Expression of fear-conditioning is accompanied by increased paired-pulse depression within the amygdala

Zinebi, Fatiha; McKernan, Margaret; Shinnick‐Gallagher, Patricia

doi:10.1016/s0091-3057(01)00684-0

Cited by 13 publications

(16 citation statements)

References 35 publications

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“…Our data demonstrate treatment dependent differences in paired pulse facilitation but no effect on paired pulse depression at IC-BLA synapses. Importantly, facilitation at short inter-stimulus intervals and depression at longer inter-stimulus intervals was previously reported at this afferent pathway (McKernan and Shinnick-Gallagher, 1997; Zinebi et al, 2002) with independent regulation of paired pulse facilitation and depression occurring at single synapses (Chen et al, 2004). …”

Section: Resultsmentioning

confidence: 65%

“…Paired-pulse ratios were reduced in WD slices at IC-BLA glutamatergic afferents similar to presynaptic effects of fear conditioning (Zinebi et al, 2002). Additional experiments identified WD dependent decreases of failure rates that support increased release probability at these thalamic inputs.…”

Section: Discussionmentioning

confidence: 97%

“…However, nothing is known about the impact of CIE/WD on thalamic IC-inputs. Since IC (thalamic) inputs express presynaptic forms of plasticity (Zinebi et al, 2002), we hypothesized that CIE and WD could enhance presynaptic function at IC-BLA glutamatergic afferents.…”

Section: Introductionmentioning

confidence: 99%

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Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

et al. 2013

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Amygdala glutamatergic neurotransmission regulates withdrawal induced anxiety-like behaviors following chronic ethanol exposure. The lateral/basolateral amygdala receives multiple glutamatergic projections that contribute to overall amygdala function. Our lab has previously shown that rat cortical (external capsule) afferents express postsynaptic alterations during chronic intermittent ethanol exposure and withdrawal. However, thalamic (internal capsule) afferents also provide crucial glutamatergic input during behavioral conditioning, and they have not been studied in the context of chronic drug exposure. We report here that these thalamic inputs express altered presynaptic function during withdrawal from chronic ethanol exposure. This is characterized by enhanced release probability, as exemplified by altered paired-pulse ratios and decreased failure rates of unitary events, and increased concentrations of synaptic glutamate. Quantal analysis further implicates a withdrawal-dependent enhancement of the readily-releasable pool of vesicles as a probable mechanism. These functional alterations are accompanied by increased expression of vesicle associated protein markers. These data demonstrate that chronic ethanol modulation of glutamate neurotransmission in the rat lateral/basolateral amygdala is afferent-specific. Further, presynaptic regulation of lateral/basolateral amygdala thalamic inputs by chronic ethanol may be a novel neurobiological mechanism contributing to the increased anxiety-like behaviors that characterize withdrawal.

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Section: Resultsmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 97%

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Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

et al. 2013

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“…This has been shown, mostly in LAd, by extra- and intracellular recordings of CS-evoked firing in vivo (80, 139, 390, 404, 414, 419) and by recordings of synaptic responses to afferent stimulation in brain slices in vitro obtained from fear-conditioned animals (301, 502, 538). These studies demonstrated the associative nature of the plasticity, established LA as the site of plasticity, and provided support for a causal relationship between LA plasticity and fear memory (reviewed by (274)).…”

Section: Synaptic Plasticity In the Amygdala Related To Conditionmentioning

confidence: 93%

Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear

Pape¹,

Paré

2010

Physiological Reviews

880

870

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The last ten years have witnessed a surge of interest for the mechanisms underlying the acquisition and extinction of classically conditioned fear responses. In part, this results from the realization that abnormalities in fear learning mechanisms likely participate to the development and/or maintenance of human anxiety disorders. The simplicity and robustness of this learning paradigm, coupled to the fact that the underlying circuitry is evolutionarily well conserved makes it an ideal model to study the basic biology of memory and identify genetic factors and neuronal systems that regulate the normal and pathological expressions of learned fear. Critical advances have been made in determining how modified neuronal functions upon fear acquisition become stabilized during fear memory consolidation and how these processes are controlled in the course of fear memory extinction. With these advances, came the realization that activity in remote neuronal networks must be coordinated for these events to take place. In this paper, we review these mechanisms of coordinated network activity and the molecular cascades leading to enduring fear memory, and allowing for their extinction. We will focus on Pavlovian fear conditioning as a model and the amygdala as a key component for the acquisition and extinction of fear responses.

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“…Functional inactivation (Muller et al, 1997; Wilensky et al, 1999) or lesions (Amorapanth et al, 2000; LeDoux et al, 1990a; Nader et al, 2001) in the LA result in inability to acquire/recall fear memory. We previously demonstrated that synaptic plasticity recorded after FPS involves alterations in N-methyl-D-aspartate receptor (NMDARs) and non-NMDAR neurotransmission in the thalamic-LA (Th-LA) neural circuit (McKernan and Shinnick-Gallagher, 1997; Zinebi et al, 2002; Zinebi et al, 2001; Zinebi et al, 2003). …”

Section: Introductionmentioning

confidence: 99%

Fear potentiated startle increases phospholipase D (PLD) expression/activity and PLD-linked metabotropic glutamate receptor mediated post-tetanic potentiation in rat amygdala

Krishnan

Scott

Pollandt

et al. 2016

Neurobiology of Learning and Memory

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Long-term memory (LTM) of fear stores activity dependent modifications that include changes in amygdala signaling. Previously, we identified an enhanced probability of release of glutamate mediated signaling to be important in rat fear potentiated startle (FPS), a well-established translational behavioral measure of fear. Here, we investigated short- and long-term synaptic plasticity in FPS involving metabotropic glutamate receptors (mGluRs) and associated downstream proteomic changes in the thalamic-lateral amygdala pathway (Th-LA). Aldolase A, an inhibitor of phospholipase D (PLD), expression was reduced, concurrent with significantly elevated PLD protein expression. Blocking the PLD-mGluR signaling significantly reduced PLD activity. While transmitter release probability increased in FPS, PLD-mGluR agonist and antagonist actions were occluded. In the unpaired group (UNP), blocking the PLD-mGluR increased while activating the receptor decreased transmitter release probability, consistent with decreased synaptic potentials during tetanic stimulation. FPS Post-tetanic potentiation (PTP) immediately following long-term potentiation (LTP) induction was significantly increased. Blocking PLD-mGluR signaling prevented PTP and reduced cumulative PTP probability but not LTP maintenance in both groups. These effects are similar to those mediated through mGluR7, which is co-immunoprecipitated with PLD in FPS. Lastly, blocking mGluR-PLD in the rat amygdala was sufficient to prevent behavioral expression of fear memory. Thus, our study in the Th-LA pathway provides the first evidence for PLD as an important target of mGluR signaling in amygdala fear-associated memory. Importantly, the PLD-mGluR provides a novel therapeutic target for treating maladaptive fear memories in posttraumatic stress and anxiety disorders.

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Expression of fear-conditioning is accompanied by increased paired-pulse depression within the amygdala

Cited by 13 publications

References 35 publications

Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear

Fear potentiated startle increases phospholipase D (PLD) expression/activity and PLD-linked metabotropic glutamate receptor mediated post-tetanic potentiation in rat amygdala

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