Elsevier

Peptides

Volume 8, Issue 3, May–June 1987, Pages 505-513
Peptides

Article
Oxytocin, oxytocin antagonist, TRH, and hypothalamic paraventricular nucleus stimulation effects on gastric motility

https://doi.org/10.1016/0196-9781(87)90017-9Get rights and content

Abstract

The roles of thyrotropin releasing hormone (TRH) and oxytocin as central regulators of gastric motility were investigated. Picomolar (4 picomoles) quantities of TRH injected into the dorsal motor nucleus of the vagus (DMN) elicited a significant increase in gastric motility while the same quantity of oxytocin elicited a reduction in phasic contractile activity and tone. The action of these peptides mimics the excitatory and inhibitory effects of stimulating the paraventricular nucleus of the hypothalamus (PVN); it is likely that this hypothalamic structure regulates gastric function through its peptidergic connections with medullary vagal structures. This hypothesis is supported by our observations that injections of an oxytocin antagonist into the DMN produced a disinhibition of gastric motility and an increase in the motility evoked by subsequent PVN stimulation. Vagotomy eliminated all subsequent central effects on motility of these peptides.

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      Thus, restoring the brain-peripheral organs hormonal interactions, e.g. OT, CCK, leptin, BDNF, IGF-1, and estrogen (Fig. 5, Section 7.6) during the lactation period, abrogating the development of hypertension by correcting the weaving of the normal homeostatic mechanisms that control blood pressure, circadian rhythms, and glucocorticoids plasma levels (Bass and Takahashi, 2010; Guyenet, 2006; McCann et al., 2002; Seckl and Walker, 2004; Staab and Maser, 2010), highly important for a proper influence of emotional arousal on memory and behavior (Bush, 2010; LaBar and Cabeza, 2006; Moffitt et al., 2011; Uvnäs-Moberg et al., 2005). OT and CCK-8 can affect the same physiological mechanisms, e.g. gastric functions (Flanagan et al., 1992; Liu et al., 2005; Rogers and Hermann, 1987), and behaviors, such as food intake (Blevins et al., 2003; Morton et al., 2006; Olson et al., 1991a,b; Shillabeer and Davison, 1987), induction of maternal behavior (Linden et al., 1987; Pedersen, 1997), modulation of lordosis behavior (Bloch et al., 1987; Sohlström et al., 2002; Uvnäs-Moberg, 1997), anxiety and stress response circuitries (Dauge and Lena, 1998; Luckman et al., 1993; Ravard and Dourish, 1990; Windle et al., 1997, 2004; Zetler, 1985), and nociception and analgesia (Stock and Uvnäs-Moberg, 1988; Wiesenfeld-Hallin and Xu, 2001; Yang et al., 2007). SON oxytocinergic neurons coexpress CCK and both are co-released from the neurosecretory granules of the neural lobe in the hypothalamic-neurohypophyseal system as a result of neural activity.

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