Chronic ethanol intake inhibits both the vasoactive intestinal peptide binding and the associated cyclic AMP production in rat enterocytes

Jiménez, Juan; Calvo, Juan R.; Molinero, Patrocinio; Goberna, R.; Guerrero, Juan M.

doi:10.1016/0306-3623(92)90135-7

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…Chronic ethanol treatment has been shown to decrease both VIP binding and stimulation of adenylate cyclase activity in rat enterocytes [13] and pinealocytes [14]. However, we did not observe any significant change either on VIP binding or on VIP-receptor coupling to G protein in rat prostatic membranes in that condition.…”

Section: Discussioncontrasting

confidence: 62%

“…Ethanolinduced desensitization of many adenylate cyclase signal-transduction systems is frequently related to altered function and/or expression of G proteins [12]. In the case of VIP, chronic ethanol treatment has been shown to decrease neuropeptide binding and its stimulatory effect on adenylate cyclase activity in rat enterocytes [13] and pinealocytes [14], as well as VIP mRNA levels in neurons of the central nervous system (CNS) [15]. On the other hand, ethanol elicited an increase of VIP levels in a secretory epithelium such as the rat gastric mucosa [16], whereas VIP plasma levels also augmented after alcohol intake [17].…”

Section: Introductionmentioning

confidence: 99%

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G-protein regulation of adenylate cyclase activity in rat prostatic membranes after chronic ethanol ingestion

et al. 1998

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Section: Discussioncontrasting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

G-protein regulation of adenylate cyclase activity in rat prostatic membranes after chronic ethanol ingestion

et al. 1998

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“…VIP mRNA is decreased in the suprachiasmatic nucleus with chronic alcohol use [147], and alcohol inhibits alpha adrenergic potentiation of VIP-regulated cAMP and cGMP responses [148]. Additionally, VIP binding is altered with alcohol administration [149,150]. Taken together, these data suggest that some of the neurological deficits in fetal alcohol syndrome may be related to a reduction of VIP activity in early embryogenesis.…”

Section: Vip In Fetal Alcohol Syndromementioning

confidence: 54%

Vasoactive Intestinal Peptide in Neurodevelopmental Disorders:Therapeutic Potential

Hill¹

2007

CPD

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Abstract:Vasoactive intestinal peptide (VIP) mediates important events during the development of the nervous system. VIP can stimulate neuronogenesis as well as differentiation and neurite outgrowth; it can promote the survival of neurons and assist in neuronal repair; it is also anti-inflammatory and can modulate immune responses. In addition, VIP is necessary for the normal growth and development of the early postimplantation mouse embryo during the period when the major embryonic events are neural tube formation, neuronogenesis and expansion of the vascular system. Receptors for VIP appear during early postimplantation embryogenesis in the rodent and exhibit changing localization patterns throughout the development of the brain. During embryogenesis, unregulated VIP may have major and permanent consequences on the formation of the brain and may be a participating factor in disorders of neurodevelopment. VIP has been linked to autism, Down syndrome and fetal alcohol syndrome. This paper will review the role of VIP in neurodevelopment, its known involvement in neurodevelopmental disorders and propose ways in which VIP might be of therapeutic value.

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“…This results in growth abnormalities which are prevented when ADNF and ADNP, both regulated by VIP, are used. As blockage of VIP during mouse embryogenesis also results in microcephaly, growth restriction and developmental delays [50,51], neurological deficits in fetal alcohol syndrome may be related to an alcohol-induced imbalance of VIP during early embryogenesis. Additionally, VIP binding is altered with alcohol administration [49].…”

Section: Vip In Fetal Alcohol Syndromementioning

confidence: 99%

VIP in Neurological Diseases: More Than A Neuropeptide

Morell

Souza-Moreira²,

González‐Rey³

2012

EMIDDT

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A hallmark in most neurological disorders is a massive neuronal cell death, in which uncontrolled immune response is usually involved, leading to neurodegeneration. The vasoactive intestinal peptide (VIP) is a pleiotropic peptide that combines neuroprotective and immunomodulatory actions. Alterations on VIP/VIP receptors in patients with neurodenegerative diseases, together with its involvement in the development of embryonic nervous tissue, and findings found in VIP-deficient mutant mice, have showed the relevance of this endogenous peptide in normal physiology and in pathologic states of the central nervous system (CNS). In this review, we will summarize the role of VIP in normal CNS and in neurological disorders. The studies carried out with this peptide have demonstrated its therapeutic effect and render it as an attractive candidate to be considered in several neurological disorders linked to neuroinflammation or abnormal neural development.

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Chronic ethanol intake inhibits both the vasoactive intestinal peptide binding and the associated cyclic AMP production in rat enterocytes

Cited by 8 publications

References 22 publications

G-protein regulation of adenylate cyclase activity in rat prostatic membranes after chronic ethanol ingestion

G-protein regulation of adenylate cyclase activity in rat prostatic membranes after chronic ethanol ingestion

Vasoactive Intestinal Peptide in Neurodevelopmental Disorders:Therapeutic Potential

VIP in Neurological Diseases: More Than A Neuropeptide

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