Receptor presynaptic

S. Kalsner and T. C. Westfall, eds., Presynaptic Receptors and the Question of Autoregulation of Meurotransmitter Release, Vol. 604, Annals of the New York Academy of Science, New York, 1990. 

Psychostimulants. Figure 2 Dopamine molecules have two different possible targets. Both ways are initially increased by DAT inhibition caused by methylphenidate pre- and postsynaptic dopamine receptors. Stimulation of postsynaptic receptors results in inhibition of presynaptic action potential generation. On the other hand, presynaptic receptor stimulation leads to a transmission inhibition of action potentials. Therefore, both mechanisms are responsible for a decrease in vesicular depletion of dopamine into the synaptic cleft (adapted from [2]). 

Fig. 8.3 Chemokines are neuromodulators. Some chemokines can be synthesized, as their own receptor, by the same neuron (a). A chemokine released by exocytosis can modulate the electrical activity of neurons after binding to its own presynaptic receptor (autoreceptor). Chemokines can also act on other neurons and glial cells (astrocytes and microgha) which express chemokine receptors (b). (Adapted from Rostene and Melik-Parsadaniantz, Pour la Science 2008, 369 66-72)...

A disadvantage of using synaptosomes is that they cannot be used to study transmitter release evoked by propagated nerve impulses, but the release, like that from intact neurons, is Ca +-dependent and K+-sensitive. Pharmacological studies using synaptosomes have also provided evidence that the amount of transmitter that is released following their depolarisation is regulated by the activation of presynaptic receptors. 

Evidence suggests that co-transmitters in a terminal have their own autoreceptors and, in some cases, activation of their own presynaptic receptor can influence the release of the co-stored, classical transmitter. For instance, activation of P2Y-autoreceptors by ATP is thought to affect the release of noradrenaline from sympathetic neurons. However, in other cases, feedback modulation of release of classical and their associated co-transmitters seems to have separate control mechanisms. This would suggest that either the two types of transmitter are concentrated in different nerve terminals or that mechanisms for regulating release target different vesicles located in different zones of the terminal (Burnstock 1990). 

Overall, it remains to be seen whether or not changes in the release of 5-HT in the terminal field parallel changes in the firing rate of neurons in the Raphe nuclei. Certainly the network of hetero- and presynaptic receptors, described above, could make it feasible to adjust 5-HT release in the terminal field despite the clock-like firing... 

Despite the paucity of nicotinic receptors in the brain there is considerable evidence that AzD is less common among smokers. Whether this is due to the action of inhaled nicotine is uncertain, but nicotine is known to stimulate presynaptic receptors on cholinergic nerve terminals which, unlike the muscarinic ones, result in increased ACh release. 

Langer, S.Z. Presynaptic receptors and their role in the regulation of transmitter release. Brit J Pharmacol 60 481-497, 1977. 

G0 was isolated as an other PTx-ribosylated G-protein which co-purifies with G, but which does not inhibit adenylate cyclase. There are two main isoforms (G0l and Go2), with additional splice-variants. G0 is particularly abundant in the nervous system, comprising up to 1% of membrane proteins. Its main function is to reduce the opening probability of those voltage-gated Ca2+ channels (N- and P/Q-type) involved in neurotransmitter release. Hence, it is largely responsible for the widespread auto-inhibition of transmitter secretion by presynaptic receptors and this effect is mediated through released py subunits. 

ACh regulates the cortical arousal characteristic of both REM sleep and wakefulness (Semba, 1991, 2000 Sarter Bruno, 1997, 2000). Medial regions of the pontine reticular formation (Figs. 5.2 and 5.7) contribute to regulating both the state of REM sleep and the trait of EEG activation. Within the medial pontine reticular formation, presynaptic cholinergic terminals (Fig. 5.1) that release ACh also are endowed with muscarinic cholinergic receptors (Roth et al, 1996). Autoreceptors are defined as presynaptic receptors that bind the neurotransmitter that is released from the presynaptic terminal (Kalsner, 1990). Autoreceptors provide feedback modulation of transmitter release. Autoreceptor activation... 

Fredholm, B. B. (1990b). Differential sensitivity to blockade by 4-aminopyridine of presynaptic receptors regulating [3H]acetylcholine release from rat hippocampus. J. Neurochem. 54 (4), 1386-90. 

Langer SZ (1997). 25 years since the discovery of presynaptic receptors Present knowledge and future perspectives. Trends in Pharmacological Sciences, 18, 95-99. 

Presynaptic receptor A receptor, either an autoreceptor or heteroreceptor, located on the presynaptic neuronal membrane which regulates the release of the neurotransmitter. 

Zahniser, N. R. and Doolen, S. Chronic and acute regulation of Na+/Cl"-dependent neurotransmitter transporters drugs, substrates, presynaptic receptors, and signaling systems. Pharmacol. Ther. 92 21-55, 2001. 

Histamine is stored within and released from neurons but a neuronal transporter for histamine has not been found. Newly synthesized neuronal histamine is transported into TM neuronal vesicles by the vesicular monoamine transporter VMAT2 [16]. Both in vivo and in vitro studies show that depolarization of nerve terminals activates the exocytotic release of histamine by a voltage- and calcium-dependent mechanism. Once released, histamine activates both postsynaptic and presynaptic receptors. Unlike the nerve terminals from other amine transmitters, however, histaminergic nerve terminals do not exhibit a high-affinity uptake system for histamine [5, 9, 23]. Astrocytes may contain a histamine transport system. 

Kainate receptors have recently been implicated in the induction of EIP in the mossy fibers (49,85). Unlike EIP in the area CA1, induction of mossy-fiber EIP is independent of NMDA-receptor activation and involves presynaptic mechanisms (105). Synaptic activation of the facilitatory presynaptic receptor can account for the role of KA receptors in the induction of mossy-fiber LIP by maintaining a high level of release during high-frequency transmission (77). Furthermore, following induction of LTP, the presynaptic kainate receptor-mediated facilitation of synaptic transmission is lost, suggesting that the mechanism by which presynaptic kainate receptors facilitate... 

Larsson, O. M., Falch, E., Schousboe, A., and Krogsgaard-Larsen, P. (1991) GABA uptake inhibitors Kinetics and molecular pharmacology, in Presynaptic Receptors, and Neuronal Transporters (Langer, S. Z., Galzin, A. M., and Costentin, J., eds.), Pergamon Press, Oxford, UK, pp. 197-200. 

McGehee DS, Heath MJ, Gelber S, Devay P, Role LW. (1995). Nicotine enhancement of fast excitatory synaptic transmission in CNS by presynaptic receptors. Science. 269(5231) 1692-96. 

Human HRS encoded by a gene, which consists of four exons on chromosome 20, was demonstrated in 1987 and cloned recently [17]. HRS has initially been identified in the central and peripheral nervous system as presynaptic receptors controlling the release of histamine and other neurotransmitters (dopamine, serotonin. 

The superfusion of isolated nerve terminals ( synaptosomes ) is a widely used technique for interrogating the pharmacological properties of presynaptic receptors and their biochemical mechanisms. Physiological buffer continuously flows over a layer of synaptosomes loaded with radiolabelled transmitter, such that released transmitter is removed in the perfusate and collected. A key feature of this methodology is that it eliminates transmitter crosstalk between different boutons, enabling presynaptic events to be studied in isolation (Raiteri and Raiteri 2000). 

HTjg and 5-HTjq receptors are structurally and functionally similar and act as inhibitory presynaptic receptors. S-HTjg receptors occur in most mammalian brains whereas 5-HTjq receptors are located in primates and the guinea pig brain. 

The central nervous actions of nicotine are thought to be mediated largely by presynaptic receptors that facilitate transmitter release from excitatory aminoacidergic (glutamatergic) nerve terminals in the cerebral cortex. Nicotine increases vigilance and the ability to concentrate. The effect reflects an enhanced readiness to perceive external stimuli (attentiveness) and to respond to them. 

Presynaptic a2A and a2c i aceptors can be distinguished functionally and may thus serve independent presynaptic functions. In mouse atria, the a2A subtype inhibited noradrenaline release at hi stimulation frequencies whereas the a2c-receptors operated at lower levels of sympathetic nerve stimulation (Hein et al. 1999). Moreover, inhibition of noradrenaline release mediated by the a2A-suhtype occurred much faster than inhibition by the a2c-receptor. These findings indicate that two presynaptic receptors in the inhibitory feedback loop of transmitter release may differentially regulate synaptic transmission. 

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