Role of brain neurotransmitters on neurotensin-induced gastric cytoprotection

De, Hernandez; Da, Stanley; Ja, Melvin; Aj, Prange

doi:10.1016/0091-3057(85)90266-7

Cited by 28 publications

(11 citation statements)

References 22 publications

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“…This assumption follows the evidence that the dopamine system provides an additional background also for Robert's stomach cytoprotection 13,[137][138][139][140][141] and gastric lesions appear after dopamine antagonists, MPTP, and reserpine. 132,133,135 Thus, for BPC 157 application as a cytoprotective agent, we could likely envisage an analogy with the counteraction of the stomach lesion induced by NSAIDs much like the counteraction of all others adverse of NSAIDs effects, including the central disturbances.…”

Section: Bpc 157 Stomach Cytoprotection Concept → Wound Heal-supporting

confidence: 56%

Stable Gastric Pentadecapeptide BPC 157, Robert's Stomach Cytoprotection/Adaptive Cytoprotection/Organoprotection, and Selye's Stress Coping Response: Progress, Achievements, and the Future

et al. 2020

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We reviewed again the significance of the stable gastric pentadecapeptide BPC 157 as a likely mediator of Robert's stomach cytoprotection/adaptive cytoprotection and organoprotection and as novel mediator of Selye's stress coping response to reestablish homeostasis. Specific points of BPC 157 therapy and the original concept of Robert's cytoprotection/adaptive cytoprotection/organoprotection are discussed, including the beneficial effects of BPC 157. First, BPC 157 protects stomach cells and maintains gastric integrity against various noxious agents (Robert's killing cell by contact) and is continuously present in the gastric mucosa and gastric juice. Additionally, BPC 157 protects against the adverse effects of alcohol and nonsteroidal anti-inflammatory drugs on the gastric epithelium and other epithelia, that is, skin, liver, pancreas, heart (organoprotection), and brain, thereby suggesting its use in wound healing. Additionally, BPC 157 counteracts gastric endothelial injury that precedes and induces damage to the gastric epithelium and generalizes "gastric endothelial protection" to protection of the endothelium of other vessels (thrombosis, prolonged bleeding, and thrombocytopenia). BPC 157 also has an effect on blood vessels, resulting in vessel recruitment that circumvents vessel occlusion and the development of additional shunting and rapid bypass loops to rapidly reestablish the integrity of blood flow (ischemic/ reperfusion colitis, duodenal lesions, cecal perforation, and inferior vena caval occlusion). Lastly, BPC 157 counteracts tumor cachexia, muscle wasting, and increases in pro-inflammatory/procachectic cytokines, such as interleukin-6 and tumor necrosis factor-α, and significantly corrects deranged muscle proliferation and myogenesis through changes in the expression of FoxO3a, p-AKT, p-mTOR, and p-GSK-3β (mitigating cancer cachexia).

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Section: Bpc 157 Stomach Cytoprotection Concept → Wound Heal-supporting

confidence: 56%

Stable Gastric Pentadecapeptide BPC 157, Robert's Stomach Cytoprotection/Adaptive Cytoprotection/Organoprotection, and Selye's Stress Coping Response: Progress, Achievements, and the Future

et al. 2020

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“…The occurrence of gastric erosions is also inhibited by icv treatment with CRF (31-33), vasopressin (34), IL-1 (22), neurotensin (35), or oxytocin (36), whereas mortality and the severity of gastric erosions caused by cysteamine are augmented by sc treatment with 22K human GH (37)(38)(39). We found that ip or icv administration of rPRL suppressed RSW-induced hypocalcemia and gastric erosions.…”

Section: Discussionmentioning

confidence: 82%

“…Briefly, sections were thaw-mounted on glass slides and fixed in 4% paraformaldehyde. 35 S-labeled antisense and sense (control) cRNA probes for PRLR(L) (15) and CRF (23) (1.2 kb CRF cDNA, provided by T. Imaki) were used under conditions described in detail previously (15,23). The general hybridization buffer contained 50% deionized formamide, with final washes in 0.1ϫ standard saline citrate containing 1 mm dithiothreitol at 60 C for 30 min.…”

Section: Ishh For Prlr(l) Mrna and Crf Mrnamentioning

confidence: 99%

Prolactin Prevents Acute Stress-Induced Hypocalcemia and Ulcerogenesis by Acting in the Brain of Rat

et al. 2004

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Stress causes hypocalcemia and ulcerogenesis in rats. In rats under stressful conditions, a rapid and transient increase in circulating prolactin (PRL) is observed, and this enhanced PRL induces PRL receptors (PRLR) in the choroid plexus of rat brain. In this study we used restraint stress in water to elucidate the mechanism by which PRLR in the rat brain mediate the protective effect of PRL against stress-induced hypocalcemia and ulcerogenesis. We show that rat PRL acts through the long form of PRLR in the hypothalamus. This is followed by an increase in the long form of PRLR mRNA expression in the choroid plexus of the brain, which provides protection against restraint stress in water-induced hypocalcemia and gastric erosions. We also show that PRL induces the expression of PRLR protein and corticotropin-releasing factor mRNA in the paraventricular nucleus. These results suggest that the PRL levels increase in response to stress, and it moves from the circulation to the cerebrospinal fluid to act on the central nervous system and thereby plays an important role in helping to protect against acute stress-induced hypocalcemia and gastric erosions.

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“…1992; Kalivas 1993; Hanson and Keefe 1999; Zahm et al. 2001) and NT release (Hernandez et al. 1985; Wagstaff et al.…”

Section: Discussionmentioning

confidence: 99%

Methylphenidate alters basal ganglia neurotensin systems through dopaminergic mechanisms: a comparison with cocaine treatment

Alburges

Hoonakker

Horner

et al. 2011

Journal of Neurochemistry

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J. Neurochem. (2011) 117, 470–478. Abstract Methylphenidate (MPD) is a psychostimulant widely used to treat behavioral problems such as attention deficit hyperactivity disorder. MPD competitively inhibits the dopamine (DA) transporter. Previous studies demonstrated that stimulants of abuse, such as cocaine (COC) and methamphetamine differentially alter rat brain neurotensin (NT) systems through DA mechanisms. As NT is a neuropeptide primarily associated with the regulation of the nigrostriatal and mesolimbic DA systems, the effect of MPD on NT‐like immunoreactivity (NTLI) content in several basal ganglia regions was assessed. MPD, at doses of 2.0 or 10.0 mg/kg, s.c., significantly increased the NTLI contents in dorsal striatum, substantia nigra and globus pallidus; similar increases in NTLI were observed in these areas after administration of COC (30.0 mg/kg, i.p.). No changes in NTLI occurred within the nucleus accumbens, frontal cortex and ventral tegmental area following MPD treatment. In addition, the NTLI changes in basal ganglia regions induced by MPD were prevented when D1 (SCH 23390) or D2 (eticlopride) receptor antagonists were coadministered with MPD. MPD treatment also increased dynorphin (DYN) levels in basal ganglia structures. These findings provide evidence that basal ganglia, but not limbic, NT systems are significantly affected by MPD through D1 and D2 receptor mechanisms, and these NTLI changes are similar, but not identical to those which occurred with COC administration. In addition, the MPD effects on NT systems are mechanistically distinct from the effects of methamphetamine.

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Role of brain neurotransmitters on neurotensin-induced gastric cytoprotection

Cited by 28 publications

References 22 publications

Stable Gastric Pentadecapeptide BPC 157, Robert's Stomach Cytoprotection/Adaptive Cytoprotection/Organoprotection, and Selye's Stress Coping Response: Progress, Achievements, and the Future

Stable Gastric Pentadecapeptide BPC 157, Robert's Stomach Cytoprotection/Adaptive Cytoprotection/Organoprotection, and Selye's Stress Coping Response: Progress, Achievements, and the Future

Prolactin Prevents Acute Stress-Induced Hypocalcemia and Ulcerogenesis by Acting in the Brain of Rat

Methylphenidate alters basal ganglia neurotensin systems through dopaminergic mechanisms: a comparison with cocaine treatment

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