Figure 4
From: Somatostatin triggers rhythmic electrical firing in hypothalamic GHRH neurons
Inhibition of GHRH neuron synaptic currents by SST.
(A) Raw traces showing spontaneous glutamatergic currents in female GHRH neurons held at −50mV (a, b and c represent before, during and after SST, respectively and correspond to the regions shown in (C)). (B) Glutamatergic current frequency in male GHRH neurons following 100 nM SST superfusion. (C) As for (B) but showing a reduction in current density in SST-treated female slices. (D) Bar graph showing proportion of GHRH neurons displaying reduced glutamatergic currents in response to SST (n = 17 for males and n = 7 for females). Mean latencies for the effects were 3.4 ± 0.4 min and 4.6 ± 0.5 min in males and females, respectively. (E) Raw traces showing spontaneous GABAergic currents in male GHRH neurons (a, b and c represent before, during and after SST, respectively and correspond to the region shown in (F)). (F) SST reduces GABAergic current density in male GHRH neurons. (G) As for (F) but showing a less potent action of SST to reduce currents in females. (H) Bar graph showing proportion of GHRH neurons displaying reduced GABAergic currents in response to SST (n = 10 for males and n = 8 for females). Mean latencies for the effects were 3.8 ± 0.6 min and 3.8 ± 0.7 min in males and females, respectively. (I,J) The sst1 agonist CH-275 increased miniature GABAergic current (mIPSC) intervals, but not their amplitude, in male GHRH neurons (recorded in the continued presence of 500nM tetrodotoxin). *P < 0.05 and ***P < 0.005 versus control (t = 0 min) (paired Student’s t- test). Under control conditions, intervals (I) and amplitudes (J) were respectively 0.4 ± 0.1 s and 16 ± 3 pA.
