Asymmetrical Synaptic Cooperation between Cortical and Thalamic Inputs to the Amygdale

Fonseca, Rosalina

doi:10.1038/npp.2013.178

Cited by 25 publications

(37 citation statements)

References 45 publications

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“…Recent studies also demonstrate that knockout of CB1 specifically localized to glutamatergic terminals facilitates LTP induction at excitatory synapses while deletion of GABAergic CB1 serves to impair induction of this LTP [42]. This if note as the internal capsule BLA CB1 receptor population specifically restricts LTP induction during associative plasticity following coincident activation of both internal and external capsule inputs into the BLA [41]. Thus, the functional impairment of CB1 receptors on BLA glutamatergic terminals by chronic ethanol may ultimately help facilitate the development of ethanol-induced plasticity at these synapses and so contribute to the development of withdrawal-induced anxiogenesis [2, 5].…”

Section: 0 Discussionmentioning

confidence: 99%

“…We have previously demonstrated that chronic ethanol induces dramatic up-regulation of presynaptic function at glutamatergic projections arriving to the BLA from the internal capsule/stria terminalis [5]. These synapses are potently influenced by the eCB system [40, 41]. Within the current experiments, we evaluated CB1-modulation of glutamatergic transmission at this BLA input during both acute and chronic ethanol exposure.…”

Section: 0 Introductionmentioning

confidence: 96%

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Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala

Robinson

Alexander²,

Bluett

et al. 2016

Neuropharmacology

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The endogenous cannabinoid (eCB) system has been suggested to play a key role in ethanol preference and intake, the acute effects of ethanol, and in the development of withdrawal symptoms following ethanol dependence. Ethanol-dependent alterations in glutamatergic signaling within the lateral/basolateral nucleus of the amygdala (BLA) are critical for the development and expression of withdrawal-induced anxiety. Notably, the eCB system significantly regulates both glutamatergic and GABAergic synaptic activity within the BLA. Chronic ethanol exposure significantly alters eCB system expression within regions critical to the expression of emotionality and anxiety-related behavior, including the BLA. Here, we investigated specific interactions between the BLA eCB system and its functional regulation of synaptic activity during acute and chronic ethanol exposure. In tissue from ethanol naïve-rats, a prolonged acute ethanol exposure caused a dose dependent inhibition of glutamatergic synaptic activity via a presynaptic mechanism that was occluded by CB1 antagonist/inverse agonists SR141716a and AM251. Importantly, this acute ethanol inhibition was attenuated following 10 day chronic intermittent ethanol vapor exposure (CIE). CIE exposure also significantly down-regulated CB1-mediated presynaptic inhibition at glutamatergic afferent terminals but spared CB1-inhibition of GABAergic synapses arising from local inhibitory-interneurons. CIE also significantly elevated BLA N-arachidonoylethanolamine (AEA or anandamide) levels and decreased CB1 receptor protein levels. Collectively, these data suggest a dynamic regulation of the BLA eCB system by acute and chronic ethanol.

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Section: 0 Discussionmentioning

confidence: 99%

Section: 0 Introductionmentioning

confidence: 96%

Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala

Robinson

Alexander²,

Bluett

et al. 2016

Neuropharmacology

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“…Given that the STC hypothesis is based on the sharing of intracellular PRPs, the cooperative paradigm relies on two assumptions: (a) that weak and strong stimulated synapses belong to two different axonal pools—no presynaptic overlap; and (b) that weak and strong synapses are mapped in the same post‐synaptic neuron—post‐synaptic overlap. Although there is now evidence for single‐cell STC, their original findings, and many others following, had no information regarding the spatial organization of inputs, whether inputs were completely independent or even if inputs co‐terminate in the same neuronal population.…”

Section: Synaptic Tagging and Capture And The Compartmentalization Ofmentioning

confidence: 99%

Actin remodeling, the synaptic tag and the maintenance of synaptic plasticity

2020

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Activity‐dependent plasticity of synaptic connections is a hallmark of the mammalian brain and represents a key mechanism for rewiring neural circuits during development, experience‐dependent plasticity, and brain disorders. Cellular models of memory, such as long‐term potentiation and long‐term depression, share common principles to memory consolidation. As for memory, the maintenance of synaptic plasticity is dependent on the synthesis of de novo protein synthesis. The synaptic‐tagging and capture hypothesis states that the maintenance of synaptic plasticity is dependent on the interplay between input‐specific synaptic tags and the allocation or capture of plasticity‐related proteins (PRPs) at activated synapses. The setting of the synaptic tag and the capture of PRPs are independent processes that can occur separated in time and different groups of activated synapses. How are these two processes orchestrated in time and space? Here, we discuss the synaptic‐tagging and capture hypothesis in the light of neuronal compartmentalization models and address the role of actin as a putative synaptic tag. If different groups of synapses interact by synaptic‐tagging and capture mechanisms, understanding the spatial rules of such interaction is key to define the relevant neuronal compartment. We also discuss how actin modulation can allow an input‐specific capture of PRPs and try to conciliate the temporal dynamics of synaptic actin with the maintenance of plasticity. Understanding how multiple synapses interact in time and space is fundamental to predict how neurons integrate information and ultimately how memory is acquired.

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“…Since the inhibition of CB1R increased competition and considering that competition is determined by a source-to-sink balance, then CB1R inhibition may increase the sink (tag) or decrease the source (PRPs). Although CB1R inhibition is associated with a decrease in protein synthesis, by modulation of the mTOR pathway, the observation that inhibiting CB1R promotes cooperation (Fonseca, 2013), does not support the hypothesis that CB1R inhibition decreases the source. An alternative hypothesis is that inhibition of CB1R increases the sink, which goes in line with CB1R inhibition promoting cooperation.…”

Section: Figure 4 Competition Is Abolished If Prps Availability Is Imentioning

confidence: 85%

“…Indeed, two previous reports have shown that CB1R inhibition downregulates the activity of the mTOR pathway (Busquets- Puighermanal et al, 2013). However, since CB1R inhibition promotes cooperation (Fonseca, 2013), it is highly unlikely that it decreases PRPs synthesis. Also, we did not observe any effect on LTP maintenance, under AM281 application, when the thalamic S2 input was not stimulated.…”

Section: Figure 6 Model Of Synaptic Cooperation and Competitionmentioning

confidence: 98%

Temporal gating of synaptic competition in the lateral amygdala by cannabinoid receptor modulation of the thalamic input

Drumond

Madeira

Fonseca

2019

Preprint

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The acquisition of fear memories involves plasticity of the thalamic and cortical pathways to the lateral amygdala (LA). The maintenance of synaptic plasticity requires the interplay between input-specific synaptic tags and the allocation of plasticity-related proteins (PRPs). Based on this interplay, weakly activated synapses can express long-lasting synaptic plasticity by cooperation with strongly activated ones. Increasing the number of activated synapses can shift cooperation to competition. Synaptic cooperation and competition can determine whether two events, separated in time, are linked or selected. The rules that determine whether synapses cooperate or compete are unknown. We found that synaptic cooperation and competition, in the LA, are determined by the temporal sequence of cortical and thalamic stimulation and that the strength of the synaptic tag is modulated by the endocannabinoid signalling. This modulation is particularly effective in thalamic synapses, suggesting a critical role of endocannabinoids in restricting thalamic plasticity. Also, we found that PRPs availability is modulated by the action-potential firing of neurons, shifting competition to cooperation. Our data present the first evidence that pre-synaptic modulation of synaptic activation, by the cannabinoid signalling, function as a temporal gating mechanism limiting synaptic cooperation and competition.

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Asymmetrical Synaptic Cooperation between Cortical and Thalamic Inputs to the Amygdale

Cited by 25 publications

References 45 publications

Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala

Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala

Actin remodeling, the synaptic tag and the maintenance of synaptic plasticity

Temporal gating of synaptic competition in the lateral amygdala by cannabinoid receptor modulation of the thalamic input

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