Long-Term Plasticity of Endocannabinoid Signaling Induced by Developmental Febrile Seizures

Chen, Kang; Ratzliff, Anna; Hilgenberg, Lutz G.W.; Gulyás, Attila I.; Freund, Tamás F.; Smith, Martin A.; Dinh, T. P.; Piomelli, Daniele; Mackie, Ken; Soltész, Iván

doi:10.1016/s0896-6273(03)00499-9

Cited by 188 publications

(178 citation statements)

References 48 publications

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“…Independently of this issue, the take home message remains that, in the hippocampus, cannabinoidmediated retrograde inhibition appears to pertain mainly to GABAergic synapses . This is further illustrated by a recent report, showing that in an animal model of febrile seizures, DSI but not DSE is selectively enhanced through an increase in the expression of presynaptic CB1Rs on hippocampal, CCK-positive interneurons (Chen et al, 2003).…”

Section: Calcium Dependence Of Dsementioning

confidence: 74%

“…CB1R activation does not seem to affect mIPSCs (Hoffman & Lupica, 2000;Chen et al, 2003, but see later) and, likewise, hippocampal DSI was reported to affect 12 M.A. Diana & A. Marty DSI/DSE: two forms of CB1R-mediated plasticity mIPSCs frequency only minimally (Pitler & Alger, 1994).…”

Section: Hippocampal Dsi Involves the Regulation Of N-type Calcium Chmentioning

confidence: 85%

“…In slices, these values correspond to the inhibition obtained with saturating concentration of a cannabinoid exogenous agonist, showing that standard DSI induction protocols are able to saturate presynaptic CBIRs. The maximal inhibition for DSE is slightly smaller than DSI for the synapses between cerebellar parallel fibers and Purkinje cells , whereas it is markedly smaller for the DSE of climbing fibers to Purkinje cell synapses (Kreitzer & Regehr, 2001a; and for hippocampal DSE (Ohno-Shosaku et al, 2002b;Chen et al, 2003). These differences could arise from a reduced number of functional CB1Rs, from a distinct location of CB1Rs on presynaptic glutamatergic terminals with respect to the postsynaptic endcannabinoid release machinery, or from a different sensitivity (possibly associated to a different isoform, see later) of endocannabinoid receptors to endogenous agonists (Ohno-Shosaku et al, 2002b).…”

Section: Expression Mechanisms Of Dsi/dsementioning

confidence: 91%

“…In addition hippocampal DSI was soon shown to be absent in CB1R-deficient mice . In a short period of time, the endocannabinoid-and CB1R-related nature of DSI has been confirmed in the hippocampus and extended to several systems: for GABAergic synapses onto cerebellar Purkinje cells (Kreitzer & Regehr, 2001b;Diana et al, 2002;Yoshida et al, 2002;Figure 2a), cultured rat hippocampal neurons (Ohno-Shosaku et al, 2001), hippocampal dentate granule cells in particular pathological conditions (Chen et al, 2003), cortical pyramidal cells (Trettel & Levine, 2003) and neurons of the substantia nigra (Yanovsky et al, 2003).…”

Section: Dsi and Dsementioning

confidence: 93%

“…Finally, we already mentioned that in a novel animal model of human fever-induced seizures, CB1R expression is upregulated on CCK-positive GABAergic terminals (Chen et al, 2003); this induces a specific increase of DSI with respect to control animals, whereas DSE is not modified. This study opens the way for a role of DSI in pathological states.…”

Section: Functional Consequences Of the Specific Localization Of Cb1rmentioning

confidence: 97%

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Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Diana

Marty

2004

British J Pharmacology

235

177

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Depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE) are two related forms of short-term synaptic plasticity of GABAergic and glutamatergic transmission, respectively. They are induced by calcium concentration increases in postsynaptic cells and are mediated by the release of a retrograde messenger, which reversibly inhibits afferent synapses via presynaptic mechanisms. We review here:(1) The evidence accumulated during the 1990s that has led to the conclusion that DSI/DSE rely on retrograde signaling. (2) The more recent research that has led to the identification of endocannabinoids as the retrograde messengers responsible for DSI/DSE. (3) The possible mechanisms by which presynaptic type 1 cannabinoid receptors reduce synaptic efficacy during DSI/DSE. (4) The possible modes of induction of DSI/DSE by physiological activity patterns, and the partially conflicting evaluations of the calcium concentration increases required for cannabinoid synthesis. (5) Finally, the relation between DSI/DSE and other forms of long-and short-term synaptic inhibition, which were more recently associated with the production of endocannabinoids by postsynaptic cells.We conclude that recent studies on DSI/DSE have uncovered a specific and original mode of action for endocannabinoids in the brain, and that they have opened new avenues to understand the role of retrograde signaling in central synapses.

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Section: Calcium Dependence Of Dsementioning

confidence: 74%

Section: Hippocampal Dsi Involves the Regulation Of N-type Calcium Chmentioning

confidence: 85%

Section: Expression Mechanisms Of Dsi/dsementioning

confidence: 91%

Section: Dsi and Dsementioning

confidence: 93%

Section: Functional Consequences Of the Specific Localization Of Cb1rmentioning

confidence: 97%

See 3 more Smart Citations

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Diana

Marty

2004

British J Pharmacology

235

177

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Marijuana: Pharmacology and Interaction with the Endocannabinoid System

Wiley

Martin

2007

Handbook of Contemporary Neuropharmacology

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Marijuana is one of the most widely used illicit psychoactive substances in the U.S. Recently, negative perceptions of marijuana as an abused substance have been tempered somewhat by the idea that it may also have medicinal properties. Regardless of perception of marijuana, however, investigation of its active substituents and their mechanism of action led to the discovery of an endocannabinoid system that is activated by marijuana as well as by several endogenous cannabinoids, including anandamide and 2‐arachidonylglycerol. In this chapter, we review the pharmacology of marijuana and discuss how its interaction with the endocannabinoid system may have implications for understanding the physiology of this system.

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Initial loss but later excess of GABAergic synapses with dentate granule cells in a rat model of temporal lobe epilepsy

Thind

Yamawaki

Phanwar

et al. 2009

J of Comparative Neurology

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Many patients with temporal lobe epilepsy display neuron loss in the dentate gyrus. One potential epileptogenic mechanism is loss of GABAergic interneurons and inhibitory synapses with granule cells. Stereological techniques were used to estimate numbers of gephyrin-positive punctae in the dentate gyrus, which were reduced short-term (5 days after pilocarpine-induced status epilepticus) but later rebounded beyond controls in epileptic rats. Stereological techniques were used to estimate numbers of synapses in electron micrographs of serial sections processed for postembedding GABA-immunoreactivity. Adjacent sections were used to estimate numbers of granule cells and glutamic acid decarboxylase-positive neurons per dentate gyrus. GABAergic neurons were reduced to 70% of control levels short-term, where they remained in epileptic rats. Integrating synapse and cell counts yielded average numbers of GABAergic synapses per granule cell, which decreased short-term and rebounded in epileptic animals beyond control levels. Axo-shaft and axo-spinous GABAergic synapse numbers in the outer molecular layer changed most. These findings suggest interneuron loss initially reduces numbers of GABAergic synapses with granule cells, but later, synaptogenesis by surviving interneurons over-shoots control levels. In contrast, the average number of excitatory synapses per granule cell decreased short-term but recovered only toward control levels, although in epileptic rats excitatory synapses in the inner molecular layer were larger than in controls. These findings reveal a relative excess of GABAergic synapses and suggest that reports of reduced functional inhibitory synaptic input to granule cells in epilepsy might be attributable not to fewer but instead to abundant but dysfunctional GABAergic synapses.

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Long-Term Plasticity of Endocannabinoid Signaling Induced by Developmental Febrile Seizures

Cited by 188 publications

References 48 publications

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Marijuana: Pharmacology and Interaction with the Endocannabinoid System

Initial loss but later excess of GABAergic synapses with dentate granule cells in a rat model of temporal lobe epilepsy

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