neurotransmitter filled packets in the presynaptic neuron are called quanta.
neurotransmitter filled packets in the presynaptic neuron are called quanta.
neurotransmitter filled packets in the presynaptic neuron are called?
quanta
when the motor nerve is stimulated there is a delay of only 0.5 to 0.8 msec between the arrival of the nerve impulse in the motor nerve terminals and the first response of the endplate the arrival of the motor nerve action potential at the presynaptic neuron terminal opens voltage-dependent calcium channels and ca ions flow from the extracellular fluid into the presynaptic neuron's cytosol. this influx of ca causes several hundred neurotransmitter-containing vesicles to fuse with the presynaptic neuron's cell membrane through snare proteins to release their acetylcholine quanta by exocytosis. the endplate depolarization by the released acetylcholine is called an endplate potential (epp). the epp is accomplished when ach binds the nicotinic acetylcholine receptors (nachr) at the motor end plate, and causes an influx of sodium ions. this influx of sodium ions generates the epp (depolarization), and triggers an action potential which travels along the sarcolemma and into the muscle fiber via the t-tubules (transverse tubules) by means of voltage-gated sodium channels. the conduction of action potentials along the t-tubules stimulates the opening of voltage-gated ca channels which are mechanically coupled to ca release channels in the sarcoplasmic reticulum. the ca then diffuses out of the sarcoplasmic reticulum to the myofibrils so it can stimulate contraction. the endplate potential is thus responsible for setting up an action potential in the muscle fiber which triggers muscle contraction. the transmission from nerve to muscle is so rapid because each quantum of acetylcholine reaches the endplate in millimolar concentrations, high enough to combine with a receptor with a low affinity, which then swiftly releases the bound transmitter.
neuromuscular junction
südhof started his independent research career in neuroscience since 1986 and open the field of molecular neuroscience for synaptic transmission especially from the presynaptic nerve terminal perspective. until südhof began his work, majority of neuroscience research was aimed at the postsynaptic neuron and its role in learning and memory. indeed, thomas südhof is credited with discovering much of the machinery mediating neurotransmitter release and presynaptic plasticity in his 21 years at ut southwestern. südhof began with the discovery of synaptotagmins and their role in neurotransmitter release from the presynaptic neuron. synaptotagmin, a transmembrane protein found in neurosecretory vesicles, functions as a calcium sensor triggering vesicle fusion and neurotransmitter release. stimulation of a neuron results in an increase in intracellular calcium concentration. after binding calcium ion to a region in its cytosolic domain, vesicular synaptotagmin promotes quick or slow neurotransmitter release from the presynaptic neuron via interaction with regulatory and fusion related proteins such as members of the snare complex. südhof also discovered rims and muncs (most notably munc13 and munc18), soluble proteins which aid in the fusion of neurotransmitter vesicles to the nerve cell membrane and play an important role in synaptic plasticity. in addition, südhof's research uncovered the role of many other proteins facilitating vesicle binding, fusion, and resultant neurotransmitter release from the presynaptic neuron, including members of the snare complex: synaptobrevin, in the vesicular membrane, syntaxin, in the cell membrane, and snap25, which is tethered to the cytosolic side of the cell membrane via cysteine-linked palmitoyl chains and holds the complex of four helices together. südhof was also responsible for elucidating the action of tetanus and botulinum toxins, which selectively cleave synaptobrevin and snap25, respectively, inhibiting vesicle fusion with the presynaptic membrane.
thomas c. südhof