Illness-induced taste aversions in normal and bulbectomized hamsters

Hobbs, Stephen H.; Clingerman, Harold; Elkins, Ralph L.

doi:10.1016/0031-9384(76)90070-6

Cited by 10 publications

(4 citation statements)

References 23 publications

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“…This observation provides some evidence that the emetic reflex is degenerate in rodents. Some potentially emetic stimuli have been used in mice, hamsters, and rabbits to induce conditioned flavour avoidance or pica (measures of malaise; see below) and have failed to induce emesis (e.g., Hobbs et al, 1976;Fox, 1977;Santucci et al, 2000;Christian et al, 2001;Santucci et al, 2002;Yamamoto et al, 2002a). However, before stating that all rodents and lagomorphs lack an emetic reflex it may be wise to undertake further formal studies of this phenomenon using a wide range of doses and stimuli.…”

Section: The Vomiting Reflex Is Lacking In Some Speciesmentioning

confidence: 99%

“…Hamster Cytotoxic drugs: Cyclophosphamide (Hobbs et al, 1976) Intragastric irritants: LiCl (Fox, 1977) Apomorphine (Nowlis et al, 1980) Nicotine (Etscorn et al, 1986) Other: 2-deoxy-D-glucose (Dibattista, 1988) Human Cytotoxic drugs: Chemotherapy (Rudd and Andrews, 2005) Chemotherapy (Schwartz et al, 1996) Intragastric irritants: Ipecac (Jackson and Smith, 1978), Copper sulfate (Liu et al, 2001) Ipecac (Jackson and Smith, 1978) Motion (Yates et al, 1998) (Arwas et al, 1989) Apomorphine (Schofferman, 1976) Morphine (Bailey et al, 1993) Radiation (Cordts et al, 1987) (Carrell et al, 1986) Hormones and neurotransmitters: CCK (Miaskiewicz et al, 1989) Other: Pregnancy (Weigel and Weigel, 1989), Reduced intracranial pressure (Mokri, 2004) Pregnancy (Bayley et al, 2002) Pregnancy (Corbett et al, 2003;Lopez et al, 2004), Gastric bypass surgery (Kushner et al, 2004) Monkey Cytotoxic drugs: Cisplatin (Fukui et al, 1993) Cyclophosphamide (Hikami et al, 1990) Intragastric irritants: Copper sulfate (Fukui et al, 1993) LiCl (Bergman and Glowa, 1986) Motion (Wilpizeski et al, 1987) (Wilpizeski et al, 1987) Radiation (Brizzee, 1956) Nicotine (Spealman, 1983) Hormones and neurotransmitters: CCK (Perera et al, 1993) Mouse Cytotoxic drugs: Cisplatin …”

Section: Emesismentioning

confidence: 99%

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

Andrews

Horn

2006

Autonomic Neuroscience

221

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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Section: The Vomiting Reflex Is Lacking In Some Speciesmentioning

confidence: 99%

Section: Emesismentioning

confidence: 99%

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

Andrews

Horn

2006

Autonomic Neuroscience

221

201

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“…The olfactory bulbs have important connections with the corticomedial amygdala and with other areas of the limbic system (Lammers, 1972). The rostral portions of the olfactory bulbs have been found to be involved in the acquisition of conditioned taste aversions in both species (Hobbs, Clingerman, & Elkins, 1976; Elkins, Fras~r, & Hobbs, Note 2). In rats, at least, the disruptive effect of bulbectomy on baitshyness is probably not related to the sensory function of the olfactory bulbs.…”

Section: Limbic Systemmentioning

confidence: 99%

Brain mechanisms of conditioned taste aversion learning: A review of the literature

Gaston

1978

Psychobiology

135

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“…This evidence, reviewed by Cain (1974), rests primarily upon the ob servation that peripherally induced anosmia frequently does not result in the same behavioral changes as those produced by direct surgical insult to the olfactory bulbs. With respect to the acquisition of aversions to flavor s which have been paired with internal malaise (bait shyness), at least partial attenuation results from bilateral olfactory-bulb lesions in both rats and ham ster s, even if the posterior bulbar layers are spared (e.g., Dine & Smith, 1966;Hankins, Garcia, & Rusiniak, 1973;Hobbs, Clingerman & Elkins, 1976;Elkins & Hobbs, Note I). Conversely, no disruption of baitshyness occurs if anosmia is produced by intranasal application of zinc sulfate (Dine & Smith, 1966;Hankins et al ., 1973).…”

mentioning

confidence: 99%