Presynaptic modulation of the release of GABA by GABAA receptors in pars compacta and by GABAB receptors in pars reticulata of the rat substantia nigra

Florán, Benjamí­n; Silva, Isaac; Nava, Cesar; Aceves, Jorge

doi:10.1016/0014-2999(88)90008-8

Cited by 65 publications

(25 citation statements)

References 38 publications

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“…A large body of physiologic data suggests that GABA B receptors act as inhibitory autoreceptors on GABAergic neurons, regulating the release of GABA from their axon terminals (Floran et al, 1988;Giralt et al, 1990;Bonanno and Raiteri, 1992;Morishita and Sastry, 1995;Bonanno et al, 1997). However, we observed only low GABA B R1-LI in the regions that contain cell bodies or terminals of GABAergic projection neurons, where GABA B -mediated autoinhibitory effects of GABA have been reported (Floran et al, 1988;Giralt et al, 1990;Seabrook et al, 1991;Morishita and Sastry, 1995).…”

Section: Discussionmentioning

confidence: 37%

“…However, we observed only low GABA B R1-LI in the regions that contain cell bodies or terminals of GABAergic projection neurons, where GABA B -mediated autoinhibitory effects of GABA have been reported (Floran et al, 1988;Giralt et al, 1990;Seabrook et al, 1991;Morishita and Sastry, 1995). To investigate this question more thoroughly, we analyzed the coexpression pattern of GABA B R1 and of GAD (a marker of GABAergic cell bodies and terminals).…”

Section: Discussionmentioning

confidence: 82%

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Immunohistochemical localization of GABAB receptors in the rat central nervous system

et al. 1999

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Section: Discussionmentioning

confidence: 37%

Section: Discussionmentioning

confidence: 82%

Immunohistochemical localization of GABAB receptors in the rat central nervous system

et al. 1999

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“…Thus, GABA B receptors are in position to modulate the release of GABA, as shown in the rat striatum and SN (Wilson and Wilson, 1985;Floran et al, 1988;Giralt et al, 1990;Seabrook et al, 1991;Nisenbaum et al, 1992Nisenbaum et al, ,1993Hausser and Yung, 1994;Stanford and Lacey, 1996;Shen and Johnson, 1997;Chan et al, 1998;Chen et al, 1998;Giustizieri et al, 2005). Surprisingly, despite the strong presynaptic expression of GABA B receptors in GABAergic terminals in the GP (Chen et al, 2004), presynaptic modulation of GABA release does not appear to be mediated by GABA B receptors (Hashimoto and Kuriyama, 1997).…”

Section: Gaba B Receptorsmentioning

confidence: 99%

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

2006

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GABA and glutamate, the main transmitters in the basal ganglia, exert their effects through ionotropic and metabotropic receptors. The dynamic activation of these receptors in response to released neurotransmitter depends, among other factors, on their precise localization in relation to corresponding synapses. The use of high resolution quantitative electron microscope immunocytochemical techniques has provided in-depth description of the subcellular and subsynaptic localization of these receptors in the CNS. In this article, we review recent findings on the ultrastructural localization of GABA and glutamate receptors and transporters in the basal ganglia, at synaptic, extrasynaptic and presynaptic sites. The anatomical evidence supports numerous potential locations for receptor-neurotransmitter interactions, and raises important questions regarding mechanisms of activation and function of synaptic versus extrasynaptic receptors in the basal ganglia.

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“…Wilcox & Dichter, 1994). The presence of presynaptic GABAA receptors in the nervous system (Richards et al 1987;Floran et al 1988;Peng & Frank, 1989;Zhang & Jackson, 1993) suggests that cis-mission may exist in vivo as a form of immediate presynaptic signalling in the absence of any collateral or interneurone. The functional consequence of such self-signalling in GABAergic neurones will depend on the Cl-ion gradient.…”

Section: Discussionmentioning

confidence: 99%

“…All of these results suggest the presence of autaptic contacts in cultured hippocampal neurones. However, since it has been demonstrated that GABAA receptors are present on presynaptic terminals in different parts of the brain (Floran, Silva, Nava & Aceves, 1988;Zhang & Jackson, 1993) indirect immunocytofluorescence using methods established previously (Schaffner, Behar, Nadi & Barker, 1993 and, at -80 mV, had a decay that could be fitted satisfactorily by an exponential with a time constant > 20 ms, which became longer at more positive holding potentials (see Fig. 5Ba and Bb).…”

mentioning

confidence: 99%

Fast presynaptic GABAA receptor‐mediated Cl‐ conductance in cultured rat hippocampal neurones.

Vautrin

Schaffner

Barker

1994

The Journal of Physiology

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1. Hippocampal neurones cultured from the 18-day-old embryonic rat for 3 days to 3 weeks were recorded with Cl--filled patch pipettes. Spontaneous synaptic currents, which reversed at the equilibrium potential for Cl-ions (Ec1) and were blocked by the GABAA (y-aminobutyric acid) receptor antagonists bicuculline or picrotoxin, were recorded in every culture. At 25°C and -80 mV they decayed with a time constant > 20 ms that invariably increased at positive potentials. After 2 weeks, 50-75% of all neurones were GABA immunoreactive. 2. In pairs-recordings, coincident synaptic currents in both cells were either spontaneous or evoked by stimulation of one cell. In the presence of tetrodotoxin and using pipettes containing lidocaine (lignocaine) N-ethyl bromide, coincident spontaneous Cl-transients still occurred in both neurones far more frequently than expected by chance. 3. Holding the potential of one neurone at a positive value reversed the synaptic transients in that cell and, in half of the cells, increased the frequency of coincident events in both cells. 4. In neurones where depolarization increased the frequency of coinciding events and all regenerative current apparent at the soma was abolished, short depolarizing pulses occasionally evoked all-or-none, pre-and postsynaptic currents with matching transmission failures and identical delays in transmission. 5. The results suggest that the same pulse of GABA simultaneously activates GABAA receptor-coupled Cl-channels on both sides of the same synaptic cleft, producing immediate auto-transmission in the absence of collaterals or interneurones.

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Presynaptic modulation of the release of GABA by GABAA receptors in pars compacta and by GABAB receptors in pars reticulata of the rat substantia nigra

Cited by 65 publications

References 38 publications

Immunohistochemical localization of GABAB receptors in the rat central nervous system

Immunohistochemical localization of GABAB receptors in the rat central nervous system

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

Fast presynaptic GABAA receptor‐mediated Cl‐ conductance in cultured rat hippocampal neurones.

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