Luteinizing hormone (LH) acts through PKA and XXXX to modulate T-type @entity460 currents and intracellular @entity460 transients in @entity19 Leydig cells.

@entity251 @entity72930 @entity19 @entity668 @entity4515 @entity866 @entity6164 @entity460 @entity141 @entity9501
LH increases the intracellular @entity141 concentration ([ @entity141 ](i)) in @entity19 Leydig cells, in a process triggered by @entity460 influx through T-type @entity141 channels. Here we show that LH modulates both T-type @entity141 currents and [ @entity141 ](i) transients through the effects of PKA and @entity6164 . LH increases the peak @entity460 current (at -20mV) by 40%. A similar effect is seen with @entity4515 . The effect of LH is completely blocked by the PKA inhibitors @entity9501 and a synthetic inhibitory peptide ( @entity72930 ), but only partially by @entity668 ( @entity6164 inhibitor). LH and the blockers induced only minor changes in the voltage dependence of activation, inactivation or deactivation of the currents. @entity866 (blocker of PKA and @entity6164 ) impaired the [ @entity141 ](i) changes induced by LH. A similar effect was seen with @entity9501 . Although @entity4515 slowly increased the [ @entity141 ](i) the subsequent addition of LH still triggered the typical transients in [ @entity141 ](i). @entity668 also does not avoid the @entity141 transients, showing that blockage of @entity6164 is not sufficient to inhibit the LH induced [ @entity141 ](i) rise. In summary, these two kinases are not only directly involved in promoting @entity251 synthesis but also act on the overall @entity460 dynamics in Leydig cells, mostly through the activation of PKA by LH.
