Autoradiographic distribution of brainstem substance P binding sites in humans: Ontogenic study and relation to Sudden Infant Death Syndrome (SIDS)

Summary The precise distribution of substance P (SP) binding sites in the human brainstem was investigated in normal cases (3 fetuses and 24 newborns) and in 9 cases of Sudden Infant Death Syndrome (SIDS) by in vitro quantitative autoradiography.We discussed the widely but uneven distribution of SP binding sites as regards to the role of SP in brainstem cardio-respiratory ontogenic control and its possible involvement in SIDS.     

Communicating hydrocephalus induced by mechanically increased amplitude of the intraventricular cerebrospinal fluid pulse pressure: rationale and method

To elucidate some of the brain stem mechanisms involved in tongue motility, extracellular microelectrode recordings were made from single neurons in the region of the hypoglossal nucleus in 10 decerebrate and 23 anesthetized (chloralose) adult cats. The antidromic response characteristics and the synaptically evoked responses of 71 motoneurons that supplied tongue protrusive (P) or retrusive (R) muscles were documented. Protrusive motoneurons could be synaptically excited by temporomandibular joint (TMJ), glossopharyngeal (IX), and/or superior laryngeal (SLN) nerve stimuli, whereas R motoneurons could be activated by lingual and/or IX nerve stimulation. Conditioning effects revealed that the inhibition of the antidromic responses was shorter in duration than the inhibitory effects noted when synaptically evoked responses were conditioned. Conditioning stimuli delivered to the lingual, TMJ, IX, and SLN nerves were most effective in inhibiting the synaptically evoked responses of P and R motoneurons for conditioning-test intervals of as much as 400 ms. Those conditioning stimuli which also could synaptically activate a motoneuron tended to facilitate the cell's synaptically evoked responses at conditioning-test intervals of about 10 ms, whereas conditioning stimuli which did not synaptically activate the cell resulted in only the long-lasting inhibition.     

Obstructive sleep apnea: Electromyographic and fiberoptic studies

Seventeen predominantly obstructive sleep apnea patients and four normal controls (all adult males) underwent one or both investigative protocols: (A) A fiberoptic endoscope was introduced intranasally into the pharynx and subjects were monitored continuously and filmed intermittently during wakefulness and sleep. (B) Muscles selected because of their anatomical importance in maintaining the oropharynx during the respiratory cycle were electromyographically implanted intraorally or, in tracheostomy patients, at time of surgery, and subjects were polygraphically monitored during wakefulness and sleep. In both protocols, standard electroencephalogram, chin electromyogram (EMG), electrooculogram (EOG), and respiration were monitored simultaneously. During fiberoptic studies obstructive apnea during sleep first appeared as a partial or total invagination of the posterolateral pharyngeal walls, while the laryngeal inlet remained patent. EMG recordings showed normal firing patterns in patients during unobstructed sleep. During sleep-induced obstructive apnea, however, a significant decrease or complete disappearance of EMG activity was observed in the palatoglossus, palatopharyngeus, genioglossus, superior and middle constrictors of the pharynx, and stylopharyngeus. The obstruction involves absence, during inspiration, of the activity in the pharyngeal dilators needed to counteract the loads abruptly imposed by intrathoracic negative pressure changes.     

The effects of nicotine on the alpha-7 and beta-2 nicotinic acetycholine receptor subunits in the developing piglet brainstem

Exposure to cigarette smoke is a major risk factor for sudden infant death syndrome (SIDS). We tested the hypothesis that nicotine increases expression of the nicotinic acetylcholine receptor (nAChR) subunits α7 and β2 in a piglet model. Piglets exposed to 2 mg/kg/day nicotine for 14 days postnatally (n = 14) were compared to non-exposed controls (n = 14), (equal gender proportions). Immunohistochemistry was performed to identify and quantify changes in, α7 and β2 nAChR subunits in 8 nuclei of the medulla at both the rostral and caudal levels. Compared to controls, nicotine exposed piglets had decreased α7 in the rostral dorsal motor nucleus of the vagus (rDMNV) (p = 0.01), and increased β2 in the caudal DMNV (cDMNV) (p = 0.05), caudal nucleus of the spinal trigeminal tract (cNSTT) (p = 0.03) and caudal nucleus of the solitary tract (cNTS) (p = 0.04). Analysis by gender showed that in the control group, compared to males, females had higher β2 in the caudal hypoglossal (cXII) (p < 0.01) and caudal inferior olivary (p = 0.04) nuclei, while in the nicotine group females had higher β2 in the cDMNV (p = 0.02). Compared to control males, nicotine exposed males had lower β2 in the cXII (p < 0.01). Overall, changes in α7 were specific to nicotine exposure with no gender differentiation. Changes in β2 were more widespread but showed gender-specific effects. These findings provide evidence that early postnatal exposure to nicotine significantly affects nAChR subunit expressions in the developing brainstem.