analogous process of depression in the visual cortex (V1) may also be GluR1 dependent. Suturing the eyelid of a mouse (monocular deprivation, MD) for 3d at the height of the critical period (P26-P29) has been reported to cause a robust 30-50% depression of the layer 2/3 V1 response to visual stimulation after eye reopening (Cang et al., 2005). This depression occurs both in the binocular region of V1 which receives input from both eyes, and the monocular region which only receives contralateral eye input. Using intrinsic signal imaging we compared the cortical responses of anesthetised mice following either normal visual experience or three days of monocular visual experience at the height of the critical period. Eye lid suture was conducted under 2% isoflurane anaesthetic administered in oxygen, while imaging was carried out under 0.8-1% isoflurane administered in oxygen and supplemented with a single intramuscular injection of 25µg chlorprothixene. The baseline V1 responses to visual stimulation in both the binocular and monocular areas were attenuated in GluR1-/- mice by around 40% (for example in the binocular area, WT mean ± SEM: 27.8x10-5 ± 3.5x10-5, n=6; GluR1-/- mean ± SEM: 16.4x10-5 ± 1.7x10-5, n=10, t-test: p<0.01). In binocular cortex, 3d of MD resulted in a percentage depression of closed eye responses relative to genotype baseline which did not differ significantly between genotypes (WT mean depression ± SEM: 49% ± 6%, n=5, t-test: p<0.01; GluR1-/- mean depression ± SEM: 41% ± 4%, n=9, t-test: p<0.05). In contrast, in the monocular region of V1, 3d of MD resulted in a percentage response depression in WT mice, while no significant depression was observed in GluR1-/- mice (WT mean depression ± SEM: 37% ± 4%, n=9, t-test: p<0.05; GluR1-/- mean depression ± SEM: 7% ± 1%). Our findings suggest that depression mechanisms operate differently in monocular and binocular regions of visual cortex and that only the former is GluR1 dependent. This suggests that GluR1 may be more important for homosynaptic depression mechanisms not requiring direct competition for depression to occur and that other mechanisms occur in binocular cortex.
Where applicable, experiments conform with Society ethical requirements