Protected substantia nigra pars compacta (SNc) dopaminergic neuronal cell bodies and striatal nerve terminals
Other research, such as that led by Charles Liberman, a professor of otology and lanyngology at Harvard Medical School, is looking into regenerating the damaged auditory nerve terminals
, reestablishing the broken links to hair cells.
Capsaicin-sensitive sensory nerve terminals
with local and systemic efferent functions: facts and scopes of an unorthodox neuroregulatory mechanism.
A team of researchers led by JosEa Lemos from the University of Massachusetts Medical School examined the mechanisms at play during secretion of vasopressin from nerve terminals
in the posterior pituitary gland, which releases the neuropeptide into the blood so that it can make its way to the kidney and regulate water retention.
These cells, called solitary chemosensory cells, detect potential irritants and pass along the alert to pain-sensing nerve terminals
The toxin binds to cholinergic nerve terminals
and proteolytically inactivates SNAP-25, a synaptosomal-associated protein utilized in synaptic vesicle fusion with the nerve terminal
Immunoglobulins inhibit pathophysiological effects of anti-GQ1b-positive sera at motor nerve terminals
through inhibition of antibody binding.
By acting specifically on motor nerve terminals
at the neuromuscular junction, it inhibits the release of acetylcholine from the cholinergic nerve endings and exhibits muscle relaxant effects.
Morphological studies conducted during the late 1960s and early 1970s suggested that both human and experimental ACR neurotoxicities were associated with cerebellar Purkinje cell death and degeneration of distal axons and nerve terminals
in the peripheral and central nervous systems (PNS and CNS, respectively) (reviewed by LoPachin 2004; LoPachin and Lehning 1994; LoPachin et al.
The release of neurotransmitters is fulfilled via complex Ca+2-dependent, regulated exocytosis from specialized secretory organelles, called small synaptic vesicles (SVs), located in presynaptic nerve terminals
Botulinum toxin acts presynaptically at cholinergic nerve terminals
by preventing acetylcholine exocytosis and release and causes muscle paresis which can last for two to three months (1,2).
This enzyme converts the amino acid tyrosine into the metabolite tyramine which stimulates the release of neurotransmitters such as dopamine from adrenergic nerve terminals
while blocking the neurotransmitters' reuptake.