cleft

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Related to synaptic cleft: postsynaptic membrane
See: rift, split
References in periodicals archive ?
For example, the treatment increased the number of synapses, the percentage of perforated synapses, the synaptic active zone length, the PSD thickness, and the synaptic curvature while narrowing the synaptic cleft and reducing the percentage of flat synapses.
A possible mechanism is that EA increases Th expression and decreases DAT expression, and upon neuronal excitation (action potential) DA is released into the synaptic cleft in brain.
Therefore, we conclude that neonatal propofol exposure alters the endogenous glutamate level in the synaptic cleft with TTX application.
As a whole, data show that the blockage of presynaptic [A.sub.2A] adenosine receptors by ZM241385 contributes more to recover the blockage of neuromuscular transmission produced by a non-depolarizing muscular relaxants exhibiting inhibitory acetylcholinesterase activity in their molecules when the level of acetylcholine in the synaptic cleft is not yet causing intense [M.sub.1]/[M.sub.2] muscarinic receptors activity on motor nerve terminal, i.e.
The amount of neurotransmitters terminating on these spines depends on their concentration in the synaptic cleft. If the concentration of neurotransmitters is high they can frequently bind with the receptors located on spine's surface to increase the potential and open more voltage controlled ion channels.
2) NO CLOUD FORMATION TO 10, 000 FOLD EFFECT: As a result of diffusion, NO cloud is formed at synaptic cleft. (1, 3) NO travels backward across a chemical synapse to bind to the axon terminal (NO receptor/sGC) of a presynaptic neuron for regulation of ANT this process is called as the retrograde neurotransmission (RNT).
Tricyclic antidepressants (TCA), monoamine oxidase inhibitors (MAOIs), selective serotonin reuptake inhibitors (SSRIs) and serotonin noradrenaline reuptake inhibitors (SNRIs) all increase the concentration of monoamine neurotransmitters in the synaptic cleft, with varying degrees of specificity.
SSRIs, as the name suggests, exert their effect mainly by blocking the reuptake of serotonin in neuronal synapse and increasing the level of serotonin in the synaptic cleft. Duloxetine and venlafaxine are serotonin-norepinephrine reuptake inhibitors (SNRIs), which can lead to increased concentration of both serotonin and norepinephrine in the synaptic cleft and potentiate their neuromodulatory effects.
When a nerve impulse reaches the end of the motor neuron, ACh is released from the presynaptic nerve ending into the synaptic cleft. Ach diffuses across the synaptic space and interacts with specific acetylcholine receptors on the postsynaptic muscle fiber membrane, resulting in a response by the muscle fiber.
In the photoreceptors of Loligo pealei, spine synapses were associated with a narrow 2-4-nm synaptic cleft, which suggests the possibility of electrical junctions (Cohen, 1973).
The gap between the neuron and the hair cell is the synaptic cleft (see Figs.
These neurotransmitters are then released into a gap called the synaptic cleft, where they relay their message by binding with receptors on the post-synaptic membrane of the neighboring cell.