Calcium-independent release of amino acid neurotransmitters: Fact or artifact?

Bernáth, Sándor

doi:10.1016/0301-0082(92)90035-d

Cited by 175 publications

(69 citation statements)

References 452 publications

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“…K ϩ depolarization can stimulate GABA release from both nerve terminals and glial cells (Bernath, 1992). GABA release from glial cells is stimulated only when concentrations of K ϩ higher than 50 to 60 mM are used and not Ca 2ϩ -dependent (Bernath, 1992).…”

Section: Discussionmentioning

confidence: 99%

Cannabinoid Agonists Stimulate [³H]GABA Release in the Globus Pallidus of the Rat When G_iProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors

González¹,

Paz²,

Florán³

et al. 2008

J Pharmacol Exp Ther

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The motor effects of cannabinoids in the globus pallidus appear to be caused by increases in interstitial GABA. To elucidate the mechanism of this response, we investigated the effect of the selective cannabinoid type 1 receptor (CB1) cannabinoid agonist arachidonyl-2-chloroethylamide (ACEA) on [ 3 H]GABA release in slices of the rat globus pallidus. ACEA had two effects: concentrations between 10 Ϫ8 and 10 Ϫ6 M stimulated release, whereas higher concentrations (IC 50 Ϸ 10 Ϫ6 M) inhibited it. Another cannabinoid agonist, WIN-55,212-2, also had bimodal effects on release. Studies of cAMP production indicate that under conditions of low G i/o , availability the coupling of CB1 receptors with G i/o proteins can be changed into CB1:G s/olf coupling; therefore, we determined the effects of conditions that limit G i/o availability on (S)-5-aminosulfonyl-N-[(1-ethyl-2-pyrrolidinyl)methyl]-2-methoxybenzamidersqb]or depleting dopamine with reserpine inhibited the ACEA-induced stimulation of release. Thus, the D2 dependence of stimulation is consistent with the proposal that D2 receptors reduce G i/o proteins available for binding to the CB1 receptor. In summary, CB1 receptor activation has dual effects on GABA release in the globus pallidus. Low concentrations stimulate release through a process that depends on activation of dopamine D2 receptors that may limit G i/o protein availability. Higher concentrations of cannabinoid inhibit GABA release through mechanisms that are independent of D2 receptor activation.

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Section: Discussionmentioning

confidence: 99%

Cannabinoid Agonists Stimulate [³H]GABA Release in the Globus Pallidus of the Rat When G_iProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors

González¹,

Paz²,

Florán³

et al. 2008

J Pharmacol Exp Ther

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“…As to the overflows evoked by KCl, their sensitivity to TTX was inversely related to the depolarizing K + concentration: TTX inhibited by about 60% and 30%, respectively, the overflows of [ 3 H]glycine evoked by 15 and 20 mmol/L KCl. Although transmitter release elicited by K + depolarization from synaptosomes is generally considered to be TTXresistant (Tibbs et al 1989;Bernath 1992), exocytosis of [ 3 H]noradrenaline evoked by low KCl concentrations (9 and 12 mmol/L KCl) from rat hippocampal synaptosomes was strongly inhibited by TTX (Raiteri et al 1990). Thus, also in the light of the uncertainties still existing on the significance of glycinergic transmission in the hippocampus, the first important result of this work is that glycine can be exocytotically released from GLYT2-bearing nerve endings in this brain region.…”

Section: Discussionmentioning

confidence: 99%

“…Veratridine is often used as a releasing stimulus (see Bernath 1992). The alkaloid activates Na + channels in the plasma membrane of nerve endings causing massive entry of Na + ions followed by depolarization and opening of Ca 2+ channels.…”

Section: Discussionmentioning

confidence: 99%

Glycinergic nerve endings in hippocampus and spinal cord release glycine by different mechanisms in response to identical depolarizing stimuli

Luccini¹,

Romei²,

Raiteri³

2008

Journal of Neurochemistry

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Studies on hippocampal glycine release are extremely rare. We here investigated release from mouse hippocampus glycinergic terminals selectively pre‐labelled with [3H]glycine through transporters of the GLYT2 type. Purified synaptosomes were incubated with [3H]glycine in the presence of the GLYT1 blocker NFPS to abolish uptake (∼ 30%) through GLYT1. The non‐GLYT1‐mediated uptake was entirely sensitive to the GLYT2 blocker Org25543. Depolarization during superfusion with high‐K+ (15–50 mmol/L) provoked overflows totally dependent on external Ca2+, whereas in the spinal cord the 35 or 50 mmol/L KCl‐evoked overflow (higher than that in hippocampus) was only partly dependent on extraterminal Ca2+. In the hippocampus, the Ca2+‐dependent 4‐aminopyridine (1 mmol/L)‐evoked overflow was five‐fold lower than that in spinal cord. The component of the 10 μmol/L veratridine‐induced overflow dependent on external Ca2+ was higher in the hippocampus than that in spinal cord, although the total overflow in the hippocampus was only half of that in the spinal cord. Part of the veratridine‐evoked hippocampal overflow occurred by GLYT2 reversal and part by bafilomycin A1‐sensitive exocytosis dependent on cytosolic Ca2+ generated through the mitochondrial Na+/Ca2+ exchanger. As glycine sites on NMDA receptors are normally not saturated, understanding mechanisms of glycine release should facilitate pharmacological modulation of NMDA receptor function.

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“…Part of this effect may be clue to interactions of NMDA with the high-affinity glutamate uptake-carrier and reduced glutamate uptake. It remains to be determined whether such mechanisms are physiologically relevant (see Erecinska, 1987;Bernath, 1992). Furthermore, receptor-activated Ca: + mobilization from internal stores may in principle induce transmitter release directly.…”

Section: The Impact Of Presynaptic Receptor Activation On the Stimulumentioning

confidence: 99%

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

Verhage

Ghijsen

Silva

1994

Progress in Neurobiology

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Calcium-independent release of amino acid neurotransmitters: Fact or artifact?

Cited by 175 publications

References 452 publications

Cannabinoid Agonists Stimulate [³H]GABA Release in the Globus Pallidus of the Rat When G_iProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors

Cannabinoid Agonists Stimulate [³H]GABA Release in the Globus Pallidus of the Rat When G_iProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors

Glycinergic nerve endings in hippocampus and spinal cord release glycine by different mechanisms in response to identical depolarizing stimuli

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

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Calcium-independent release of amino acid neurotransmitters: Fact or artifact?

Cited by 175 publications

References 452 publications

Cannabinoid Agonists Stimulate [3H]GABA Release in the Globus Pallidus of the Rat When GiProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors

Cannabinoid Agonists Stimulate [3H]GABA Release in the Globus Pallidus of the Rat When GiProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors

Glycinergic nerve endings in hippocampus and spinal cord release glycine by different mechanisms in response to identical depolarizing stimuli

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

Contact Info

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Cannabinoid Agonists Stimulate [³H]GABA Release in the Globus Pallidus of the Rat When G_iProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors

Cannabinoid Agonists Stimulate [³H]GABA Release in the Globus Pallidus of the Rat When G_iProtein-Receptor Coupling Is Restricted: Role of Dopamine D2 Receptors