Endogenous cannabinoid signaling at inhibitory interneurons

Younts, Thomas J.; Castillo, Pablo E.

doi:10.1016/j.conb.2013.12.006

Cited by 45 publications

(32 citation statements)

References 132 publications

(176 reference statements)

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“…In the hippocampus, where CB 1 receptors are predominantly expressed at inhibitory terminals (Freund et al, 2003), eCBs exert a profound effect on inhibition by reducing GABA release in a transient (Wilson and Nicoll, 2001) or long-lasting manner by triggering long-term depression (LTD) of inhibition (iLTD) (Chevaleyre and Castillo, 2003) (for a review, see Younts and Castillo, 2014). Disinhibition can robustly shift the excitatory-inhibitory balance in a network and by this means contribute to associative learning (Letzkus et al, 2015).…”

Section: Ecb Signaling At Hippocampal and Neocortical Synapsesmentioning

confidence: 99%

Synaptic functions of endocannabinoid signaling in health and disease

et al. 2017

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Endocannabinoids (eCBs) are a family of lipid molecules that act as key regulators of synaptic transmission and plasticity. They are synthetized “on demand” following physiological and/or pathological stimuli. Once released from postsynaptic neurons, eCBs typically act as retrograde messengers to activate presynaptic type 1 cannabinoid receptors (CB1) and induce short- or long-term depression of neurotransmitter release. Besides this canonical mechanism of action, recent findings have revealed a number of less conventional mechanisms by which eCBs regulate neural activity and synaptic function, suggesting that eCB-mediated plasticity is mechanistically more diverse than anticipated. These mechanisms include non-retrograde signaling, signaling via astrocytes, participation in long-term potentiation, and the involvement of mitochondrial CB1. Focusing on paradigmatic brain areas, such as hippocampus, striatum, and neocortex, we review typical and novel signaling mechanisms, and discuss the functional implications in normal brain function and brain diseases. In summary, eCB signaling may lead to different forms of synaptic plasticity through activation of a plethora of mechanisms, which provide further complexity to the functional consequences of eCB signaling.

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Section: Ecb Signaling At Hippocampal and Neocortical Synapsesmentioning

confidence: 99%

Synaptic functions of endocannabinoid signaling in health and disease

et al. 2017

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“…Late postnatal CPF also inhibits the endocannabinoid metabolizing enzymes FAAH and MAGL and increases endocannabinoid levels in the brain (Carr and others 2013; Carr and others 2011; Carr and others 2014). Since the endocannabinoid signaling is involved in central nervous system functions such as modulation of mood, learning and memory, neurogenesis, cell differentiation, cell migration, neuronal specification and synaptogenesis (Anavi-Goffer and Mulder 2009; Younts and Castillo 2014), more studies investigating CPF-mediated interference in this system during this and other periods of development are warranted. Some deleterious effects are smaller in magnitude when compared to earlier periods of exposure.…”

Section: Organophosphates (Ops)mentioning

confidence: 99%

Developmental neurotoxicity of succeeding generations of insecticides

Abreu‐Villaça

Levin

2017

Environment International

136

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Insecticides are by design toxic. They must be toxic to effectively kill target species of insects. Unfortunately, they also have off-target toxic effects that can harm other species, including humans. Developmental neurotoxicity is one of the most prominent off-target toxic risks of insecticides. Over the past seven decades several classes of insecticides have been developed, each with their own mechanisms of effect and toxic side effects. This review covers the developmental neurotoxicity of the succeeding generations of insecticides including organochlorines, organophosphates, pyrethroids, carbamates and neonicotinoids. The goal of new insecticide development is to more effectively kill target species with fewer toxic side effects on non-target species. From the experience with the developmental neurotoxicity caused by the generations of insecticides developed in the past advice is offered how to proceed with future insecticide development to decrease neurotoxic risk.

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“…; Lourenco et al . ; Younts and Castillo ) and varies as a result of the heterogeneity in the interneuron populations (Mendez and Bacci ). Homeostatic plasticity mechanisms and manipulation of neuronal activity have been shown to induce different types of presynaptic alterations in GABAergic synapses, including changes in neurotransmitter release probability (Kim and Ryan ), as well as in the loading of synaptic vesicles (De Gois et al .…”

Section: Plasticity Of Gabaergic Synapsesmentioning

confidence: 99%

“…Presynaptic plasticity is mainly associated with the modulation of GABA release (Pitler and Alger 1992;Mendez and Bacci 2011;Iremonger et al 2013;Lourenco et al 2014;Younts and Castillo 2014) and varies as a result of the heterogeneity in the interneuron populations (Mendez and Bacci 2011). Homeostatic plasticity mechanisms and manipulation of neuronal activity have been shown to induce different types of presynaptic alterations in GABAergic synapses, including changes in neurotransmitter release probability (Kim and Ryan 2010), as well as in the loading of synaptic vesicles (De Gois et al 2005;Hartman et al 2006;Lau and Murthy 2012) and in the protein levels of GAD65, the enzyme responsible for the production of GABA at the synapse (Peng et al 2010).…”

Section: Plasticity Of Gabaergic Synapsesmentioning

confidence: 99%

Role of GABA_AR trafficking in the plasticity of inhibitory synapses

Mele

Leal

Duarte

2016

Journal of Neurochemistry

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Neuronal excitability depends on the balance between inhibitory and excitatory neurotransmission, which in the CNS are mainly mediated by GABA and glutamate respectively. The plasticity of glutamatergic synapses and the underlying molecular mechanisms have been characterized to a large extent. In comparison, much less is known regarding the plasticity of GABAergic synapses, which is also important in the maintenance of the excitatory/inhibitory balance. GABAergic synapses, similarly to the glutamatergic synapses, adjust their strength depending on the pattern of neuronal activity. These alterations take place in the pre-and postsynaptic compartments, and short-and long-term alterations have been described. At the postsynaptic level the plasticity of inhibitory synapses is largely mediated by modulation of the expression, localization and function of GABA A receptors, by mechanisms involving the participation of scaffold proteins and structural molecules. This review is focused on the key mechanisms that regulate GABA A receptor trafficking in response to alterations in neuronal activity or to stimulation of plasma membrane receptors. These alterations in GABAergic neurotransmission are important in the refinement of the pattern of activity of neuronal networks.

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Endogenous cannabinoid signaling at inhibitory interneurons

Cited by 45 publications

References 132 publications

Synaptic functions of endocannabinoid signaling in health and disease

Synaptic functions of endocannabinoid signaling in health and disease

Developmental neurotoxicity of succeeding generations of insecticides

Role of GABA_AR trafficking in the plasticity of inhibitory synapses

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Endogenous cannabinoid signaling at inhibitory interneurons

Cited by 45 publications

References 132 publications

Synaptic functions of endocannabinoid signaling in health and disease

Synaptic functions of endocannabinoid signaling in health and disease

Developmental neurotoxicity of succeeding generations of insecticides

Role of GABAAR trafficking in the plasticity of inhibitory synapses

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Role of GABA_AR trafficking in the plasticity of inhibitory synapses