An Arterially Perfused Decerebrate Preparation of Suncus Murinus (House Musk Shrew) for the Study of Emesis and Swallowing

Abstract

Arterially perfused, decerebrate preparations of the insectivore, Suncus murinus were made to determine whether the emetic reflex could be activated in such a preparation using a range of stimuli shown to be emetic in conscious or anaesthetised Suncus. Efferent phrenic and vagus nerve activities and electromyograms (EMGs) from the temporalis, abdominal oesophagus and trapezius muscles were recorded, as well as longitudinal shortening of the oesophagus and dorso‐ventral movements of the thorax. The preparations swallowed spontaneously every 0.6 to 6.5 min. The duration of a swallow was 3.1 ± 0.3 s (recorded as the time taken for the oesophagus to shorten and recover to its resting position) and the oesophagus shortened by 3.5 ± 0.4 mm during a swallow. The emetic reflex was activated by electrical stimulation (30 Hz, 10‐20 V, 0.2 ms pulse width, for 30 s) of abdominal vagal afferents (latency < 30 s) or by arterial perfusion with either 40 nM of the capsaicin analogue resiniferatoxin (latency 1.7 ± 0.6 min), 6 μM nicotine (latency 1.6 ± 0.1 min) or 1 μM of the phosphodiesterase IV inhibitor CP‐80,633 (latency 8.9 ± 3.9 min). These emetic stimuli produced somatic and visceral movements in Suncus preparations indicative of activation of the emetic reflex. There were pronounced contractions of the thorax that occurred simultaneously with oesophageal shortening and mouth opening, separated by thorax expansion and a burst of phrenic nerve activity. During emetic‐like episodes, oesophageal shortenings were only 0.84 ± 0.1 s in duration, faster than the duration of shortening observed during swallowing (cf. swallowing, 3.1 ± 0.3 s; P < 0.0001). The shortening of the oesophagus during emetic‐like episodes was 6.2 ± 0.4 mm, which was greater than the shortening seen during swallowing (cf. swallowing, 3.5 ± 0.4 mm; P < 0.0001). We conclude that the emetic reflex can be activated in our Suncus preparations and that this non‐sentient small adult animal model can now be used to study the neurophysiology and pharmacology of swallowing and emesis.

Chemotherapy agent cisplatin induces 48-h Fos expression in the brain of a vomiting species, the house musk shrew (Suncus murinus)

“…DMN neurons make extensive projections to the upper gastrointestinal tract (e.g., in musk shrew, Ref. 74) and possibly initiate the giant retrograde contraction that moves intestinal contents back to the stomach before emesis, and the nucleus ambiguous likely participates in the esophageal shortening that occurs during vomiting (66). Therefore, cisplatin-induced Fos expression in the DMN might reflect the activation of motor outputs related to emesis.…”

Why is the neurobiology of nausea and vomiting so important?

“…In vivo preparations showing retching or vomiting responses have been developed for the cat, dog, ferret, and house musk shrew (e.g., Smith, Paton, & Andrews, 2002;Fukuda et al, 2003;Umezaki, Zheng, Shiba, & Miller, 1997;Van, Oland, Mackie, Davison, & Sharkey, 2003). Since prodromal outputs, including nausea, are connected to the emetic circuitry this level of analysis should yield insights into brain pathways that also mediate prodromal responses (Fig.…”

Pharmacogenetics of Chemotherapy-Induced Nausea and Vomiting

“…Early studies using experimental animals, such as dogs, cats and ferrets [13][14][15], suggested the existence of a 'vomiting center' in the hindbrain. The nucleus of the solitary tract (NTS) is involved in the integration of afferent inputs by emetic stimuli in the medulla oblongata [16][17][18].…”