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After stroke, the EE caused increased dendritic growth, enhanced sensorimotor recovery, increased synaptic plasticity and production of trophic factors, as well as reduced apoptosis (Geibig et al., 2012)

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Once in the cortex, upregulation of KCC2 is necessary for the reduction of interneuron motility through the drop of neuronal chloride, a process which is also a precondition for the inhibitory effects of the neurotransmitter GABA and glycine in the CNS (Yeo et al., 2013)

doi:10.13005/ojc/300340 Regulska E, Karpiska J (2012) Photocatalytic degradation of olanzapine in aqueous and river waters suspension of titanium dioxide

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Cerebellar ataxia rehabilitation trial in degenerative cerebellar diseases