The functional analysis revealed that astrocyte-specific expression of Adra1a in global knockout mice completely restored the amplitudes of arousal-dependent transient as well as sustained V1 astrocyte Ca 2+ responses, and there was only a weak trend toward a restoration of the time to peak, with responses clearly not being faster than in wild-type mice ( Figures 3 D–3F).
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Impaired neuromodulator crosstalk delays arousal-dependent astroglia Ca<sup>2+</sup> activation in mouse models of Alzheimer's disease.
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