Figure 6: Attenuation of ghrelin-mediated enhancement of firing in CA1 pyramidal neurons from Tg mice.
From: Peptide hormone ghrelin enhances neuronal excitability by inhibition of Kv7/KCNQ channels

(a) KCNQ currents of example CA1 pyramidal neurons in wild type (WT) and Tg mice recorded by nystatin-perforated patch clamp recording under standard deactivation protocol from the holding potential of −20 to −40 mV. Note the pronounced deactivation relaxation (arrow in left panel) of WT mice, which was absence in the example neuron of Tg mice. (b) Statistical analysis of amplitude of native KCNQ current (IKCNQ) in WT (n=7) and Tg (n=11) mice (each bar represents the mean±s.e.m. *P<0.05, WT versus Tg; t=2.279, unpaired t-test.). (c) The example CA1 pyramidal neuron of WT mice fired spontaneous action potential at 0.6 Hz. A concentration of 100 nM ghrelin significantly increased firing rate to 1.2 Hz. (d) Collective data of all neurons recorded. Ghrelin increased the firing rate of all neurons (8/8) in WT mice (**P<0.01, Ghrelin versus Control, t=7.570, Paired t-test). (e) Raw traces showing that ghrelin did not change the firing rate of the example neuron in Tg mice. (f) In Tg mice, the firing rate of neurons (8/11) was not increased in the presence of 100 nM ghrelin (n.s. ghrelin versus control, t=1.112, Paired t-test). (g) Statistical analysis of d and f. Each bar represents the mean±s.e.m.