ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Presynaptic GABAB autoreceptor modulation of P/Q-type calcium channels and GABA release in rat suprachiasmatic nucleus neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Systematic review of drugs that modify the circadian system's phase-shifting responses to light exposure.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Pooled it
- Structural Basis of GABAAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Restoring GABAFrontiers in molecular neuroscience · 2024Article
- Cleomin Exerts Acute Antinociceptive Effects in Mice via GABAPharmaceuticals (Basel, Switzerland) · 2023Article
- ERK1/2-Dependent Phosphorylation of GABAInternational journal of molecular sciences · 2023Article
- Targeting the interaction of GABABrain pathology (Zurich, Switzerland) · 2023Article
- GABACurrent topics in behavioral neurosciences · 2022Review
- Protein phosphatase 2A regulation of GABAFrontiers in molecular neuroscience · 2022Article
- Targeting the Interaction of GABAFrontiers in pharmacology · 2022Article
- Diurnal properties of tonic and synaptic GABAJournal of neurophysiology · 2021Article
- Article
- Diurnal properties of voltage-gated CaThe Journal of physiology · 2020Article
- GABAThe Journal of physiology · 2019Article
- Enhanced Postsynaptic GABANeuroscience · 2018Article
- Safety Challenges of Using High Dose Baclofen for Alcohol Use Disorder: A Focused Review.Frontiers in psychiatry · 2018Review
- GABA transporters regulate tonic and synaptic GABAJournal of neurophysiology · 2017Article
- GABAPhysiological reports · 2017Article
- The dynamics of GABA signaling: Revelations from the circadian pacemaker in the suprachiasmatic nucleus.Frontiers in neuroendocrinology · 2017Review
- GABAB receptor-mediated frequency-dependent and circadian changes in synaptic plasticity modulate retinal input to the suprachiasmatic nucleus.The Journal of physiology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
GABA is the primary transmitter released by neurons of the suprachiasmatic nucleus (SCN), the circadian clock in the brain. Whereas GABAB receptor agonists exert a significant effect on circadian rhythms, the underlying mechanism by which GABAB receptors act in the SCN has remained a mystery. We found no GABAB receptor-mediated effect on slow potassium conductance, membrane potential, or input resistance in SCN neurons in vitro using whole-cell patch-clamp recording. In contrast, the GABAB receptor agonist baclofen (1-100 microM) exerted a large and dose-dependent inhibition (up to 100%) of evoked IPSCs. Baclofen reduced the frequency of spontaneous IPSCs but showed little effect on the frequency or amplitude of miniature IPSCs in the presence of tetrodotoxin. The activation of GABAB receptors did not modulate postsynaptic GABAA receptor responses. The depression of GABA release by GABAB autoreceptors appeared to be mediated primarily through a modulation of presynaptic calcium channels. The baclofen inhibition of both calcium currents and evoked IPSCs was greatly reduced (up to 100%) by the P/Q-type calcium channel blocker agatoxin IVB, suggesting that P/Q-type calcium channels are the major targets involved in the modulation of GABA release. To a lesser degree, N-type calcium channels were also involved. The inhibition of GABA release by baclofen was abolished by a pretreatment with pertussis toxin (PTX), whereas the inhibition of whole-cell calcium currents by baclofen was only partially depressed by PTX, suggesting that G-protein mechanisms involved in GABAB receptor modulation at the soma and axon terminal may not be identical. We conclude that GABAB receptor activation exerts a strong presynaptic inhibition of GABA release in SCN neurons, primarily by modulating P/Q-type calcium channels at axon terminals.
Indexed as
Identifiers
9465016PMC6792632W1893009693What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.