Proceedings of The Physiological Society

Physiology 2015 (Cardiff, UK) (2015) Proc Physiol Soc 34, PC108

Poster Communications

Riding the waves of astrocytic calcium: the role of astrocytes in experience-dependent plasticity

S. Glazewski1, J. B. Butcher1, R. E. Sims2, H. R. Parri2

1. School of Life Sciences, Keele University, Keele, United Kingdom. 2. School of Life & Health Sciences, Aston University, Birmingham, United Kingdom.


  • Figure 1: Average KO undeprived and SWE (deprived and intact) responses when stimulating P and S (error bars: SEM).

  • Figure 2: Average WT SWE and KO SWE (deprived and intact) responses when stimulating P and S (error bars: SEM).

There is increasing evidence that astrocytes partner neurons in synaptic communication and plasticity. They sense the same synaptic inputs and respond with intracellular [Ca2+] elevations, which correlate with gliotransmitter release (1). While there is evidence for astrocytic involvement in neuronal plasticity (NP) in vitro (2), the impact of astrocytes on NP in vivo is less established. Deflection of a single whisker leads to a substantial neuronal firing in its corresponding cortical representation (principal input, P) which dominates responses elicited by the stimulation of immediately adjacent whiskers (surround input, S). This pattern of dominance can be altered, a phenomenon known as experience-dependent plasticity (EDP), through whisker deprivation. Removal of all but one whisker (single whisker experience (SWE)), leads to an expansion of the cortical representation of the intact whisker into the territory of the immediately surrounding whiskers in layers 2/3, while the responses of the deprived inputs get depressed. We compared the magnitude of responses to whisker deflections collected from the barrel cortex of C57BL/6J wild type and IP3-R2 knockout mice, either undeprived (WT:n=8, KO:n=5) or deprived (SWE for 18 days) with 5-9 days of whisker regrowth (WT:n=11, KO:n=9). In IP3-R2 KO mice spontaneous and G-protein-coupled receptors-mediated increases in astrocytic [Ca2+] elevations have been shown to be impaired (3-5). Mice were anaesthetised with urethane (1.5 g/kg body weight, i.p.) and extracellular data was collected in-vivo by recording layer 2/3 cells in the barrel cortex while stimulating P and S (50 deflections of 1o were delivered for 10 ms at 1 Hz per each whisker). The Mann-Whitney U-test was used to compare data which is expressed as spikes per stimulus±SEM. Undeprived WT and KO animals did not differ concerning the magnitude of whisker-evoked responses (WT, P:1.43±0.27, S:0.36±0.05; KO, P:0.97±0.06, S:0.24±0.05; p>0.05). Comparison of the WT undeprived and WT SWE animals showed a significant difference in the S responses (WT undeprived, S: 0.36±0.05; WT SWE, intact whisker S (IWS): 0.92±0.14, deprived whisker S in the intact representation (DWS): 0.09±0.03; p<0.05) as did a comparison of the undeprived and deprived KO mice (KO: undeprived S:0.24±0.05; KO SWE IWS:0.80±0.13, DWS:0.05±0.01; p<0.01, Fig 1). In both WT and KO animals IWS responses were potentiated while the DWS responses were depressed when compared to their respective undeprived S (p<0.05). Comparison of the SWE deprived WT and KO mice revealed no significant differences (P-deprived/P-intact/IWS/DWS for WT SWE: 0.72±0.17, 1.57±0.21, 0.92±0.14, 0.09±0.04 and for KO SWE: 0.71±0.17, 1.54±0.26, 0.80±0.13, 0.05±0.01 respectively; p>0.05, Fig 2). These results show that the impairment of the astrocytic IP3-R2 mechanism does not affect neuronal EDP.

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