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This mechanism is distinct from the previously postulated mechanisms for the inhibition of EPSPs by the activity of HCN channels ( h currents, particularly in late developmental stages, suggesting developmental stage-dependent serotonergic modulation of MTN frequency selectivity (Tanaka et al., 2019)

however, phosphorylation at the serine 518 residue, by Rac 1dependent p21activated kinase (PAK) and cAMPdependent protein kinase A 4, 162, results in a more closed conformation, which is associated with loss of activity 163

Theunis, A

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