Similarities of the neuronal circuit for the induction of fictive vomiting between ferrets and dogs

Onishi, Takako; Mori, Takashi; Yanagihara, Mamoru; Furukawa, Naohiro; Fukuda, Hiroyuki

doi:10.1016/j.autneu.2007.03.002

Cited by 29 publications

(49 citation statements)

References 24 publications

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“…Electrophysiological data demonstrated that central pattern generator neurons driven by the mNTS, 62 as well as nearby neurons associated with the prodromic signs of vomiting (i.e., hypersalivation, tachypnea), fired in a rhythmic pattern synchronized to the retching and vomiting motor sequences induced by vagal stimulation. 53,78,218 In the decerebrate dog model, this neuronal activity was abolished along with the actual emesis-associated behaviors upon application of NK 1 receptor antagonists, 70,81 a finding recently reproduced in the ferret. 53 In addition, intraperitoneal administration of GR73632 increases Fos expression in the central pattern generator of vomiting least shrews, which suggests that this locus is an important anatomical emetic substrate of SP (Ray, Chebolu, and Darmani, submitted for publication).…”

Section: Dorsal Vagal Complexmentioning

confidence: 81%

“…The central pattern generator appears to be heavily innervated with NK 1 receptor-containing fibers, and information from pharmacological studies suggests that glutamatergic neurotransmissionviaAMPA/kainatereceptorsisalsoinvolved. 53,61,77,81 3. Dopamine: Synthesis, Storage, Release, Degradation, and Receptors Dopamine (DA) is a neurotransmitter in both the CNS and the periphery.…”

Section: Central Pattern Generator Areamentioning

confidence: 99%

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Evidence for a Re-Evaluation of the Neurochemical and Anatomical Bases of Chemotherapy-Induced Vomiting

2009

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Section: Dorsal Vagal Complexmentioning

confidence: 81%

Section: Central Pattern Generator Areamentioning

confidence: 99%

Evidence for a Re-Evaluation of the Neurochemical and Anatomical Bases of Chemotherapy-Induced Vomiting

2009

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“…As with the AP, the discussed diverse emetogenic receptors are also present in the NTS [20,36,41,42,43,44,45,46,47,48,49]. After integrating the central and peripheral signals relating to emesis or other GI activity, inhibitory GABAergic and excitatory glutamatergic primary NTS neurons project to neurons in the DMNX and to the central pattern generator area (CPG) [40,50]. The DMNX also receives afferents from vagal nodose ganglion neurons, and sends efferents to the enteric nervous system (ENS), as well as to the emetic CPG postulated to be dorsomedial to the nucleus ambiguus and retrofacial nucleus which coordinate peristaltic activity and its reversal during emesis [51,52,53,54].…”

Section: Cinv Emetic Circuitsmentioning

confidence: 99%

Mechanisms of Broad-Spectrum Antiemetic Efficacy of Cannabinoids against Chemotherapy-Induced Acute and Delayed Vomiting

Darmani

2010

Pharmaceuticals

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Chemotherapy-induced nausea and vomiting (CINV) is a complex pathophysiological condition and consists of two phases. The conventional CINV neurotransmitter hypothesis suggests that the immediate phase is mainly due to release of serotonin (5-HT) from the enterochromaffin cells in the gastrointestinal tract (GIT), while the delayed phase is a consequence of release of substance P (SP) in the brainstem. However, more recent findings argue against this simplistic neurotransmitter and anatomical view of CINV. Revision of the hypothesis advocates a more complex, differential and overlapping involvement of several emetic neurotransmitters/modulators (e.g. dopamine, serotonin, substance P, prostaglandins and related arachidonic acid derived metabolites) in both phases of emesis occurring concomitantly in the brainstem and in the GIT enteric nervous system (ENS) [1]. No single antiemetic is currently available to completely prevent both phases of CINV. The standard antiemetic regimens include a 5-HT3 antagonist plus dexamethasone for the prevention of acute emetic phase, combined with an NK1 receptor antagonist (e.g. aprepitant) for the delayed phase. Although NK1 antagonists behave in animals as broad-spectrum antiemetics against different emetogens including cisplatin-induced acute and delayed vomiting, by themselves they are not very effective against CINV in cancer patients. Cannabinoids such as Δ9-THC also behave as broad-spectrum antiemetics against diverse emetic stimuli as well as being effective against both phases of CINV in animals and patients. Potential side effects may limit the clinical utility of direct-acting cannabinoid agonists which could be avoided by the use of corresponding indirect-acting agonists. Cannabinoids (both phyto-derived and synthetic) behave as agonist antiemetics via the activation of cannabinoid CB1 receptors in both the brainstem and the ENS emetic loci. An endocannabinoid antiemetic tone may exist since inverse CB1 agonists (but not the corresponding silent antagonists) cause nausea and vomiting.

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“…In addition, Fukuda's electrophysiological studies demonstrated that neurons in the LTF had appropriate firing patterns to coordinate the respiratory muscle contractions that result in vomiting (20). Furthermore, administration of emetic drugs or stimulation of gastrointestinal afferents evoked the expression of the intermediate-early gene c-fos by a large number of LTF neurons (12,26,27,36,41).…”

mentioning

confidence: 97%

Responses of neurons in the caudal medullary lateral tegmental field to visceral inputs and vestibular stimulation in vertical planes

Moy

Miller

Catanzaro

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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The dorsolateral reticular formation of the caudal medulla, or the lateral tegmental field (LTF), has been classified as the brain's "vomiting center", as well as an important region in regulating sympathetic outflow. We examined the responses of LTF neurons in cats to rotations of the body that activate vestibular receptors, as well as to stimulation of baroreceptors (through mechanical stretch of the carotid sinus) and gastrointestinal receptors (through the intragastric administration of the emetic compound copper sulfate). Approximately half of the LTF neurons exhibited graviceptive responses to vestibular stimulation, similar to primary afferents innervating otolith organs. The other half of the neurons had complex responses, including spatiotemporal convergence behavior, suggesting that they received convergent inputs from a variety of vestibular receptors. Neurons that received gastrointestinal and baroreceptor inputs had similar complex responses to vestibular stimulation; such responses are expected for neurons that contribute to the generation of motion sickness. LTF units with convergent baroreceptor and vestibular inputs may participate in producing the cardiovascular system components of motion sickness, such as the changes in skin blood flow that result in pallor. The administration of copper sulfate often modulated the gain of responses of LTF neurons to vestibular stimulation, particularly for units whose spontaneous firing rate was altered by infusion of drug (median of 459%). The present results raise the prospect that emetic signals from the gastrointestinal tract modify the processing of vestibular inputs by LTF neurons, thereby affecting the probability that vomiting will occur as a consequence of motion sickness.

show abstract

Similarities of the neuronal circuit for the induction of fictive vomiting between ferrets and dogs

Cited by 29 publications

References 24 publications

Evidence for a Re-Evaluation of the Neurochemical and Anatomical Bases of Chemotherapy-Induced Vomiting

Evidence for a Re-Evaluation of the Neurochemical and Anatomical Bases of Chemotherapy-Induced Vomiting

Mechanisms of Broad-Spectrum Antiemetic Efficacy of Cannabinoids against Chemotherapy-Induced Acute and Delayed Vomiting

Responses of neurons in the caudal medullary lateral tegmental field to visceral inputs and vestibular stimulation in vertical planes

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