Examples of using Nerve terminals in English and their translations into Greek
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This causes an increase in nerve terminals in the endometrium.
Internalisation and release of the toxin into the cytosol of the nerve terminals 3.
Inhibition of acetylcholine release from nerve terminals at the neuromuscular junction.
Extracellular binding of the toxin to specific acceptors on motor nerve terminals 2.
The CB1 receptor is present mainly in skeletal sympathetic nerve terminals, thus regulating the adrenergic tonic restrain of bone formation.
It prevents the re-uptake, andhence the inactivation of noradrenaline and serotonin at nerve terminals.
In this process,the substance of this drug actively works in the nerve terminals and inhibits the release of acetylcholine.
The nerve terminals of the neuromuscular junction no longer respond to nerve impulses, and secretion of the neurotransmitter is prevented(chemical denervation).
This combination of more sensitive cells and more nerve terminals leads to chronic pain.
Pseudo-ephedrine is a nasal decongestant, which exerts its sympathomimetic effects indirectly,predominantly through release of adrenergic mediators from postganglionic nerve terminals.
Recovery after injection normally takes place within 3-4 months as nerve terminals sprout and reconnect with the endplate.
Noradrenaline is released from nerve terminals, leading predominantly to beta adrenoceptor activation in the bladder musculature, and hence bladder smooth muscle relaxation.
Muscle relaxation: senna can block acetylcholine at the motor nerve terminals and skeletal joints, so that muscle relaxation.
Also in the nerve terminals, aminooxyacetic acid prevents the mitochondria from utilizing pyruvate generated from glycolysis, thus leading to a bioenergetic state similar to that of hypoglycemia.
The CB1 receptor is mainly present in skeletal sympathetic nerve terminals, which regulates the adrenergic tonic restraint of the bone formation.
Recovery after intramuscular injection takes place normally within 12 weeks of injection as nerve terminals sprout and reconnect with the endplates.
Acetylcholine, released from pelvic nerve terminals, stimulates cholinergic M2 and M3 receptors, inducing bladder contraction.
Cerebral synapse maturation was retarded andthe number of functioning nerve terminals in the cerebrum was reduced, which resulted in impaired brain growth.
Binding to the cholinergic nerve terminals entry or internalisation into the nerve terminal and inhibition of acetylcholine release by intracellular poisoning within the nerve terminal.
The 5-HT3 receptors are present both peripherally on vagal nerve terminals and centrally in the chemoreceptor trigger zone of the area postrema in the medulla.
CB1 is mostly expressed on presynaptic peripheral and central nerve terminals and is believed to be responsible for psychologic effects on pleasure, memory, thought, concentration, sensory and time perceptions, and coordinated movement.
Extracellular binding of the toxin to specific acceptors on motor nerve terminals Internalisation andrelease of the toxin into the cytosol of the nerve terminals Inhibition of acetylcholine release from nerve terminals at the neuromuscular junction.
The 5-HT3 receptors are located in three sites: vagal nerve terminals in the gastrointestinal tract and chemoreceptor trigger zones located in the area postrema and the nucleus tractus solidarius of the vomiting center in the brainstem.
Meanwhile, the empty vesicle is recycled back into the nerve terminal to be used again.
When an electrical signal arrives at a nerve terminal and needs to be passed along to the next neuron, neurotransmitters, or chemical messengers, packed in vesicles mediate this process.
Once bound to the nerve terminal, the neuron takes up the toxin into a vesicle by receptor-mediated endocytosis.
Receptor-bound Botulinum neurotoxin type A is endocytosed into the nerve terminal prior to reaching its target(SNAP 25) and will eventually be degraded intracellularly.
Free circulating Botulinum neurotoxin type A molecules which have not bound to presynaptic cholinergic nerve terminal receptors will be phagocytosed or pinocytosed and degraded like any other free circulating protein.