Sensory Inputs to Intercalated Cells Provide Fear-Learning Modulated Inhibition to the Basolateral Amygdala

Asede, Douglas; Bosch, Daniel; Lüthi, Andreas; Ferraguti, Francesco; Ehrlich, Ingrid

doi:10.1016/j.neuron.2015.03.008

Cited by 89 publications

(107 citation statements)

References 63 publications

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“…Although foot shock-induced Fos activation in the sensory thalamus has not been described, electrophysiological measurements showed that foot shock and pinch do activates the sensory thalamic neurons (e.g. posterior intralaminar thalamic nuclei, PIN) (Asede et al, 2015; Bienvenu et al, 2015), as well as the PBel neurons (Bernard and Besson, 1990; Bester et al, 2000), and the PIN sends excitatory projections to both intercalated neurons and principal neurons in the LA (Asede et al, 2015; Bienvenu et al, 2015). Thus, the spino-thalamic and spino-parabrachial circuits may coordinately activate the CeA and LA to establish robust learning about threats.…”

Section: Discussionmentioning

confidence: 99%

Elucidating an Affective Pain Circuit that Creates a Threat Memory

Han

Soleiman

Soden

et al. 2015

Cell

376

450

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SUMMARY Animals learn to avoid harmful situations by associating a neutral stimulus with a painful one, resulting in a stable threat memory. In mammals, this form of learning requires the amygdala. Although pain is the main driver of aversive learning, the mechanism that transmits pain signals to the amygdala is not well resolved. Here we show that neurons expressing calcitonin gene-related peptide (CGRP) in the parabrachial nucleus are critical for relaying pain signals to the central nucleus of amygdala, and that this pathway may transduce the affective motivational aspects of pain. Genetic silencing of CGRP neurons blocks pain responses and memory formation, while their optogenetic stimulation produces defensive responses and a threat memory. The pain-recipient neurons in the central amygdala expressing CGRP receptors are also critical for establishing a threat memory. The identification of the neural circuit conveying affective pain signals may be pertinent for treating pain conditions with psychiatric comorbidities.

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Section: Discussionmentioning

confidence: 99%

Elucidating an Affective Pain Circuit that Creates a Threat Memory

Han

Soleiman

Soden

et al. 2015

Cell

376

450

View full text Add to dashboard Cite

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“…The infralimbic cortex (IL) indirectly projects to the CeM via intercalated cells in rats but not in mice Sesack 2000, 2008;Strobel et al 2015). It is thought that the ITC cells mediate extinction (Quirk et al 2003;Likhtik et al 2008) but may play a more general role in gating fear behavior, as they also receive direct sensory inputs (Asede et al 2015;Strobel et al 2015). Moreover, PL and IL receive amygdala projections originating mainly from the basal amygdala.…”

Section: Neural Circuitrymentioning

confidence: 99%

Neurobehavioral perspectives on the distinction between fear and anxiety

2015

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In this review, we discuss the usefulness of the distinction between fear and anxiety. The clinical use of the labels is ambiguous, often defining one in terms of the other. We first consider what a useful, objective, and scientifically valid definition would entail and then evaluate several fear/anxiety distinctions that have been made in the neurobiological literature. A strong distinction should specify the difference in conditions that lead to fear versus anxiety. Additionally, fear and anxiety should generate distinct sets of behaviors. Ideally, the two states should be supported by distinguishable neuroanatomical circuits. Such a conceptualization would be consistent with the National Institute of Mental Health's Research Domain Criteria (RDoc). The majority of neurobiological approaches to the fear versus anxiety distinction fail to differentiate the two states in terms of behavior, often using the exact same behavioral measures as indicators. Of the two that do, only Predatory Imminence Theory provides a distinction both in terms of cause and effect. Indeed, that approach provides a ready distinction of anxiety, fear, and panic in terms of both antecedent conditions and response selection rules. Additionally, it appeals to distinct neural circuits to generate these modes of action.Clear definitional distinctions between fear and anxiety have been elusive. There is also ambiguity in relating clinical classifications to preclinical laboratory models. The intention of this review is to describe and evaluate several neurobehavioral approaches to the distinction between fear and anxiety. A clear, research-based definition of fear and anxiety should help clarify the natural function of these brain states and point to how their dysfunction manifests as particular anxiety disorders. This relationship is becoming increasingly important with the National Institute of Mental Health's adoption of Research Domain Criteria (RDoc), which specifically attempts to link preclinical research with clinical phenomenology. The purpose of the RDoc systems is to ". . .to translate rapid progress in basic neurobiological and behavioral research to an improved integrative understanding of psychopathology and the development of new and/or optimally matched treatments for mental disorders" (National Institute of Mental Health 2013).To accomplish this goal, we will first consider the characteristics of a good definitional distinction between fear and anxiety. Then, after briefly reviewing the circuitry responsible for fear and anxiety, we will evaluate several neurobehavioral models with respect to those characteristics. Parsing the strengths and weaknesses of these models as well as analyzing the mechanisms and circuitry that underlie fear learning may point toward a better understanding of the fear/anxiety distinction. It should also help forge a clearer relationship between these models and specific anxiety disorders. We also clarify the relationship of the RDoc criteria to these animal models.

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“…Yet, how nociceptive signals are detected by the BLA learning system is still unclear. Some studies suggest that the sensory discriminative component of the nociceptive information is conveyed to the BLA via a spino-thalamic tract composed of lamina I spinal cord neurons targeting the posterior intralaminar thalamic nucleus (PIN), which in turn sends excitatory projections to the BLA (Asede et al 2015;Bienvenu et al 2015). However, this hypothesis has been challenged by studies showing that fiber-sparing lesions in this area do not impair footshock learning (Brunzell and Kim 2001;Lanuza et al 2008;Herry and Johansen 2014).…”

Section: Noxious Stimulimentioning

confidence: 99%

The neural circuits of innate fear: detection, integration, action, and memorization

2016

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How fear is represented in the brain has generated a lot of research attention, not only because fear increases the chances for survival when appropriately expressed but also because it can lead to anxiety and stress-related disorders when inadequately processed. In this review, we summarize recent progress in the understanding of the neural circuits processing innate fear in rodents. We propose that these circuits are contained within three main functional units in the brain: a detection unit, responsible for gathering sensory information signaling the presence of a threat; an integration unit, responsible for incorporating the various sensory information and recruiting downstream effectors; and an output unit, in charge of initiating appropriate bodily and behavioral responses to the threatful stimulus. In parallel, the experience of innate fear also instructs a learning process leading to the memorization of the fearful event. Interestingly, while the detection, integration, and output units processing acute fear responses to different threats tend to be harbored in distinct brain circuits, memory encoding of these threats seems to rely on a shared learning system.

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Sensory Inputs to Intercalated Cells Provide Fear-Learning Modulated Inhibition to the Basolateral Amygdala

Cited by 89 publications

References 63 publications

Elucidating an Affective Pain Circuit that Creates a Threat Memory

Elucidating an Affective Pain Circuit that Creates a Threat Memory

Neurobehavioral perspectives on the distinction between fear and anxiety

The neural circuits of innate fear: detection, integration, action, and memorization

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