Calcineurin is required for TRPV1-induced long-term depression of hippocampal interneurons

Jensen, Tyron; Edwards, Jeffrey G.

doi:10.1016/j.neulet.2012.01.006

Cited by 21 publications

(11 citation statements)

References 29 publications

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“…These findings are likely to have relevance beyond the leech CNS given the similarities that we have already documented with eCB-LTD in mammals, including the involvement of presynaptic TRPV-like receptors, presynaptic activation of calcineurin, postsynaptic eCB synthesis and pre-and postsynaptic increases in intracellular Ca 2+ (Gibson et al, 2008; Yuan and Burrell, 2010; Jensen and Edwards, 2012; Yuan and Burrell, 2012). The ability to record from identifiable synapses in the leech CNS and manipulate signaling pathways in individual neurons is a powerful tool to identify critical cellular processes during synaptic plasticity and determine whether they operate pre- or postsynaptically.…”

Section: Discussionsupporting

confidence: 63%

“…For example, homer 2a is known to play an important role in regulating DAG lipase activity related to eCB-dependent synaptic plasticity (Jung et al, 2007; Roloff et al, 2010). In the case of the presynaptic neuron, translation-dependent processes may be related to proteins that directly regulate neurotransmitter release (Chevaleyre et al, 2006) or to up-stream molecules, such as calcineurin, that are known to be active in the presynaptic neuron during both CB1- and TRPV-mediated ecLTD (Heifets and Castillo, 2009; Jensen and Edwards, 2012; Yuan and Burrell, 2012). …”

Section: Discussionmentioning

confidence: 99%

“…However, recent studies have found that transient receptor potential vanilloid (TRPV) channels can also modulate endocannabinoid-mediated depression in the mammalian hippocampus, superior colliculus, nucleus accumbens, and in the leech nervous system (Di Marzo et al, 2001; Gibson et al, 2008; Maione et al, 2009; Toth et al, 2009; Chavez et al, 2010; Grueter et al, 2010; Yuan and Burrell, 2010; Li and Burrell, 2011; Yuan and Burrell, 2012). Although presynaptic (Gibson et al, 2008; Maione et al, 2009; Yuan and Burrell, 2010) and postsynaptic TRPV receptors (Chavez et al, 2010; Grueter et al, 2010) have been observed to mediate eCB-LTD, increased intracellular Ca 2+ and activation of calcineurin appear to be required in both instances (Chavez et al, 2010; Jensen and Edwards, 2012; Yuan and Burrell, 2012). …”

Section: Introductionmentioning

confidence: 99%

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Endocannabinoid-Dependent Long-Term Depression in a Nociceptive Synapse Requires Coordinated Presynaptic and Postsynaptic Transcription and Translation

Yuan

Burrell

2013

J. Neurosci.

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Endocannabinoids (eCBs) play an important role in long-term regulation of synaptic signaling in both vertebrates and invertebrates. In this study, the role of transcription- and translation-dependent processes in pre- versus post-synaptic neurons was examined during eCB-mediated synaptic plasticity in the central nervous system (CNS) of the leech. Low frequency stimulation (LFS) of non-nociceptive afferents elicits eCB-dependent long-term depression (eCB-LTD) heterosynaptically in nociceptive synapses that lasts at least 2 hrs. Bath application of emetine, a protein synthesis inhibitor, blocked eCB-LTD following afferent LFS or exogenous eCB application, indicating that this depression was translation-dependent. Bath application of actinomycin D, an irreversible RNA synthesis inhibitor, or DRB, a reversible RNA synthesis inhibitor, also prevented eCB-LTD. Selective injection of DRB or emetine into the pre- or postsynaptic neuron prior to LFS indicated that eCB-LTD required transcription/translation in the postsynaptic neuron, but only translation in the presynaptic cell. Depression observed immediately following LFS was also blocked when these transcription- and translation-dependent processes were inhibited. It is proposed that induction of eCB-LTD in this nociceptive synapse requires the coordination of presynaptic protein synthesis and postsynaptic mRNA and protein synthesis. These findings provide significant insights into both eCB-based synaptic plasticity and understanding how activity in non-nociceptive afferents modulates nociceptive pathways.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Endocannabinoid-Dependent Long-Term Depression in a Nociceptive Synapse Requires Coordinated Presynaptic and Postsynaptic Transcription and Translation

Yuan

Burrell

2013

J. Neurosci.

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“…Besides LTP, LTD is another important form of synaptic plasticity in the central nervous system [ 70 , 71 ]. Accumulating evidence has been presented to support the involvement of TRPV1 in various forms of LTD in the brain [ 24 - 26 , 32 , 33 ]. Our previous work has mapped the spatiotemporal properties of LTD in the ACC of adult mice [ 63 ].…”

Section: Resultsmentioning

confidence: 99%

“…In addition to LTP, evidence has also been provided to support the involvement of TPRV1 in various forms of LTD induction in the brain (Table 2 ). For example, TRPV1 can mediate a presynaptic form of LTD at glutamatergic synapses on hippocampal GABAergic interneurons, as revealed by both pharmacological and genetic approaches in both rats and mice [ 23 , 24 , 32 ]. On the other hand, treatment with TRPV1 agonists suppressed low-frequency stimulation-evoked LTD as well as (RS)-3,5-dihydroxyphenyl-glycine-induced acute depression in the CA1 region [ 22 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

No requirement of TRPV1 in long-term potentiation or long-term depression in the anterior cingulate cortex

Liu

Zhuo

2014

Molecular Brain

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One major interest in the study of transient receptor potential vanilloid type 1 (TRPV1) in sensory system is that it may serve as a drug target for treating chronic pain. While the roles of TRPV1 in peripheral nociception and sensitization have been well documented, less is known about its contribution to pain-related cortical plasticity. Here, we used 64 multi-electrode array recording to examine the potential role of TRPV1 in two major forms of synaptic plasticity, long-term potentiation (LTP) and long-term depression (LTD), in the anterior cingulate cortex (ACC). We found that pharmacological blockade of TRPV1 with either [(E)-3-(4-t-Butylphenyl)-N-(2,3-dihydrobenzo[b][1,4]dioxin-6-yl)acrylamide] (AMG9810, 10 μM) or N-(3-methoxyphenyl)-4-chlorocinnamide (SB366791, 20 μM) failed to affect LTP induced by strong theta burst stimulation in the ACC of adult mice. Similarly, neither AMG9810 nor SB366791 blocked the cingulate LTD induced by low-frequency stimulation. Analysis of the results from different layers of the ACC obtained the same conclusions. Spatial distribution of LTP or LTD-showing channels among the ACC network was also unaltered by the TRPV1 antagonists. Since cortical LTP and LTD in the ACC play critical roles in chronic pain triggered by inflammation or nerve injury, our findings suggest that TRPV1 may not be a viable target for treating chronic pain, especially at the cortical level.

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TRPV1 in the Central Nervous System: Synaptic Plasticity, Function, and Pharmacological Implications

Edwards

2014

Capsaicin as a Therapeutic Molecule

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Calcineurin is required for TRPV1-induced long-term depression of hippocampal interneurons

Cited by 21 publications

References 29 publications

Endocannabinoid-Dependent Long-Term Depression in a Nociceptive Synapse Requires Coordinated Presynaptic and Postsynaptic Transcription and Translation

Endocannabinoid-Dependent Long-Term Depression in a Nociceptive Synapse Requires Coordinated Presynaptic and Postsynaptic Transcription and Translation

No requirement of TRPV1 in long-term potentiation or long-term depression in the anterior cingulate cortex

TRPV1 in the Central Nervous System: Synaptic Plasticity, Function, and Pharmacological Implications

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