Neuroanatomical connections between corticotropin-releasing factor (CRF) and somatostatin (SRIF) nerve endings and thyrotropin-releasing hormone (TRH) neurons in the paraventricular nucleus of rat hypothalamus

Liao, Ning; Vaudry, Hubert; Pelletier, Georges

doi:10.1016/0196-9781(92)90172-y

Cited by 26 publications

(13 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As leptin receptor mRNA has not been detected in the paraventricular nucleus, but is mostly concentrated in the arcuate nucleus, the effect of leptin is likely indirect [72,73]. Somatostatin neurons are in close proximity to CRH neurons in the paraventricular nucleus [74] and somatostatin inhibits hypothalamic CRH release [75,76]. Catecholamines including dopamine increase CRH expression directly and indirectly [77,78].…”

Section: Corticotropin-releasing Hormonementioning

confidence: 98%

Hypothalamic Regulation of Anterior Pituitary Function

Ben-Shlomo¹,

Melmed²

2011

The Pituitary

View full text Add to dashboard Cite

Section: Corticotropin-releasing Hormonementioning

confidence: 98%

Hypothalamic Regulation of Anterior Pituitary Function

Ben-Shlomo¹,

Melmed²

2011

The Pituitary

View full text Add to dashboard Cite

“…This possibility is made less likely by the observation that growth hormone and tuberoinfundibular dopamine and somatostatin deficiency would have been expected to increase TSH levels in the bloodstream [65, 66]. A small percentage of the somatostatin-producing neurons in the arcuate nucleus do project to the paraventricular nucleus [25], however, which may be of significance as somatostatin-containing nerve terminals contact TRH-synthesizing neurons in the paraventricular nucleus [67] and somatostatin has been shown in vitro to inhibit TRH release [68, 69]. …”

Section: Discussionmentioning

confidence: 99%

Arcuate Nucleus Ablation Prevents Fasting-Induced Suppression of ProTRH mRNA in the Hypothalamic Paraventricular Nucleus

et al. 1998

View full text Add to dashboard Cite

Fasting results in reduced thyroid hormone levels and inappropriately low or normal thyroid-stimulating hormone (TSH), partly attributed to central hypothyroidism due to suppression of pro TRH gene expression in the hypothalamic paraventricular nucleus. Recently, we demonstrated that the systemic administration of leptin to fasting animals restores plasma thyroxine (T₄) and proTRH mRNA in the paraventricular nucleus to normal, suggesting that the fall in circulating leptin levels during fasting acts as a signal to hypophysiotropic neurons in the paraventricular nucleus to reset the set point for feedback regulation of pro TRH mRNA by thyroid hormone. To determine whether the effect of fasting on the hypothalamic-pituitary-thyroid axis is mediated through the hypothalamic arcuate nucleus where leptin receptors are highly concentrated, we studied the effect of fasting and exogenous leptin administration on plasma thyroid hormone levels and proTRH mRNA concentration in the paraventricular nucleus in adult animals with arcuate nucleus lesions induced pharmacologically by the neonatal administration of monosodium L-glutamate (MSG). In normal animals, fasting reduced plasma T₄ and TSH levels and the concentration of proTRH mRNA in the hypothalamic paraventricular nucleus. In contrast, neither fasting nor leptin administration to fasting MSG-treated animals had any significant effects on plasma thyroid hormone and TSH levels and proTRH mRNA in the paraventricular nucleus. These studies suggest that during fasting, the arcuate nucleus is essential for the normal homeostatic response of the hypothalamic-pituitary-thyroid axis and may serve as a critical locus to mediate the central actions of leptin on proTRH gene expression in the paraventricular nucleus.

show abstract

“…The possibility that P4 and P5 inhibit GH secretion at extrapituitary sites is supported by the demonstration of neuroanatomical interactions between P5-containing neurons and those secreting SRIF, pro-opiomelanocortinrelated peptides, neuropeptide Y, corticotrophin-releasing factor and catecholamines in the rat paraventricular nucleus (Liao et al 1991(Liao et al , 1992. Furthermore, it is now well established that the in vivo GH-releasing activity of systemic TRH is partly due to actions within the CNS that stimulate catecholamine turnover and probably sup¬ press somatostatinergic tone (Leung et al 1985, Harvey et al 1990, Harvey 1993.…”

Section: Discussionmentioning

confidence: 98%

Cryptic peptides of prepro-TRH antagonize TRH-induced GH secretion in chickens at extrapituitary sites

Harvey

Cogburn²

1996

Journal of Endocrinology

View full text Add to dashboard Cite

Complete processing of the TRH precursor in the rat hypothalamus generates TRH and a number of other "cryptic' peptides that flank the TRH progenitor sequences. Two of these peptides, P4 (Ser-Phe-Pro-Trp-Met-Glu-Ser-Asp-Val-Thr; present between amino acids 160 and 169 of rat prepro-TRH) and P5 (Phe-Ile-Asp-Pro-Gly-Leu-Gln-Arg-Ser-Trp- Glu-Glu-Lys-Glu-Gly-Glu-Gly-Val-Leu-Met-Pro-Glu; present between amino acids 178 and 199 of rat prepro-TRH), have recently been shown to modulate TRH-induced GH and thyrotrophin release from rat pituitary glands. The possibility that these peptides might modulate GH secretion in chickens was examined, since TRH is a physiological GH-releasing factor in birds. The administration of P4 and P5 (at doses of 10 and 100 micrograms/kg) consistently lowered basal plasma GH concentrations 30 and 60 min after a bolus i.v. injection. Pretreatment with P4 and P5 similarly suppressed the GH response to systemic TRH challenge. The GH-releasing activity of maximally stimulatory doses of TRH was also reduced by concomitant injections of either P4 (100 micrograms/kg) or P5 (100 micrograms/kg), which blocked the GH-releasing activity of submaximally effective doses of TRH. In marked contrast, neither P4 nor P5 significantly affected basal or TRH-induced GH release from chicken pituitary glands incubated in vitro. These results demonstrate novel actions of P4 and P5 on hypothalamic-pituitary function and, for the first time, indicate extrapituitary sites of action for these cryptic peptides in modulating anterior pituitary function.

show abstract

Neuroanatomical connections between corticotropin-releasing factor (CRF) and somatostatin (SRIF) nerve endings and thyrotropin-releasing hormone (TRH) neurons in the paraventricular nucleus of rat hypothalamus

Cited by 26 publications

References 19 publications

Hypothalamic Regulation of Anterior Pituitary Function

Hypothalamic Regulation of Anterior Pituitary Function

Arcuate Nucleus Ablation Prevents Fasting-Induced Suppression of ProTRH mRNA in the Hypothalamic Paraventricular Nucleus

Cryptic peptides of prepro-TRH antagonize TRH-induced GH secretion in chickens at extrapituitary sites

Contact Info

Product

Resources

About