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Fig. 6.2
Kisspeptin predominantly activates a sodium-dependent, nonselective cationic
(TRPC)
channel. (
a
) The kisspeptin-induced inward current (at −60 mV) was greatly reduced in low Na
+
bath solution (5 mM Na
+
/140 mM
N
-methyl- d -glucamine [NMDG
+
]), and switching back to nor-
mal aCSF (control) solution revealed
a kisspeptin sensitive inward current of 28 pA in this GnRH
neuron. (
b
,
c
) The
I
-
V
relationships of the kisspeptin-evoked current in a low Na
+
bath solution
(5 and 15 mM Na
+
) between −20 and −120 mV showed a greatly reduced inward current. (
d
) A
typical
I
-
V
relationship of the kisspeptin-induced inward current in normal aCSF (control) solu-
tion showed a larger inward current (−30 pA at −60 mV). (
e
) Summary of the effects of the extra-
cellular sodium concentration on the kisspeptin-induced inward current at −60 mV. ***
p
< 0.001,
signifi cantly different from the effects of kisspeptin under control aCSF conditions. Cell numbers
tested are indicated for each group. Error bars indicate SEM. From Zhang C, Roepke TA, Kelly
MJ, Rønnekleiv OK. Kisspeptin depolarizes gonadotropin-releasing hormone neurons through
activation of TRPC-like cationic channels. J Neurosci 2008; 28: 4423-4434. Reprinted with
permission from The Society for Neuroscience
functional distinction between these channel subtypes in CNS neurons has been
problematic because of a lack of selective pharmacological reagents. The main
exception is the discriminatory effects of lathanides to augment TRPC4, 5 channel
activity [
62
]. Whole-cell recording experiments, with K
+
channel blockers on board,
have revealed that the current-voltage relationship for the kisspeptin-induced
current in GnRH neurons resembles the current-voltage relationship of heteromeric
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