ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Sustained elevation of dendritic calcium evokes widespread endocannabinoid release and suppression of synapses onto cerebellar Purkinje cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 67 citations in OpenAlex.
- From Classical to Alternative Pathways of 2-Arachidonoylglycerol Synthesis: AlterAGs at the Crossroad of Endocannabinoid and Lysophospholipid Signaling.Molecules (Basel, Switzerland) · 2024Review
- mGluR1 Regulates the Interspike Interval Threshold for Dendritic CaExperimental neurobiology · 2023Article
- α2δ-2 is required for depolarization-induced suppression of excitation in Purkinje cells.The Journal of physiology · 2022Article
- Complex spike clusters and false-positive rejection in a cerebellar supervised learning rule.The Journal of physiology · 2019Article
- STIM1 Regulates Somatic CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- The stochastic nature of action potential backpropagation in apical tuft dendrites.Journal of neurophysiology · 2017Article
- Protein purification and cloning of diacylglycerol lipase from rat brain.Journal of biochemistry · 2016Article
- Cerebellar endocannabinoids: retrograde signaling from purkinje cells.Cerebellum (London, England) · 2015Review
- Article
- Cannabinoid-dependent potentiation of inhibition at eye opening in mouse V1.Frontiers in cellular neuroscience · 2014Article
- CA1 pyramidal cell theta-burst firing triggers endocannabinoid-mediated long-term depression at both somatic and dendritic inhibitory synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Increased 20-HETE synthesis explains reduced cerebral blood flow but not impaired neurovascular coupling after cortical spreading depression in rat cerebral cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Intermediate conductance calcium-activated potassium channels modulate summation of parallel fiber input in cerebellar Purkinje cells.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Sustained firing of cartwheel cells in the dorsal cochlear nucleus evokes endocannabinoid release and retrograde suppression of parallel fiber synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Mechanisms underlying input-specific expression of endocannabinoid-mediated synaptic plasticity in the dorsal cochlear nucleus.Hearing research · 2011Article
- The Endocannabinoid System as Pharmacological Target Derived from Its CNS Role in Energy Homeostasis and Reward. Applications in Eating Disorders and Addiction.Pharmaceuticals (Basel, Switzerland) · 2011Review
- Calcium-dependent isoforms of protein kinase C mediate posttetanic potentiation at the calyx of Held.Neuron · 2011Article
- Purine receptor-mediated endocannabinoid production and retrograde synaptic signalling in the cerebellar cortex.British journal of pharmacology · 2011Article
- Homer 1a gates the induction mechanism for endocannabinoid-mediated synaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Endocannabinoids can act as retrograde messengers that allow postsynaptic cells to regulate the strength of their synaptic inputs. In the cerebellum, Purkinje cells (PCs) release endocannabinoids through two mechanisms. Synaptic activation evokes local endocannabinoid release that relies on a pathway that involves the metabotropic glutamate receptor mGluR1 and phospholipase-C (PLC). In contrast, depolarization evokes endocannabinoid release from the entire dendritic arbor. This leads to depolarization-induced suppression of inhibitory (DSI) and excitatory (DSE) synapses by a mechanism that does not involve mGluR1 or PLC. This latter mechanism of endocannabinoid release has only been observed under artificial conditions that transiently elevate postsynaptic calcium to >5 microm. Here, we tested the possibility that this mechanism could lead to retrograde inhibition in response to more realistic calcium signals. At both climbing fiber and inhibitory synapses onto PCs, we found that prolonging the elevation of calcium significantly lowered the peak calcium required to evoke PLC-independent endocannabinoid release. This suggests that the mechanism of endocannabinoid release involved in DSI and DSE is likely to evoke endocannabinoid release in response to physiologically relevant levels of calcium. When dendritic calcium was elevated to 0.4-1 microm for 15 s or more, endocannabinoid release from PCs selectively suppressed inhibitory synapses. This suggests that inhibitory synapses are more sensitive to prolonged calcium increases. Thus, in contrast to localized retrograde inhibition evoked by synaptic activation, modest but sustained calcium elevation could globally suppress inhibitory synapses onto PCs.
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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.