Feeding induced by food deprivation is differentially reduced by G-protein α-subunit antisense probes in rats

Hadjimarkou, Maria M.; Silva, Robert M.; Rossi, Grace C.; Pasternak, Gavril W.; Bodnar, Richard J.

doi:10.1016/s0006-8993(02)03361-9

Cited by 18 publications

(20 citation statements)

References 43 publications

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“…A previous study reported that following 24 h of food deprivation, anti-Giα 2 and anti-Giα 3 significantly reduced food intake, while aODNs directed against either Giα 1 and Goα failed to significantly alter deprivation-induced feeding (Hadjimarkou et al, 2002). However, accordingly, to our data in mice not maximally stimulated to eat (4 h of fasting) only aODN against Giα 2 reduced food intake, while the silencing of other Gi/Go subunits exerted a different effect on feeding behavior.…”

Section: Discussionmentioning

confidence: 95%

“…Specifically, the role of Gs and Gq protein was observed since the deprivation-induced feeding was most effectively reduced by administration of an antisense oligodeoxynucleotide (aODN) directed against the Gsα and Gqα subunits, while anti-Giα 2 and Giα 3 exerted lesser effects, and anti-Giα 1 and Goα failed to affect deprivation-induced food intake (Hadjimarkou et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Differential contribution of Gαi/o subunits in the response to food deprivation

Sanna

Ghelardini

Galeotti

2015

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Differential contribution of Gαi/o subunits in the response to food deprivation

Sanna

Ghelardini

Galeotti

2015

European Journal of Pharmacology

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“…For these investigations, we used ODN sequences to selectively reduce brain G␣q and G␣z protein expression (4,19,22,24). The ODN sequences used in these studies are specific for their respective G␣ subunit protein sequences, as verified by a GenBank search and have been used extensively in vivo for selective targeting of G␣-subunit proteins (4,19,22,24). In agreement with previous studies (4,19,24), the current data show a sequence-specific reduction in G␣-subunit protein levels 24 h following intracerebroventricular administration of each respective ODN (25 g).…”

Section: Discussionmentioning

confidence: 99%

“…The ODN sequences used in these studies are specific for their respective G␣ subunit protein sequences, as verified by a GenBank search and have been used extensively in vivo for selective targeting of G␣-subunit proteins (4,19,22,24). In agreement with previous studies (4,19,24), the current data show a sequence-specific reduction in G␣-subunit protein levels 24 h following intracerebroventricular administration of each respective ODN (25 g). We further demonstrated the specific and selective nature of the ODN sequences using a miss-sense ODN (25 g), which did not alter CNS G␣-subunit protein levels or the cardiovascular and renal responses to intracerebroventricular N/OFQ.…”

Section: Discussionmentioning

confidence: 99%

“…In G␣-protein studies, rats (n ϭ 6 per group) were pretreated with a single intracerebroventricular injection of either saline vehicle (5 l, 48 h), PTX (1 g/5 l, 48 h) (3,13), G␣z ODN (25 g/5 l, 24 h; 5Ј-GGGCCAGTAGCCCAATGGG-3Ј), G␣q ODN (25 g/5 l, 24-h; 5Ј-GCTTGAGCTCCCGGCGGGCG-3Ј) or a scrambled ODN (25 g/5 l, 24 h; 5Ј-GGGGGAAGTAGGTCT-TGG-3Ј) (4,19,24). Following an NCBI Basic Local Alignment Search Tool (Blast) search of the Rattus norvegicus RefSeq protein database, it was confirmed that there is no similarity between the scrambled ODN sequence and any rat protein gene sequence.…”

Section: Experimental Protocolsmentioning

confidence: 99%

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Central G-alpha subunit protein-mediated control of cardiovascular function, urine output, and vasopressin secretion in conscious Sprague-Dawley rats

Wainford

Kurtz²,

Kapusta³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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The role(s) of central Galpha-proteins in the regulation of cardiovascular and renal function is unknown. We examined how inhibition/downregulation of central Galphai/Galphao, Galphaz or Galphaq proteins altered the characteristic cardiovascular (depressor), renal excretory (diuretic), and plasma AVP (inhibitory) responses to intracerebroventricular injection of nociceptin/orphanin FQ (N/OFQ) in rats. Before investigation, rats were pretreated intracerebroventricularly with saline vehicle (5 microl, 48 h, n=6), pertussis toxin (PTX; 48-h, 1 microg, n=6), or Galphaz, Galphaq, or scrambled oligodeoxynucleotide (ODN) (25 microg, 24 h, n=6 per group). On the study day, intracerebroventricular N/OFQ (5.5 nmol) or vehicle (5 microl) was injected into pretreated conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were recorded, and urine was collected for 90 min. In vehicle or scrambled ODN groups, intracerebroventricular N/OFQ decreased MAP and HR and produced water diuresis (sensitive to UFP-101, N/OFQ receptor antagonist). The hypotension and bradycardia, but not diuresis, to N/OFQ were abolished in PTX-pretreated rats. In contrast, intracerebroventricular ODN pretreatment markedly blunted (Galphaz) or augmented (Galphaq) the diuresis to intracerebroventricular N/OFQ. In separate studies, the action of central N/OFQ to decrease plasma AVP levels in naïve water-restricted rats was differentially altered by intracerebroventricular Galphaz ODN (blunted) and Galphaq ODN (augmented) pretreatment. These studies demonstrate central Galphai/Galphao activity mediates intracerebroventricular N/OFQ's cardiovascular depressor function. Alternatively, central Galphaz (inhibitory) and Galphaq (stimulatory) activity differentially modulates AVP release to control the pattern of diuresis to intracerebroventricular N/OFQ. These findings highlight the novel selective central Galpha-subunit protein-mediated control of cardiovascular vs. renal excretory function.

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Pathophysiology of anorexia in the cancer cachexia syndrome

Ezeoke

Morley

2015

Journal of Cachexia, Sarcopenia and Muscle

164

117

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Anorexia is commonly present in persons with cancer and a major component of cancer cachexia. There are multiple causes of anorexia in cancer. Peripherally, these can be due to (i) substances released from or by the tumour, e.g. pro-inflammatory cytokines, lactate, and parathormone-related peptide; (ii) tumours causing dysphagia or altering gut function; (iii) tumours altering nutrients, e.g. zinc deficiency; (iv) tumours causing hypoxia; (v) increased peripheral tryptophan leading to increased central serotonin; or (vi) alterations of release of peripheral hormones that alter feeding, e.g. peptide tyrosine tyrosine and ghrelin. Central effects include depression and pain, decreasing the desire to eat. Within the central nervous system, tumours create multiple alterations in neurotransmitters, neuropeptides, and prostaglandins that modulate feeding. Many of these neurotransmitters appear to produce their anorectic effects through the adenosine monophosphate kinase/methylmalonyl coenzyme A/fatty acid system in the hypothalamus. Dynamin is a guanosine triphosphatase that is responsible for internalization of melanocortin 4 receptors and prostaglandin receptors. Dynamin is up-regulated in a mouse model of cancer anorexia. A number of drugs, e.g. megestrol acetate, cannabinoids, and ghrelin agonists, have been shown to have some ability to be orexigenic in cancer patients.

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Feeding induced by food deprivation is differentially reduced by G-protein α-subunit antisense probes in rats

Cited by 18 publications

References 43 publications

Differential contribution of Gαi/o subunits in the response to food deprivation

Differential contribution of Gαi/o subunits in the response to food deprivation

Central G-alpha subunit protein-mediated control of cardiovascular function, urine output, and vasopressin secretion in conscious Sprague-Dawley rats

Pathophysiology of anorexia in the cancer cachexia syndrome

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