Basolateral to Central Amygdala Neural Circuits for Appetitive Behaviors

Kim, Joshua; Zhang, Xiangyu; Muralidhar, Shruti; LeBlanc, Sarah; Tonegawa, Susumu

doi:10.1016/j.neuron.2017.02.034

Cited by 381 publications

(590 citation statements)

References 71 publications

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“…CGRP PBN neurons project to the CeA and BNST 3,7 , nuclei that mediate behavioral and physiological responses to ingestive and fear-related stimuli 7,8,34 . Downstream CeA neurons express the CGRP receptor 7 , and a subpopulation of those neurons co-express protein kinase C-δ 7,35 , but the identity of downstream BNST neurons is unknown. We postulate that the CeA and BNST contribute to different aspects of behavior and/or alter behaviors over different timescales.…”

Section: Discussionmentioning

confidence: 99%

Encoding of danger by parabrachial CGRP neurons

Campos

Bowen

Roman

et al. 2018

Nature

260

275

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Animals must respond to various threats to survive. Neurons that express calcitonin gene-related peptide (CGRP) in the parabrachial nucleus (PBN) relay sensory signals that contribute to satiation and pain-induced fear behavior, but it is unknown how they encode these distinct processes. By recording calcium transients in vivo from individual CGRPPBN neurons, we reveal that most neurons are activated by noxious cutaneous (shock, heat, itch) and visceral stimuli (lipopolysaccharide). These same neurons are inhibited during feeding, but become activated during satiation, consistent with evidence that CGRPPBN neurons prevent overeating. CGRPPBN neurons are also activated during consumption of novel food or by an auditory cue that was previously paired with electrical foot shocks. Correspondingly, silencing CGRPPBN neurons attenuates expression of food neophobia and conditioned fear responses. Therefore, in addition to transducing primary sensory danger signals, CGRPPBN neurons promote affective-behavioral states that limit harm in response to potential threats.

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Section: Discussionmentioning

confidence: 99%

Encoding of danger by parabrachial CGRP neurons

Campos

Bowen

Roman

et al. 2018

Nature

260

275

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“…Moreover, both AS and AH neurons in lateral BLA do not receive PFC input, suggesting they participate in distinct circuits driven by alternative inputs. In the future, it will be interesting to explore additional pathways in this circuit, including projections to the central amygdala (CeA), which are also known to regulate both aversive (Beyeler et al, 2016; Namburi et al, 2015; Quirk et al, 2003) and appetitive behaviors (Kim et al, 2017). Finally, it will be important to determine how fear conditioning and extinction influence cell-type specific connectivity in the BLA (Arruda-Carvalho and Clem, 2014; Cho et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Prefrontal Cortex Drives Distinct Projection Neurons in the Basolateral Amygdala

2017

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SUMMARY The prefrontal cortex (PFC) regulates emotional behavior via top-down control of the basolateral amygdala (BLA). However, the influence of PFC inputs on the different projection pathways within the BLA remains largely unexplored. Here we combine whole-cell recordings and optogenetics to study these cell-type specific connections in the mouse BLA. We characterize PFC inputs onto three distinct populations of BLA neurons that project to either the PFC, ventral hippocampus or Nucleus Accumbens. We find that PFC-evoked synaptic responses are strongest at amygdala-cortical and amygdala-hippocampal neurons, and much weaker at amygdala-striatal neurons. We assess the mechanisms for this targeting, and conclude that it reflects fewer connections onto amygdala-striatal neurons. Given the similar intrinsic properties of these cells, this connectivity allows the PFC to preferentially activate amygdala-cortical and amygdala-hippocampal neurons. Together, our findings reveal how PFC inputs to the BLA selectively drive feed-back projections to the PFC and feed-forward projections to the hippocampus.

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“…Given our desire to understand the basic neuroscience of negative emotions, there has been considerable recent effort made to use modern optogenetic and chemogenetic tools to understand the coding of valence in the mouse brain subpopulations of neurons in the BLA 104 , central amygdala 105 , nucleus accumbens 106 and ventral tegmental area (VTA) 107 , and other regions appear to respond to the appetitive or aversive qualities of a stimulus, independent of its sensory features 10 . However, it is not yet known whether these neurons can be defined by their molecular properties, projection targets or some combination of these characteristics 10 .…”

Section: Altered Cognition and Moodmentioning

confidence: 99%

Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man

et al. 2018

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Post-traumatic stress disorder (PTSD) is a prevalent, debilitating and sometimes deadly consequence of exposure to severe psychological trauma. Although effective treatments exist for some individuals, they are limited. New approaches to intervention, treatment and prevention are therefore much needed. In the past few years, the field has rapidly developed a greater understanding of the dysfunctional brain circuits underlying PTSD, a shift in understanding that has been made possible by technological revolutions that have allowed the observation and perturbation of the macrocircuits and microcircuits thought to underlie PTSD-related symptoms. These advances have allowed us to gain a more translational knowledge of PTSD, have provided further insights into the mechanisms of risk and resilience and offer promising avenues for therapeutic discovery.

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Basolateral to Central Amygdala Neural Circuits for Appetitive Behaviors

Cited by 381 publications

References 71 publications

Encoding of danger by parabrachial CGRP neurons

Encoding of danger by parabrachial CGRP neurons

Prefrontal Cortex Drives Distinct Projection Neurons in the Basolateral Amygdala

Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man

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