IndraLab

Statements


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"These findings suggest that inhibition of HCN1 channels enhances excitatory synaptic transmission by altering T-type Ca 2+ channel activity."

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"Genetic deletion of HCN1 channels or pharmacological blockade in vivo of HCN channels enhanced synaptic plasticity and spatial learning and increased dendritic Ca 2+ spiking."

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"For example, in mice, genetic deletion of the HCN1 gene or pharmacological inhibition of I h by the drug ZD7288 have been shown to enhance the frequency of miniature excitatory post-synaptic potentials onto EC layer III pyramids by promoting the entry of calcium through T-type calcium channels; this suggests that I h normally limits calcium entry into the synapse and reduces neurotransmission."

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"Deletion of HCN1 may also preferentially enhance the firing of local dendritic Ca 2+ spikes, which are of particular importance for intrinsic theta oscillations and for induction of LTP at distal syna[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The decrease in pre-synaptic HCN1 activity in these synapses enhances T-type Ca 2+ channel function XREF_BIBR."