Sentences with phrase «of acetylcholine at»

Several drugs are available to increase the concentration or prolong the action of acetylcholine at the neuromuscular junction sites.

This leads to higher concentrations of acetylcholine at the dog's neuromuscular junctions.

Organophosphate insecticides inhibit acetylcholinesterase causing excess levels of acetylcholine at the nerve end paralyzing the muscle.

There are several drugs that are used to concentrate the action of acetylcholine at the neuromuscular junction sites.

Not exact matches

Specifically, intensive postmortem neurological studies of their brain tissues reveal a relatively low density of acetylcholine (a neurotransmitter) nerve sites, which, at normal densities, function in critical ways to help re-initiate breathing following a sleep - related apnea or extended breathing pauses.

In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.

In the late 1960s, Katz determined that the amount of acetylcholine in a vesicle was related to the electrical potential at the terminal of an axon — the long extension of a neuron that transmits the impulse.

The paper is «an important milestone,» says Laurent Segalat, a geneticist at the University of Lyon, France, because it finally links the worm muscular dystrophy model with defects in acetylcholine transport and breakdown.

Judy Anderson, a muscular dystrophy expert at the University of Manitoba in Winnipeg, Canada, adds that evidence for acetylcholine defects in human muscular dystrophy has been contradictory over the years, but if this preliminary finding holds up in mice and humans, it could pave the way for new drug targets.

Electrophysiological assays of human and frog nAChR revealed that one amino acid replacement, which evolved three times in poison frogs, decreased epibatidine sensitivity but at a cost of acetylcholine sensitivity.

«Essentially, they cause acetylcholine to build up in the brain, causing hyperexcitability of neurons as well as the death of some neurons, which leads to inflammation in the brain,» said Ashok K. Shetty, PhD, a professor in the Department of Molecular and Cellular Medicine at the Texas A&M College of Medicine, associate director of the Institute for Regenerative Medicine, research career scientist at the Olin E. Teague Veterans Medical Center, Central Texas Veterans Health Care System and senior author of the paper.

To narrow down the list, a team of researchers led by Henry Lester, a neuroscientist at the California Institute of Technology in Pasadena, designed a mouse with a mutant version of the a4 * acetylcholine receptor subunit.

Here's a tantalizing prospect, hinted at by a long - running thread of brain research: compounds that boost the function of certain acetylcholine circuits in the brain might also modify production of toxic beta - amyloid protein.

This ambiguity was explained by JJ Noval at NAMRL in Pensacola, when he showed that magnetic fields that vibrated in the ELF range would increase the levels of acetylcholine in the rat brainstem directly.

Dogs with myasthenia gravis either don't have the normal number of skeletal muscle cell receptors for the neurotransmitter acetylcholine when they are born (congenital myasthenia gravis), or the receptors that they do have are defective or have been damaged at some point after their birth (acquired myasthenia gravis).

Myasthenia gravis is caused by a reduction or deficiency in the number of cellular receptors for a specific neurotransmitter, acetylcholine, at the junctions between nerve endings and skeletal muscle cells.

The goals of treating a dog that has myasthenia gravis are to improve the transmission of acetylcholine between its nerve endings and muscle fiber receptors, improve its comfort and muscle stability and eliminate or at least reduce any acquired immune - related causes of its condition.