1.Effects of extracerebral dopamine on salsolinol- or thyrotropin-releasing hormone-induced prolactin (PRL) secretion in goats.
Inaba Y1, Kato Y1, Itou A1, Chiba A1, Sawai K1, Fülöp F2, Nagy GM3, Hashizume T1. Anim Sci J. 2016 Mar 20. doi: 10.1111/asj.12586. [Epub ahead of print]
The aim of the present study was to clarify the effect of extracerebral dopamine (DA) on salsolinol (SAL)-induced prolactin (PRL) secretion in goats. An intravenous injection of SAL or thyrotropin-releasing hormone (TRH) was given to female goats before and after treatment with an extracerebral DA receptor antagonist, domperidone (DOM), and the PRL-releasing response to SAL was compared with that to TRH. DOM alone increased plasma PRL concentrations and the PRL-releasing response to DOM alone was greater than that to either SAL alone or TRH alone. The PRL-releasing response to DOM plus SAL was similar to that to DOM alone, and no additive effect of DOM and SAL on the secretion of PRL was observed. In contrast, the PRL-releasing response to DOM plus TRH was greater than that to either TRH alone or DOM alone and DOM synergistically increased TRH-induced PRL secretion. The present results demonstrate that the mechanism involved in PRL secretion by SAL differs from that by TRH, and suggest that the extracerebral DA might be associated in part with the modulation of SAL-induced PRL secretion in goats.
2.L-type calcium channels and MAP kinase contribute to thyrotropin-releasing hormone induced depolarization in thalamic paraventricular nucleus neurons.
Kolaj M1, Zhang L1, Renaud LP2. Am J Physiol Regul Integr Comp Physiol. 2016 Mar 23:ajpregu.00082.2016. doi: 10.1152/ajpregu.00082.2016. [Epub ahead of print]
In rat paraventricular thalamic nucleus (PVT) neurons, activation of thyrotropin releasing hormone (TRH) receptors enhances neuronal excitability via concurrent decrease in a GIRK-like conductance and opening of a cannabinoid receptor-sensitive transient receptor potential canonical (TRPC)-like conductance. Here we investigated the calcium (Ca2+) contribution to the components of this TRH-induced response. TRH-induced membrane depolarization was reduced in the presence of intracellular BAPTA, also in media containing nominally zero [Ca2+]o, suggesting a critical role for both intracellular Ca2+release and Ca2+influx. TRH-induced inward current was unchanged by T-type Ca2+channel blockade, but was decreased by blockade of high-voltage-activated Ca2+channels (HVACCs). Both the pharmacologically isolated GIRK-like and the TRPC-like components of the TRH-induced response were decreased by nifedipine and increased by BayK8644, implying Ca2+influx via L-type Ca2+channels.
