Abstract:
:The membrane electroporation-induced inward current (IMEP) in pituitary tumor (GH3) cells was characterized. This current emerges irregularly when membrane hyperpolarizations to -200 mV with a holding potential of -80 mV were elicited. Neither E-4031 (10 μM), glibenclamide (30 μM), nor ZD7288 (30 μM) caused any effects on IMEP. The single-channel conductance and pore radius were estimated to be around 1.12 nS and 1.7 nm, respectively. LaCl3- and memantidine (MEM)-induced block of this current was also examined. The IC50 value for LaCl3- and MEM-induced inhibition of IMEP was 35 and 75 μM, respectively. However, unlike LaCl3, MEM (300 μM) did not exert any effect on voltage-gated Ca2+ current. In inside-out configuration, MEM applied to either external or internal surface of the excised patch did not suppress the activity of ATP-sensitive K+ channels expressed in GH3 cells, although glibenclamide significantly suppressed channel activity. This study provides the first evidence to show that MEM, a non-competitive antagonist of N-methyl D-aspartate receptors, directly inhibits the amplitude of IMEP in pituitary GH3 cells. MEM-mediated block of IMEP in these cells is unlinked to its inhibition of glutamate-induced currents or ATP-sensitive K+ currents. The channel-suppressing properties of MEM might contribute to the underlying mechanisms by which it and its structurally related compounds affect neuronal or neuroendocrine function.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Wu SN,Huang HC,Yeh CC,Yang WH,Lo YCdoi
10.1016/j.bbrc.2011.01.066subject
Has Abstractpub_date
2011-02-18 00:00:00pages
508-13issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(11)00109-4journal_volume
405pub_type
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