Peptidergic regulation of feeding in the dog (Canis familiaris)

Levine, Allen S.; Sievert, Chester E.; Morley, John E.; Gosnell, Blake A.; Silvis, Stephen E.

doi:10.1016/0196-9781(84)90005-6

Cited by 40 publications

(9 citation statements)

References 35 publications

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“…Although the inhibitory effects of exogenous CCK on gastric emptying and feed intake have been demonstrated clearly in rats (Debas et al, 1975;Smith et ai., 1983) and similar effects have been observed in humans (Kissilef et al, 1981), pigs (Anika et al, 1981), monkeys (Gibbs et al, 1976) and dogs (Levine et al, 1984), few reports exist that describe its effects on ruminants. McLeay and Bell (1980) showed that infusions of CCK inhibited abomasal emptying in the calf.…”

Section: Disou~ionmentioning

confidence: 64%

Immune, Growth and Carcass Responses of Ram Lambs to Active Immunization against Desulfated Cholecystokinin (CCK-8)

Trout¹,

Pekas²,

Schanbacher³

1989

Journal of Animal Science

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This study explored feed intake and carcass responses to active immunization against desulfated cholecystokinin-octapeptide (CCK-8) in ram lambs. Antibody titers 8 wk following primary immunization and booster immunizations given at 4 and 6 wk averaged greater than 1:1,000. Titers increased to greater than 1:10,000 by 16 wk following a final booster immunization at 11 wk. The antibodies developed against desulfated CCK-8 exhibited 29% and 13% cross-reactivities for sulfated CCK-8 and gastrin-17, respectively. Immunization against desulfated CCK-8 had no effect on feed intake, ADG, carcass weight or carcass quality grade. Backfat thickness and carcass yield grade were reduced (P less than .05) by immunization. Organ weights at slaughter, including those of the pancreas and small intestines, were not affected by CCK-8 immunization, with the exception of the lungs, which were 16% lighter (P less than .01) in immunized lambs. In conclusion, active immunization against desulfated CCK-8 resulted in development of high antibody titers against desulfated and sulfated CCK-8. Immunization against CCK-8 decreased fat content of the carcass but failed to affect feed intake, carcass weight or ADG.

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Section: Disou~ionmentioning

confidence: 64%

Immune, Growth and Carcass Responses of Ram Lambs to Active Immunization against Desulfated Cholecystokinin (CCK-8)

Trout¹,

Pekas²,

Schanbacher³

1989

Journal of Animal Science

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“…2B). A similar shift in the dose-response curve for the CCK-8S effect on feeding has been shown in vagotomized dogs (12).…”

mentioning

confidence: 68%

Modulation of Memory Processing by Cholecystokinin: Dependence on the Vagus Nerve

Flood

Smith

Morley

1987

Science

Self Cite

180

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Allowing mice access to food immediately after an aversive training session enhances memory retention. Cholecystokinin-octapeptide (CCK-8), which is a gastrointestinal hormone released during feeding, also enhances memory retention when administered intraperitoneally. This memory-enhancing effect of CCK-8 is blocked when the vagus nerve is cut, indicating that CCK-8 may produce its effect on memory retention by activating ascending fibers in the vagus nerve. Thus, CCK-8, a peripherally acting peptide, may mediate the memory-enhancing effects of feeding.

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“…Cat Cytotoxic drugs: Cisplatin , Cyclophosphamide (Fetting et al, 1982) Intragastric irritants: Copper sulfate (Kayashima and Hyama, 1976) Motion (Crampton and Daunton, 1983) Apomorphine (Costello and Borison, 1977) Morphine (Villablanca et al, 1984) Radiation (Rabin et al, 1986b) (Rabin et al, 1986b) Nicotine (Beleslin et al, 1981) Hormones and neurotransmitters: Angiotensin II (Rabin et al, 1986a) Other: Amphetamine (Rabin and Hunt, 1992) Dog Cytotoxic drugs: Cisplatin (Gylys et al, 1979), Cyclophosphamide (Amber et al, 1990) Intragastric irritants: Ipecac (Gardner et al, 1996), Copper sulfate (Kayashima and Hayama, 1975) LiCl (Vavilova and Kassil, 1984) Apomorphine (Harrison et al, 1972) Morphine (Lefebvre et al, 1981) Radiation (Cooper and Mattsson, 1979) Nicotine (Vig, 1990) Hormones and neurotransmitters: CCK (Levine et al, 1984), Vasopressin (Wu et al, 1985), Peptide YY (Smith et al, 1989) Ferret Cytotoxic drugs: Cisplatin, cyclophosphamide (Andrews et al, 1990) Intragastric irritants: Copper sulfate, ipecac, NaCl, KCl (Andrews et al, 1990) LiCl (Rabin and Hunt, 1992) Apomorphine (Andrews et al, 1990) Morphine (Barnes et al, 1991) Radiation (Andrews et al, 1990) Guinea pig Intragastric irritants: LiCl (Braveman, 1974) …”

Section: Emesismentioning

confidence: 99%

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

Andrews

Horn

2006

Autonomic Neuroscience

220

201

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Nausea and vomiting are amongst the most common symptoms encountered in medicine as either symptoms of diseases or side effects of treatments. In a more biological setting they are also important components of an organism's defences against ingested toxins. Identification of treatments for nausea and vomiting and reduction of emetic liability of new therapies has largely relied on the use of animal models, and although such models have proven invaluable in identification of the anti-emetic effects of both 5-hydroxytryptamine3 and neurokinin1 receptor antagonists selection of appropriate models is still a matter of debate. The present paper focuses on a number of controversial issues and gaps in our knowledge in the study of the physiology of nausea and vomiting including: The choice of species for the study of emesis and the underlying behavioural (e.g. neophobia), anatomical (e.g. elongated, narrow abdominal oesophagus with reduced ability to shorten) and physiological (e.g. brainstem circuitry) mechanisms that explain the lack of a vomiting reflex in certain species (e.g. rats); The choice of response to measure (emesis[retching and vomiting], conditioned flavour avoidance or aversion, ingestion of clay [pica], plasma hormone levels[e.g. vasopressin], gastric dysrhythmias) and the relationship of these responses to those observed in humans and especially to the sensation of nausea; The stimulus coding of nausea and emesis by abdominal visceral afferents and especially the vagus-how do the afferents encode information for normal postprandial sensations, nausea and finally vomiting?; Understanding the central processing of signals for nausea and vomiting is particularly problematic in the light of observations that vomiting is more readily amenable to pharmacological treatment than is nausea, despite the assumption that nausea represents "low" intensity activation of pathways that can evoke vomiting when stimulated more intensely.

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Peptidergic regulation of feeding in the dog (Canis familiaris)

Cited by 40 publications

References 35 publications

Immune, Growth and Carcass Responses of Ram Lambs to Active Immunization against Desulfated Cholecystokinin (CCK-8)

Immune, Growth and Carcass Responses of Ram Lambs to Active Immunization against Desulfated Cholecystokinin (CCK-8)

Modulation of Memory Processing by Cholecystokinin: Dependence on the Vagus Nerve

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

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