DAT is an integral membrane protein that removes dopamine from the synaptic cleft and deposits it into surrounding cells, thus terminating the signal of the neurotransmitter.
42.
The phosphate groups and protons form a pH buffer with a pKa of 7.2, which keeps the pH in the synaptic cleft relatively acidic.
43.
During neurosecretion / exocytosis, SNAREs play a crucial role in vesicle docking, priming, fusion, and synchronization of neurotransmitter release into the synaptic cleft.
44.
Neurotransmitters are removed from the synaptic cleft by either enzymatic degradation or re-uptake by the same presynaptic neuron, via endocytosis or specific neurotransmitter transporters.
45.
SERT, results in increased concentration of neurotransmitters, e . g . 5-HT, in the synaptic cleft, leading to improvement of depression symptoms
46.
In neurons, transporter reversal facilitates the release of neurotransmitters into the synaptic cleft, which subsequently increases the binding of these neurotransmitters at their associated neurotransmitter receptors.
47.
These neurotransmitters are released into the synaptic cleft to bind onto the receptors of the postsynaptic membrane and influence another cell, either in an inhibitory or excitatory way.
48.
MDMA activity at VMAT2 moves neurotransmitters out from synaptic vesicles and into the cytosol; MDMA activity at TAAR1 moves neurotransmitters out of the cytosol and into the synaptic cleft.
49.
They allow endogenously released acetylcholine more time to interact with its respective receptor before being inactivated by acetylcholinesterase in the synaptic cleft ( the space between nerve and muscle ).
50.
Thus amphetamines actively increases the release of these neurotransmitters into the synaptic cleft . They may have a better side-effect profile than methylphenidate cardiovascularly and potentially better tolerated.
