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Related to synaptic cleft: postsynaptic membrane
See: rift, split
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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.
When a nerve impulse reaches the end of the motor neuron, ACh is released from the presynaptic nerve ending into the synaptic cleft.
The gap between the neuron and the hair cell is the synaptic cleft (see Figs.
Here, for example, insult A targets the vesicular monoamine transporter in which DA is stored; insult B attacks the enzyme converting tyrosine to DOPA (3,4-dihydroxyphenylalanine) and thus the DA metabolic pathway; insult C strikes the metabolism of DOPAC (3,4-dihydroxyphenylacetic acid) to HVA (bomovanillic acid); and insult D hits the DA transporter that takes DA back up from the synaptic cleft postrelease.