Presynaptic regulation of neurotransmitter release in the brain: Facts and hypothesis

Chesselet, M.-F.

doi:10.1016/0306-4522(84)90058-7

Cited by 564 publications

(174 citation statements)

References 295 publications

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“…Furthermore, receptor-activated Ca: + mobilization from internal stores may in principle induce transmitter release directly. Several presynaptic receptors couple to phospholipase C activation, such as acetylcholine receptors of the muscarinic type (see for instance, Raiteri, 1982;Diamant et al, 1988), 5-HT (Kaczmarek and Levitan, 1987;Delaney et al, 1991), several neuropeptide receptors such as CGRP (Oku et al, 1988), galanin (Martire et al, 1991), vasoactive intestinal polypeptide (see for a review, Chesselet, 1984) and a recently characterized member of glutamate receptors, the metabotrope, tACPD sensitive receptor (Baskys and Malenka, 1991;Calabresi et al, 1992;Rainnie and Shinnick-Gallanger, 1992). As discussed in Section 2, there is already relatively little information as to the potency of presynaptic internal Ca :+ stores.…”

Section: The Impact Of Presynaptic Receptor Activation On the Stimulumentioning

confidence: 99%

“…Inhibition of the presynaptic stimulus-secretion coupling by presynaptic receptor activation may be more general than potentiation (see Chesselet, 1984). A well known mechanism of presynaptic inhibition is the activation of presynaptic GABA-receptors and their modulation of ionic balance by ligand-gated ion channels.…”

Section: The Impact Of Presynaptic Receptor Activation On the Stimulumentioning

confidence: 99%

“…Effectively, the voltage dependence of the Ca 2 + channels and thus of the triggering of transmitter release, is shifted to more depolarized potentials. Many other presynaptic receptors have been described to mediate inhibition of the presynaptic stimulus-secretion coupling (see Chesselet, 1984), such as ~2-adrenergic receptors (see for instance, Starke, 1977;Maura et al, 1982), adenosine A,-receptors (Prince and Stevens, 1992;Barrie and Nicholls, 1993), opioid receptors (see for instance, Hagan and Hughes, 1984;McWilliam and Campbell, 1987). For these receptors the most likely targets are presynaptic K + channels and Ca 2 + channels, either via G proteins or through intracellular messengers.…”

Section: The Impact Of Presynaptic Receptor Activation On the Stimulumentioning

confidence: 99%

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Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Verhage

Ghijsen

Silva

1994

Progress in Neurobiology

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Section: The Impact Of Presynaptic Receptor Activation On the Stimulumentioning

confidence: 99%

Section: The Impact Of Presynaptic Receptor Activation On the Stimulumentioning

confidence: 99%

Section: The Impact Of Presynaptic Receptor Activation On the Stimulumentioning

confidence: 99%

See 1 more Smart Citation

Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Verhage

Ghijsen

Silva

1994

Progress in Neurobiology

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“…Reconciling these data with the heteroexchange hypothesis of ascorbate release requires an understanding of the somewhat unique effects of stimulating terminal glutamate receptors. Thus, unlike striatal dopamine terminal receptors, which attenuate dopamine synthesis and release (Chesselet, 1984;Drukarch and Stoof, 1990), terminal NMDA and non-NMDA glutamate receptors actually facilitate glutamate release (Ferkany et al, 1982;Collins et al, 1983;Ferkany and Coyle, 1983), while increasing glutamate terminal excitability (Garcia-Munoz et al, 199 1, 1992). This presynaptic positive feedback mechanism has been suggested to contribute to glutamate-induced neurotoxicity as well as the induction of long-term potentiation (Biziere and Coyle, 1978;Garcia-Munoz et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Intraneostriatal administration of glutamate antagonists increases behavioral activation and decreases neostriatal ascorbate via nondopaminergic mechanisms

Pierce

Rebec

1993

J. Neurosci.

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Behavioral findings suggest that the effects of neostriatal glutamate and ascorbate are opposed to those of neostriatal dopamine.Recent evidence also indicates that glutamate and ascorbate are linked via a carrier-mediated heteroexchange process, suggesting that ascorbate may act through the glutamate system to influence behavior. In order to assess glutamate-ascorbate interactions and their influence on the behavioral output of the basal ganglia, glutamate and homocysteic acid (a glutamate reuptake blocker) as well as NMDA antagonists were infused into the neostriatum of freely moving rats while extracellular neostriatal ascorbate was monitored via electrochemically modified carbon-fiber electrodes. Neostriatal 3,4-dihydroxyphenylacetic acid (DO-PAC), a major dopamine metabolite, also was recorded in order to assess the dependency of any drug effect on the nigrostriatal dopamine system. lntraneostriatal infusions of L-glutamate (1 pg/pl), but not L-homocysteic acid (30 rglpl), elevated extracellular neostriatal ascorbate levels. Neither of these drugs had any effect on neostriatal DOPAC or overt behavioral activity. lntraneostriatal infusion of the noncompetitive NMDA antagonist dirocilpine (MK-801; 3 pg/pl) or the competitive NMDA antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1 -phosphonene (CPPene; 5 rg/Al) decreased neostriatal ascorbate but had no effect on neostriatal DO-PAC. Both dizocilpine and CPPene activated behavior in intact and sham-lesioned animals as well as in animals with near-total depletions of neostriatal dopamine following a 6-hydroxydopamine lesion. When administered systemically, however, dizocilpine (1 .O mg/kg) significantly increased neostriatal DOPAC. This effect appears to be regulated via midbrain NMDA receptors, in that this effect was completely abolished by electrolytic lesions of the substantia nigra pars reticulata. In addition, systemic dizocilpine substantially lowered the level of extracellular ascorbate (in both intact/sham and substantia nigra-lesioned animals), but subsequent intraneostriatal infusions of glutamate increased ascorbate levels to the'same extent as that observed in undrugged animals.Taken together, these results suggest that neostriatal NMDA receptors regulate basal, but not glutamate-stimulat-

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“…Since lesions of the LC partially denervate the medial habenulae (Kobayashi et al, 1975) it is conceivable that a transynaptic effect could alter the synthesis of P,-binding sites. It has also been suggested that neurotransmitters can act at a distance (Chesselet, 1984;Schmitt, 1984;Herkenham, 1987), which could explain the frequent occurrence of apparent mismatches between binding sites and afferent distribution in the CNS. Changes in the density of @,-binding sites in the lateral subnuclei could therefore indicate a humoral regulation by NE diffusing to this area.…”

Section: Discussionmentioning

confidence: 99%

Beta 1- and beta 2-adrenergic 125I-pindolol binding sites in the interpeduncular nucleus of the rat: normal distribution and the effects of deafferentation

1989

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The plasticity of the beta 1- and beta 2-adrenergic receptor subtypes was examined in the interpeduncular nucleus (IPN) of the adult rat. The beta-adrenergic receptor antagonist 125I-pindolol (125I-PIN) was used in conjunction with the selective subtype antagonists ICI 118,551 and ICI 89,406 to determine the subnuclear distribution of beta 1- and beta 2-adrenergic receptors in this nucleus and to correlate the receptor distribution with the distribution of both noradrenergic afferents from the locus coeruleus (LC) and non-noradrenergic afferents from the fasiculus retroflexus (FR). The density of these binding sites was examined following lesions that decreased (LC lesions) or increased (FR lesions) the density of the noradrenergic projection in the IPN. Quantitative radioautography indicated that beta 1-labeled binding sites account for the larger percentage of binding sites in the IPN. The beta 1-binding sites are densest in the those subnuclei that receive a noradrenergic projection from the LC: the central, rostral, and intermediate subnuclei. beta 1-binding sites are algo homogeneously distributed throughout the lateral subnuclei, where there is no detectable noradrenergic innervation. beta 2-binding sites have a more restricted distribution. They are concentrated in the ventral half of the lateral subnuclei, where they account for 70% of total 125I-PIN binding sites. beta 2-binding sites are also present along the ventral border of the IPN. Some of this labeling extends into the central and intermediate subnuclei. Bilateral lesions of the LC, which selectively remove noradrenergic innervation to the IPN, result in an increase in the beta 1-binding sites. Bilateral lesions of the FR, which remove the major cholinergic and peptidergic input from the IPN, elicit an increase in noradrenergic projections and a decrease in beta 1-binding sites. beta 1-binding sites thus exhibit both up-regulation and down- regulation which is correlated with the density of the noradrenergic projection. Our results suggest, therefore, that the density of beta 1- binding sites is regulated by noradrenergic input. beta 2-binding sites increase in density in response to both the LC and FR lesions, suggesting that they are postsynaptic to both of these afferents. The distribution suggests that some of these binding sites may reflect binding to glial cells. The beta 2-binding sites may therefore be regulated by both noradrenergic and non-noradrenergic mechanisms.

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Presynaptic regulation of neurotransmitter release in the brain: Facts and hypothesis

Cited by 564 publications

References 295 publications

Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Intraneostriatal administration of glutamate antagonists increases behavioral activation and decreases neostriatal ascorbate via nondopaminergic mechanisms

Beta 1- and beta 2-adrenergic 125I-pindolol binding sites in the interpeduncular nucleus of the rat: normal distribution and the effects of deafferentation

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