Presynaptic receptors definition

Presynaptic receptors for nonadrenomimetic substances (e.g., acetylcholine, adenosine) also have been found on the sympathetic presynaptic nerve ending. Their importance and role in the modulation of neurotransmission have not been definitively established. 

The majority of these compounds are agonists or partial agonists. Pure antagonists, devoid of any agonistic activity at presynaptic receptors (somatodendritic autoreceptors) or postsynaptic receptors were identified only very recently (for details of the definition of agonists, partial agonists and antagonists, see [6]). 

As previously noted, all currently available antidepressants enhance monoamine neurotransmission by one of several mechanisms. The most common mechanism is inhibition of the activity of SERT, NET, or both monoamine transporters (Table 30-2). Antidepressants that inhibit SERT, NET, or both include the SSRIs and SNRIs (by definition), and the TCAs. Another mechanism for increasing the availability of monoamines is inhibition of their enzymatic degradation (the MAOIs). Additional strategies for enhancing monoamine tone include binding presynaptic autoreceptors (mirtazapine) or specific postsynaptic receptors (5-HT antagonists and mirtazapine). Ultimately, the increased availability of monoamines for... 

Caveats include minor differences in size and shape from muscle to muscle, and fixation artifacts that can eliminate staining, especially presynaptically. In general, defects in the presynaptic terminal, such as partial retraction, are reflected less-precise definition in the postsynaptic receptors. 

Like presynaptic dopamine autoreceptors, presynaptic histamine autoreceptors are activated by the released endogenous transmitter to inhibit further histamine release, as shown by the increase in histamine release caused by antagonists at H3 receptors a definite piece of physiology. Evidence has been presented recently that cardiac postganglionic sympathetic neurons of the guinea pig synthesize and release histamine as a co-transmitter (Li et al. 2003 2006). These noradrenaline-histamine neurons possess H3 autoreceptors which, when activated, depress the release of both noradrenaline and histamine - unlike the D2-like autoreceptors of dopamine-neurotensin neurons which modulate the release of the two cotransmitters in opposite direction (see Section 2.2). It would be of interest to see whether, conversely, activation of ot2-autoreceptors inhibits the release of histamine in the guinea pig heart. 

Some authors faced with experimental data from functional studies that did not fulfilled the criteria of definition of Ii- or l2-receptors this was particularly the case in investigations concerning the possible role of pancreatic imidazoline receptors but it was also evoked with regard to sympathetic presynaptic imidazohne receptors. Such sites were provisionally named non-Il, non-l2 receptors [24,25]. 

NEUROTRANSMITTERS Transmitters may produce minimal effects on bioelectric properties, yet activate or inactivate biochemical mechanisms necessary for responses to other circuits. Alternatively, the action of a transmitter may vary with the context of ongoing synaptic events— enhancing excitation or inhibition, rather than operating to impose direct excitation or inhibition. Each chemical substance that fits within the broad definition of a transmitter may therefore require operational definition within the spatial and temporal domains of a specific ceU-ceU circuit. Those same properties may not necessarily be generalized to other cells contacted by the same presynaptic neurons differences in operation may relate to differences in postsynaptic receptors and the mechanisms by which an activated receptor produces its effects. 

Using CB, knockout animals, a study in hippocampal slices definitively showed that activation of the CB, receptor was responsible for the downstream inhibition of presynaptic VDCC in cells in which DSI was produced (Wilson et al., 2001). The investigators also showed that a specific subtype of GABAergic intemeuron is targeted by endocannabinoids. In this case, activation of CB, receptors led to the specific inhibition of N- but not P/Q- type calcium channels, and this resulted in decreased release of neurotransmitter. 

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