Electrical activation and c‐fos mRNA expression in rat neurosecretory neurones after systemic administration of cholecystokinin.

Hamamura, Mitsuko; Leng, Gareth; Emson, Piers C.; Kiyama, Hiroshi

doi:10.1113/jphysiol.1991.sp018865

Cited by 75 publications

(33 citation statements)

References 35 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Northern analysis has confirmed that probe binding is specifically to mRNA corresponding in size to that reported for rat c-fos mRNA (Wisden et al, 1990). Hybridization in the hypothalamus is localized to neuronal cell bodies, and is blocked in the presence of an excess of cold oligonucleotide and by RNase A pretreatment of tissue sections (Hamamura et al, 1991;1992 perfused with fixative for standard immunocytochemistry using a polyclonal antibody raised against the N-terminal amino acids 2-17 of the Fos protein, as previously described (Luckman, 1992 (Figure 2a). Injection of MK-329 itself had no effect on the plasma oxytocin concentration at any dose used.…”

Section: Methodsmentioning

confidence: 68%

“…The profile of neuronal activation in the hypothalamus following systemic administration of CCK has been studied using products of the immediate-early gene c-fos as a marker. Within 10 min of CCK injection, c-fos mRNA is expressed in neurones of the supraoptic and paraventricular nuclei (Hamamura et al, 1991). In the supraoptic nucleus, Fos-like immunoreactivity (Fos-LI) is found exclusively in magnocellular oxytocin neurones following CCK injection, while in the paraventricular nucleus at least three neuronal populations express Fos-LI: the CRF neurones, and both magnocellular and parvocellular oxytocin neurones (Verbalis et al, 1991b).…”

Section: Introductionmentioning

confidence: 99%

“…The in situ hybridization technique for measurement of c-fos mRNA has been described in full elsewhere (Hamamura et al, 1991;1992). The probe was a synthetic oligonucleotide (48-mer) complementary to rat c-fos mRNA (Curran et al, 1987), 3' end-labelled using a[35S]-dATP (New England Nuclear, UK) and terminal deoxynucleotidyl transferase (Pharmacia, UK).…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Luckman

Hamamura

Antonijevic

et al. 1993

British J Pharmacology

View full text Add to dashboard Cite

1 Intravenous administration of cholecystokinin (CCK) results in a transient activation of oxytocin neurones in the rat, and hence to oxytocin secretion: this activation is followed by expression of c-fos mRNA and of Fos-like immunoreactivity (Fos-LI) in magnocellular oxytocin neurones. Fos-like immunoreactivity is also induced in the regions of the brainstem that are thought to relay information from the periphery to the hypothalamus. 2 Administration of the selective CCKA receptor antagonist MK-329, but not the CCKB receptor antagonist L-365,260, prior to CCK injection, prevented oxytocin release as measured by radioimmunoassay and oxytocin neuronal activation as measured by electrophysiology and by the lack of induction of c-fos mRNA.3 MK-329 abolished the release of adrenocorticotrophic hormone (ACTH) following injection of CCK. 4 MK-329 prevented the expression of Fos-LI in the hypothalamic magnocellular nuclei and in the area postrema and dorsal vagal complex of the brainstem.5 L-365,260 had no effect on the expression of Fos-LI in the brainstem, but attenuated that seen in the hypothalamic magnocellular nuclei. 6 We conclude that CCK acts on CCKA receptors, either in the area postrema or on peripheral endings of the vagus nerve, to cause the release of hypothalamic oxytocin and ACTH. Information may be carried to the hypothalamus in part by CCK acting at CCKB receptors.

show abstract

Section: Methodsmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Luckman

Hamamura

Antonijevic

et al. 1993

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…These vagal messages initiated by the intraperitoneal or intravenous administration of CCK activate several neuronal complexes in the brain, including the nucleus tractus solitarius, the lateral parabrachial nucleus, and the central nucleus of the amygdala, as assessed by expression of the early gene product c-fos (Hamamura et al 1991). The production of early satiety by CCK does not require an intact medial hypothalamus because it occurs in human subjects with hypothalamic injury and obesity (Boosalis et al 1992).…”

mentioning

confidence: 99%

Afferent signals regulating food intake

2000

View full text Add to dashboard Cite

Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. β-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.

show abstract

“…Além disso, a vagotomia bloqueia a redução de ingestão provocada por injeção periférica de CCK, sugerindo que mensagens aferentes são geradas a nível hepático e gastroduodenal e encaminhadas ao cérebro via nervo vago. Essas mensagens ativam vários complexos neuronais cerebrais, incluindo o núcleo do trato solitário, o núcleo parabraquial lateral e o núcleo central da amíg-dala (85). É interessante que a produção de saciedade precoce pela CCK independe da integridade do hipotálamo medial, uma vez que ocorre em humanos com lesão hipotalâmica e obesidade.…”

Section: Peptídeos Agentes De Ação Periféricaunclassified

Aspectos fisiológicos do balanço energético

Mancini

Halpern

2002

Arq Bras Endocrinol Metab

View full text Add to dashboard Cite

RESUMOconhecidos. Nesta revisão, abordamos os nutrientes, monoaminas e peptídeos que podem levar a redução da ingestão e, em alguns casos, aumentar a ingestão de alimentos. Vários desses mecanismos podem levar ao desenvolvimento de novas abordagens no tratamento da obesidade ou na elucidação do mecanismo de ação de agentes farmacológicos. NUTRIENTES Agentes de Ação Periférica a. Análogos e metabólitos da hexoseA teoria glicostática (1) propõe que taxas de utilização de glicose podem ser sinais para iniciar ou ultimar a ingestão alimentar.Glicose. Uma diminuição no nível de glicose pode preceder e iniciar a alimentação em animais e humanos (2,3). Infusões periféricas de glicose diminuem a ingestão alimentar em animais experimentais, sendo o nervo vago a conexão entre os glicorreceptores periféricos e o cérebro. Quando glicose é infundida na circulação portal, a descarga de aferentes vagais é reduzida à medida que a concentração de glicose aumenta (4). A infusão de glicose ou arginina diminui a taxa de transmissão aferente e aumenta a transmissão simpática eferente ao tecido adiposo marrom (5).

show abstract

Electrical activation and c‐fos mRNA expression in rat neurosecretory neurones after systemic administration of cholecystokinin.

Cited by 75 publications

References 35 publications

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Afferent signals regulating food intake

Aspectos fisiológicos do balanço energético

Contact Info

Product

Resources

About