Abstract：
:To elucidate biophysical mechanisms underlying the Zn2+ block on the low-threshold T-type Ca2+ current (I(T)), we examined the Zn(2+)-induced alterations of gating properties of I(T) of a rat thalamic relay neuron and of alpha1G channels expressed in HEK-293 cells, using a whole-cell voltage clamp technique. The effect of Zn2+ block depended upon holding potentials but not test potentials, indicating that, the greater the inactivation, the less Zn2+ blocked I(T). Except for the inactivation near the activation threshold of I(T), no significant changes in the kinetics of activation and inactivation were induced by Zn2+. In contrast, the rates of both de-inactivation and deactivation were dramatically increased by Zn2+, and moreover the channels were rapidly re-blocked upon re-polarization under Zn2+. Furthermore, the outward current via alpha1G channel was almost insensitive to Zn2+. All these results imply that Zn2+ alters the gating properties of I(T) mainly by accelerating its deactivation process.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Noh J,Kim MK,Chung JMdoi
10.1016/j.neures.2009.12.005subject
Has Abstractpub_date
2010-04-01 00:00:00pages
353-8issue
4eissn
0168-0102issn
1872-8111pii
S0168-0102(09)02089-6journal_volume
66pub_type
杂志文章abstract：:Accumulating evidence demonstrates astrocytic crucial roles in the brain, but the molecular basis underlying astrocytic intracellular protein trafficking remains to be elucidated. The present study reports the identification of novel protein, brain-derived integrating factor-1 (BDIF1), which comprises TBC (Tre-2/Bub2/...
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