Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

Abstract

Background: The accepted function of the hypothalamic peptide, thyrotrophin-releasing hormone (TRH), is to initiate release of thyrotrophin (TSH) from the pituitary. A physiological role for TRH in lactating rats has not yet been established. Methods: Tissues were prepared from random-cycling and lactating rats and analysed using Northern blot, real time RT-PCR and quantitative in situ hybridisation.Results: This study demonstrates that TRH receptor 1 (TRHR1) mRNA expression is up-regulated in the pituitary and in discrete nuclei of the hypothalamus in lactating rats, while proTRH mRNA expression levels are increased only in the hypothalamus. The results were corroborated by quantitative in situ analysis of proTRH and TRHR1. Bromocriptine, which reduced prolactin (PRL) concentrations in plasma of lactating and nursing rats, also counteracted the suckling-induced increase in TRHR1 mRNA expression in the hypothalamus, but had an opposite effect in the pituitary. These changes were confined to the hypothalamus and the amygdala in the brain.Conclusions: The present study shows that the mechanisms of suckling-induced lactation involve region-specific regulation of TRHR1 and proTRH mRNAs in the central nervous system notably at the hypothalamic level. The results demonstrate that continued suckling is critical to maintain plasma prolactin (PRL) levels as well as proTRH and TRHR1 mRNA expression in the hypothalamus. Increased plasma PRL levels may have a positive modulatory role on the proTRH/TRHR1 system during suckling.

Tuberoinfundibular peptide of 39 residues modulates the mouse hypothalamic–pituitary–adrenal axis via paraventricular glutamatergic neurons

“…This decrease in plasma prolactin concentration can be attributed to an effect of TIP39 on a specific set of neurons and not to a general consequence of glutamate or norepinephrine release, because norepinephrine and glutamate (Bregonzio et al, 1998; Kapoor et al, 1993; Nagy et al, 2005; Pohl et al, 1989) increase prolactin secretion when directly infused into the central nervous system. Prolactin secretion is under diverse and complex regulation exerted by the dopamine neurons in the arcuate nucleus (Christian et al, 2007; Kawano and Daikoku, 1987; Meites, 1977), some PVN neuropeptides including vasoactive intestinal polypeptide (Mezey and Kiss, 1985) and thyrotropin‐releasing hormone (Fjeldheim et al, 2005), and some classical neurotransmitters such as glutamate (Bregonzio et al, 1998) and serotonin (Rittenhouse et al, 1993). The infusion of TIP39 into the PVN does not permit identification of the exact pathway of prolactin inhibition, but it very likely involves indirect or direct activation of dopamine neurons in the arcuate nucleus.…”

Novel Potential Regulators of Maternal Adaptations During Lactation: Tuberoinfundibular Peptide 39 and Amylin

“…Prolactin secretion may also be affected by several neuropeptides (36). The regulatory roles of thyrotrophin‐releasing hormone (37–39) and opioid peptides (40–43) are best established. Peptide products of pro‐opiomelanocortin and other peptides in the arcuate nucleus involved in the control of food intake (44,45) may also participate in mechanisms leading to elevated food intake during pregnancy and lactation (46,47).…”