Presynaptic long-term depression mediated by Gi/o-coupled receptors

Atwood, Brady K.; Lovinger, David M.; Mathur, Brian N.

doi:10.1016/j.tins.2014.07.010

Cited by 100 publications

(113 citation statements)

References 120 publications

(145 reference statements)

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“…Like CB1-dependent LTD, several other forms of LTD are known to depend on activation of a presynaptically localized G i/o -coupled receptor (Atwood et al, 2014b). Given the known interactions between EtOH and the opioid system (Volpicelli et al, 1992;Drews and Zimmer, 2010), and that activation of these G i/o -coupled opioid receptors is capable of inducing striatal presynaptic LTD (Atwood et al, 2014a), we next assessed whether EtOH-LTD occurs in an opioid receptor-dependent fashion.…”

Section: Fsi-msn Etoh-ltd Is Dor Dependentmentioning

confidence: 99%

“…Naltrindole blocked EtOH-LTD at the FSI-MSN synapse (oIPSC amplitude = 97.65 ± 7.32% of baseline, t = 0.32, df = 7, p = 0.76, Figure 3c), and the EtOH effect in this condition differed from control EtOH-LTD (control EtOH-LTD oIPSC amplitude 66.67 ± 6.54%, t = 3.16, df = 14, p = 0.01). To determine if this form of LTD is labile or static (Atwood et al, 2014b), we applied naltrindole (1 μM) to slices 15 min after EtOH washout (Figure 3d). EtOH-LTD did not return to baseline in the presence of naltrindole, suggesting this form of LTD is static (oIPSC following EtOH application = 75.95 ±3.07% of baseline, t = 6.23, df = 5, p = 0.02; oIPSC in naltrindole = 63.58 ± 9.91% of baseline, t = 3.58, df = 5, p = 0.02).…”

Section: Fsi-msn Etoh-ltd Is Dor Dependentmentioning

confidence: 99%

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Ethanol Disinhibits Dorsolateral Striatal Medium Spiny Neurons Through Activation of A Presynaptic Delta Opioid Receptor

Patton

Roberts

Lovinger

et al. 2015

Neuropsychopharmacol

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The dorsolateral striatum mediates habit formation, which is expedited by exposure to alcohol. Across species, alcohol exposure disinhibits the DLS by dampening GABAergic transmission onto this structure's principal medium spiny projection neurons (MSNs), providing a potential mechanistic basis for habitual alcohol drinking. However, the molecular and circuit components underlying this disinhibition remain unknown. To examine this, we used a combination of whole-cell patch-clamp recordings and optogenetics to demonstrate that ethanol potently depresses both MSN-and fast-spiking interneuron (FSI)-MSN GABAergic synaptic transmission in the DLS. Concentrating on the powerfully inhibitory FSI-MSN synapse, we further show that acute exposure of ethanol (50 mM) to striatal slices activates delta opioid receptors that reside on FSI axon terminals and negatively couple to adenylyl cyclase to induce a long-term depression of GABA release onto both direct and indirect pathway MSNs. These findings elucidate a mechanism through which ethanol may globally disinhibit the DLS.

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Section: Fsi-msn Etoh-ltd Is Dor Dependentmentioning

confidence: 99%

Section: Fsi-msn Etoh-ltd Is Dor Dependentmentioning

confidence: 99%

Ethanol Disinhibits Dorsolateral Striatal Medium Spiny Neurons Through Activation of A Presynaptic Delta Opioid Receptor

Patton

Roberts

Lovinger

et al. 2015

Neuropsychopharmacol

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“…In most studies, the D2-R mediated inhibition of excitatory corticostriatal transmission has been characterized as long-term depression (LTD), a form of long-lasting activity dependent plasticity implicated in motor learning and adaptive motor responses (Andre et al, 2010; Atwood et al, 2014; Cepeda et al, 2001; Hsu et al, 1995; Maura et al, 1988). LTD at corticostriatal synapses requires co-activation of D2-Rs and group-1 metabotropic glutamate receptors (mGlu-R1), encompassing mGlu-R 1 and mGlu-R 5 subtypes.…”

Section: Introductionmentioning

confidence: 99%

Dopamine-dependent corticostriatal synaptic filtering regulates sensorimotor behavior

et al. 2015

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Summary Modulation of corticostriatal synaptic activity by dopamine is required for normal sensorimotor behaviors. After loss of nigrostriatal dopamine axons in Parkinson's disease, l-DOPA and dopamine D2-like receptor agonists are used as replacement therapy, although these drugs also trigger sensitized sensorimotor responses including dyskinesias and impulse control disorders. In mice, we lesioned dopamine projections to left dorsal striatum and assayed unilateral sensorimotor deficits with the corridor test as well as presynaptic corticostriatal activity with the synaptic vesicle probe, FM1-43. Sham-lesioned mice acquired food equivalently on both sides, while D2 receptor activation filtered the less active corticostriatal terminals, a response that required coincident co-activation of mGlu-R5 metabotropic glutamate and CB1 endocannabinoid receptors. Lesioned mice did not acquire food from their right, but overused that side following treatment with l-DOPA. Synaptic filtering on the lesioned side was abolished by either l-DOPA or a D2 receptor agonist, but when combined with a CB1 receptor antagonist, l-DOPA or D2 agonists normalized both synaptic filtering and behavior. Thus, high-pass filtering of corticostriatal synapses by the coordinated activation of D2, mGlu-R5, and CB1 receptors is required for normal sensorimotor response to environmental cues.

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“…Specifically, several of the components involved in the induction and expression of long-term plasticity have also been shown to play critical roles in short-term forms of plasticity such as paired pulse facilitation, and on the synaptic filters that they mediate (Atwood et al, 2014;Bouchard et al, 2003;De Pitta et al, 2011;Dittman et al, 2000;Emptage et al, 2001;Fioravante and Regehr, 2011;Fortune and Rose, 2001;Regehr, 2012;Siegelbaum, 2000;Zucker, 1989Zucker, , 1999Zucker and Regehr, 2002). …”

Section: Degeneracy In the Expression Of Synaptic Plasticitymentioning

confidence: 99%

Degeneracy in hippocampal physiology and plasticity

Rathour

Narayanan

2017

Preprint

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Degeneracy, defined as the ability of structurally disparate elements to perform analogous function, has largely been assessed from the perspective of maintaining robustness of physiology or plasticity. How does the framework of degeneracy assimilate into an encoding system where the ability to change is an essential ingredient for storing new incoming information? Could degeneracy maintain the balance between the apparently contradictory goals of the need to change for encoding and the need to resist change towards maintaining homeostasis? In this review, we explore these fundamental questions with the mammalian hippocampus as an example encoding system. We systematically catalog lines of evidence, spanning multiple scales of analysis, that demonstrate the expression of degeneracy in hippocampal physiology and plasticity. We assess the potential of degeneracy as a framework to achieve encoding and homeostasis without cross-interferences, and postulate that multiscale parametric and interactional complexity could establish disparate routes towards accomplishing these conjoint goals. These disparate routes then provide several degrees of freedom to the encodinghomeostasis system in accomplishing its tasks in an input-and state-dependent manner. Finally, the expression of degeneracy spanning multiple scales offers an ideal reconciliation to several outstanding controversies, through the recognition that the seemingly contradictory disparate observations are merely alternate routes that the system might recruit towards accomplishment of its goals. Juxtaposed against the ubiquitous prevalence of degeneracy and its strong links to evolution, it is perhaps apt to add a corollary to Theodosius Dobzhansky's famous quote and state "nothing in physiology makes sense except in the light of degeneracy".peer-reviewed)

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Presynaptic long-term depression mediated by Gi/o-coupled receptors

Cited by 100 publications

References 120 publications

Ethanol Disinhibits Dorsolateral Striatal Medium Spiny Neurons Through Activation of A Presynaptic Delta Opioid Receptor

Ethanol Disinhibits Dorsolateral Striatal Medium Spiny Neurons Through Activation of A Presynaptic Delta Opioid Receptor

Dopamine-dependent corticostriatal synaptic filtering regulates sensorimotor behavior

Degeneracy in hippocampal physiology and plasticity

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