Neuron
ArticlePre- and postsynaptic GABAB receptors in the hippocampus have different pharmacological properties
References (27)
- et al.
Pertussis toxin blocks the outward currents evoked by opiate and α2-agonists in locus coeruleus neurons
Brain Res.
(1986) - et al.
Pre- and postsynaptic effects of baclofen in the rat hippocampal slice
Brain Res.
(1985) - et al.
Phaclofen, a peripheral and central baclofen antagonist
Brain Res.
(1987) - et al.
Baclofen selectively inhibits excitatory synaptic transmission in the hippocampus
Brain Res.
(1981) - et al.
Phorbol esters enhance transmitter release in rat hippocampal slices
Brain Res.
(1987) - et al.
A simpler chamber for recording from submeged brain slices
J. Neurosci. Meth.
(1981) Pertussis toxin blocks a late inhibitory postsynaptic potential in hippocampal CA3 neurons
Neurosci. Lett.
(1987)- et al.
A G-protein couples serotonin and GABAB receptors to the same channels in hippocampus
Science
(1986) - et al.
Baclofen selectively inhibits transmission at synapses made by axons of CA3 pyramidal cells in the hippocampal slice
J. Pharmacol. Exp. Ther.
(1982) - et al.
Protein kinase C regulates ionic conductance in hippocampal neurons: electrophysiological effects of phorbol esters
Phorbol esters induce transient internalization without degradation of unoccupied epidermal growth factor receptors
Actions and Interactions of GABA and Benzodiazepines
(-) Baclofen decreases neurotransmitter release in the mammalian CNS by an action at a novel GABA receptor
Nature
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The effect of GABA-B receptors in the basolateral amygdala on passive avoidance memory impairment induced by MK-801 in rats
2021, Behavioural Brain ResearchPresynaptic Excitation via GABA<inf>B</inf> Receptors in Habenula Cholinergic Neurons Regulates Fear Memory Expression
2016, CellCitation Excerpt :Thus, the habenulo-interpeduncular pathway can regulate both fear extinction and the overall fear response intensity. Because GABAB activity had been thought previously to produce only inhibitory responses (Chalifoux and Carter, 2011; Dutar and Nicoll, 1988a, 1988b; Gassmann and Bettler, 2012; Newberry and Nicoll, 1984), it at first appears counterintuitive that both the activity of habenula cholinergic neurons and the activity of GABAB receptors in their axonal terminals play similar behavioral roles. Our finding that GABAB mediates strong presynaptic excitation resolves this paradox.
Role of GABA<inf>B</inf> receptors in learning and memory and neurological disorders
2016, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Although we are far from understanding the full contribution of altered GABAergic signaling to these behaviors, diseases, and disorders, it is possible that some of the differences observed in the behavioral outcomes and across populations may be due to distinct populations of these receptors. Pre- and postsynaptic GABAB receptors in the CA1 (Dutar and Nicoll, 1988) and the somatosensory cortex (Deisz et al., 1993) in rats demonstrate different pharmacological properties. The function of the GABAB1 receptor isoforms may be different, as well (Kasten and Boehm, 2015).
Post-endocytotic deubiquitination and degradation of the metabotropic γ-aminobutyric acid receptor by the ubiquitin-specific protease 14
2016, Journal of Biological ChemistryCitation Excerpt :Whether USP family members act similarly on GABAB or other GPCRs also remains a largely unanswered question, although USP8 has been shown to promote CXCR4 trafficking and degradation (24). A role for PKC in the regulation of GABAB had been previously suggested, as PKC has been shown to phosphorylate GABAB (5) and down-regulate synaptic activity of the receptor (36). Although the role of PKC-mediated phosphorylation in GABAB ubiquitination remains to be investigated, phosphorylation of other substrates, such as the gap junction protein connexin-43 (42) and the organic anion transporter-1 (43) by PKC has been shown to promote their ubiquitination, resulting in their degradation and internalization, respectively.
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