TY - JOUR
T1 - Blockade of ionotropic quisqualate receptor desensitization by wheat germ agglutinin in cultured postnatal rat hippocampal neurons
AU - Liu Lin Thio, Lin Thio
AU - Clifford, D. B.
AU - Zorumski, C. F.
PY - 1992
Y1 - 1992
N2 - The effects of the lectin wheat germ agglutinin (WGA) on quisqualate- gated currents were examined in postnatal rat hippocampal neurons using recordings from whole cells and outside-out membrane patches. Rapid applications of quisqualate to whole cells and outside-out patches evoked a current that desensitized to a steady-state level. WGA blocked desensitization by increasing the steady-state current amplitude without altering the current-voltage (I-V) relationship or pharmacology of the current. In outside-out patches quisqualate (2.5-1,000 μM) elicited bursts of channel openings having conductances of 2.7, 6.3, and 13 pS. The mean burst length for all conductances was 8.6 ± 0.6 ms (mean ± SE) and exhibited little voltage (-110 to +80 mV) or concentration (2.5-1,000 μM) dependence. Treating patches with 580 nM WGA produced no change in conductance, but the mean burst length for 100 μM quisqualate increased from 9.0 ± 1.1 to 16 ± 3.2 ms. Fluctuation analysis of whole cell currents evoked by 1 μM quisqualate at -80 mV revealed an increase in the time constant from 8.7 ± 0.5 to 13 ± 1.0 ms after treatment with 580 nM WGA. This treatment produced no change in the estimated single-channel conductance. These findings suggest that an increase in channel burst length, rather than an increase in single-channel conductance, contributes to the WGA-induced augmentation of the steady-state quisqualate current.
AB - The effects of the lectin wheat germ agglutinin (WGA) on quisqualate- gated currents were examined in postnatal rat hippocampal neurons using recordings from whole cells and outside-out membrane patches. Rapid applications of quisqualate to whole cells and outside-out patches evoked a current that desensitized to a steady-state level. WGA blocked desensitization by increasing the steady-state current amplitude without altering the current-voltage (I-V) relationship or pharmacology of the current. In outside-out patches quisqualate (2.5-1,000 μM) elicited bursts of channel openings having conductances of 2.7, 6.3, and 13 pS. The mean burst length for all conductances was 8.6 ± 0.6 ms (mean ± SE) and exhibited little voltage (-110 to +80 mV) or concentration (2.5-1,000 μM) dependence. Treating patches with 580 nM WGA produced no change in conductance, but the mean burst length for 100 μM quisqualate increased from 9.0 ± 1.1 to 16 ± 3.2 ms. Fluctuation analysis of whole cell currents evoked by 1 μM quisqualate at -80 mV revealed an increase in the time constant from 8.7 ± 0.5 to 13 ± 1.0 ms after treatment with 580 nM WGA. This treatment produced no change in the estimated single-channel conductance. These findings suggest that an increase in channel burst length, rather than an increase in single-channel conductance, contributes to the WGA-induced augmentation of the steady-state quisqualate current.
UR - http://www.scopus.com/inward/record.url?scp=0027051386&partnerID=8YFLogxK
U2 - 10.1152/jn.1992.68.6.1917
DO - 10.1152/jn.1992.68.6.1917
M3 - Article
C2 - 1283404
AN - SCOPUS:0027051386
SN - 0022-3077
VL - 68
SP - 1917
EP - 1929
JO - Journal of neurophysiology
JF - Journal of neurophysiology
IS - 6
ER -