GABA and glycine in synaptic vesicles: storage and transport characteristics

Burger, Peter; Hell, Johannes; Mehl, E.; Krasel, Cornelius; Lottspeich, Friedrich; Jahn, Reinhard

doi:10.1016/0896-6273(91)90267-4

Cited by 177 publications

(140 citation statements)

References 31 publications

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“…On the other hand, the finding that patch responses induced by low micromolar concentrations of GABA have a faster decay [Jones and Westbrook (1995) and this study] closer to that of the mIPSCs (see Table 1) could be consistent with the proposal that synaptic GABA transients occur in such a low range (Frerking et al, 1995). It should be noted, however, that the concentration of GABA in synaptic vesicles is high (Burger et al, 1991); therefore, its peak cleft concentration could reach the hundreds of micromolar to millimolar range.…”

Section: Comparison Between Mipscs and Patch Responses To Brief Pulsesupporting

confidence: 36%

Properties of GABA_AReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons

Galarreta

Hestrin

1997

J. Neurosci.

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Rapid applications of GABA (from 10 M to 10 mM) to outsideout patches were used to study the role that the kinetic properties of GABA A receptors play in determining the time course of IPSCs in neocortical pyramidal neurons. Currents induced by rapid applications of brief (1 msec) pulses of GABA (1 mM) showed a biexponential decay phase that seems to involve the entry of GABA A receptors into desensitized states. This conclusion is based on the similar fast decay kinetics of the response to brief and prolonged pulses of GABA and on the correlation between the degree of paired-pulse depression and the decay rate of the currents induced by brief pulses.Under nonequilibrium conditions we found that the concentration-response curve of pyramidal GABA A receptors has an EC 50 of 185 M (GABA pulse of 1 msec). The decay time course of the patch currents in response to brief applications of GABA was insensitive to agonist concentrations at the range from 50 M to 10 mM. Faster decay rates were observed only in response to pulses of 10 M GABA. These data are compatible with the suggestion that briefer openings derive from a monoliganded state and that these are negligible when receptor activation is Ͼ2%. Assuming that GABA transients at neocortical synapses are fast, a several millimolar GABA concentration would be needed to saturate the postsynaptic GABA A receptors.

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Section: Comparison Between Mipscs and Patch Responses To Brief Pulsesupporting

confidence: 36%

Properties of GABA_AReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons

Galarreta

Hestrin

1997

J. Neurosci.

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“…The machineries necessary for both synaptic and nonsynaptic GlyR-mediated transmission have been reported to be present in the hippocampus. In particular, synaptoneurosomes obtained from adult rat hippocampus contain glycine and release it by both vesicular and nonvesicular mechanisms (Burger et al, 1991;Engblom et al, 1996). Expression of ␤ heteromeric GlyRs in the developing hippocampus (Malosio et al, 1991;Chattipakorn and McMahon, 2002;Kondratskaya et al, 2004) indicate the synaptic location of GlyRs, because the ␤ subunit is required for receptor clustering (Kirsch et al, 1993;Meyer et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Glycine Receptors in CNS Neurons as a Target for Nonretrograde Action of Cannabinoids

Lozovaya

Yatsenko²,

Beketov³

et al. 2005

J. Neurosci.

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At many central synapses, endocannabinoids released by postsynaptic cells act retrogradely on presynaptic G-protein-coupled cannabinoid receptors to inhibit neurotransmitter release. Here, we demonstrate that cannabinoids may directly affect the functioning of inhibitory glycine receptor (GlyR) channels. In isolated hippocampal pyramidal and Purkinje cerebellar neurons, endogenous cannabinoids anandamide and 2-arachidonylglycerol, applied at physiological concentrations, inhibited the amplitude and altered the kinetics of rise time, desensitization, and deactivation of the glycine-activated current (I Gly ) in a concentration-dependent manner. These effects of cannabinoids were observed in the presence of cannabinoid CB1/CB3, vanilloid receptor 1 antagonists, and the G-protein inhibitor GDP␤S, suggesting a direct action of cannabinoids on GlyRs. The effect of cannabinoids on I Gly desensitization was strongly voltage dependent. We also demonstrate that, in the presence of a GABA A receptor antagonist, GlyRs may contribute to the generation of seizure-like activity induced by short bursts (seven stimuli) of high-frequency stimulation of inputs to hippocampal CA1 region, because this activity was diminished by selective GlyR antagonists (strychnine and ginkgolides B and J). The GlyR-mediated rhythmic activity was also reduced by cannabinoids (anandamide) in the presence of a CB1 receptor antagonist. These results suggest that the direct inhibition of GlyRs by endocannabinoids can modulate the hippocampal network activity.

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“…Eupergit C1Z methacrylate microbeads (1 mm diameter; Röhm Pharmaceuticals, Darmstadt, Germany) were blocked with glycine or conjugated with affinity-purified goat anti-rabbit-IgG antibodies (IgG; Sigma) as previously described (Burger et al, 1991;Fattorini et al, 2009). Affinity-purified anti-VGLUT1, -VGLUT2 and -VGAT antibodies (Synaptic Systems) were conjugated with the covalently bound secondary antibodies, generating IgG-coated anti-VGLUT1, anti-VGLUT2 or anti-VGAT beads.…”

Section: Synaptic Vesicle Immunoisolationmentioning

confidence: 99%

Presynaptic NMDA receptors: dynamics and distribution in developing axons in vitro and in vivo

Gill

Droubi

Giovedì

et al. 2014

Journal of Cell Science

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BSTRACTDuring cortical development, N-methyl-D-aspartate (NMDA) receptors (NMDARs) facilitate presynaptic terminal formation, enhance neurotransmitter release and are required in presynaptic neurons for spike-timing-dependent long-term depression (tLTD). However, the extent to which NMDARs are found within cortical presynaptic terminals has remained controversial, and the subsynaptic localization and dynamics of axonal NMDARs are unknown. Here, using live confocal imaging and biochemical purification of presynaptic membranes, we provide strong evidence that NMDARs localize to presynaptic terminals in vitro and in vivo in a developmentally regulated manner. The NR1 and NR2B subunits (also known as GRIN1 and GRIN2B, respectively) were found within the active zone membrane, where they could respond to synaptic glutamate release. Surprisingly, NR1 also appeared in glutamatergic and GABAergic synaptic vesicles. During synaptogenesis, NR1 was mobile throughout axons -including growth cones and filopodia, structures that are involved in synaptogenesis. Upon synaptogenic contact, NMDA receptors were quickly recruited to terminals by neuroligin-1 signaling. Unlike dendrites, the trafficking and distribution of axonal NR1 were insensitive to activity changes, including NMDA exposure, local glutamate uncaging or action potential blockade. These results support the idea that presynaptic NMDARs play an early role in presynaptic development.

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GABA and glycine in synaptic vesicles: storage and transport characteristics

Cited by 177 publications

References 31 publications

Properties of GABA_AReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons

Properties of GABA_AReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons

Glycine Receptors in CNS Neurons as a Target for Nonretrograde Action of Cannabinoids

Presynaptic NMDA receptors: dynamics and distribution in developing axons in vitro and in vivo

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GABA and glycine in synaptic vesicles: storage and transport characteristics

Cited by 177 publications

References 31 publications

Properties of GABAAReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons

Properties of GABAAReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons

Glycine Receptors in CNS Neurons as a Target for Nonretrograde Action of Cannabinoids

Presynaptic NMDA receptors: dynamics and distribution in developing axons in vitro and in vivo

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Properties of GABA_AReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons

Properties of GABA_AReceptors Underlying Inhibitory Synaptic Currents in Neocortical Pyramidal Neurons