Elsevier

Current Opinion in Neurobiology

Volume 49, April 2018, Pages 141-147
Current Opinion in Neurobiology

New perspectives on central amygdala function

https://doi.org/10.1016/j.conb.2018.02.009Get rights and content

Highlights

  • Central amygdala circuits mediate defensive and appetitive responses.

  • Central amygdala circuit activity is controlled by local inhibitory interactions.

  • Central amygdala circuits mediate state-dependent and scalable action selection.

The central nucleus of the amygdala (CEA) is a striatum-like structure orchestrating a diverse set of adaptive behaviors, including defensive and appetitive responses [1, 2, 3]. Studies using anatomical, electrophysiological, imaging and optogenetic approaches revealed that the CEA network consists of recurrent inhibitory circuits comprised of precisely connected functionally and genetically defined cell types that can select and control specific behavioral outputs [3, 4, 5•, 6•, 7, 8•, 9, 12]. While bivalent functionality of the CEA in adaptive behavior has been clearly demonstrated, we are just beginning to understand to which degree individual CEA circuit elements are functionally segregated or overlapping. Importantly, recent studies seem to suggest that optogenetic manipulations of the same, or overlapping cell populations can give rise to distinct, or sometimes even opposite, behavioral phenotypes [5•, 6•, 9, 10, 11•, 12]. In this review, we discuss recent progress in our understanding of how defined CEA circuits can control defensive and appetitive behaviors, and how seemingly contradictory results could point to an integrated concept of CEA function.

Section snippets

The CEA and defensive responses

For nearly six decades, the CEA has been demonstrated to play a fundamental role in defensive responding (see [13]). Electrical stimulation and lesion studies were subsequently complemented by neurophysiological and pharmacological approaches culminating in the view that the CEA is a vital output station controlling and mediating a panoply of physiological and behavioral changes occurring in the face of threat (Figure 1) [1, 2]. For example, it has been repeatedly demonstrated that acute

The CEA, feeding behavior, and appetitive responses

The CEA is involved in the processing of rewarding events and the generation of appetitive behavioral responses [3, 30]. This is consistent with the existence of gustatory-related responses in the CEA [31, 32], and with its defined anatomical connectivity with reward-related, gustatory-related and feeding-related centers [33]. For example, optogenetic stimulation of neurons expressing the serotonin 2A receptor can elicit voracious feeding [11], as can activation of specific projection pathways

CEA cellular subpopulations mediate various and specific functions

As outlined above, there is extensive evidence for specific functional roles of CEA cellular populations in processing aversive as well as appetitive information and for the generation of distinct behavioral responses. The concept that distinct molecularly identified populations reflect specific functional roles has taken us a long way in understanding how the CEA generates adaptive behaviors. However, taken together, recent findings suggest this concept may not be sufficient to explain the

Conclusions and outlook

In general, as our circuit dissection tools are becoming ever sharper and the level of specificity in our experimental approaches increases, the likelihood of identifying specific functions of individual circuit elements increases. This has shifted our focus away from particular brain areas as functional units towards the emerging view of state-dependent functional assemblies of circuits distributed across many brain regions underlying definable brain functions, such as survival behaviors. As a

Conflict of interest statement

Nothing declared.

References and recommended reading

Papers of particular interest, published within the period of review, have been highlighted as:

  • • of special interest

Acknowledgements

This work has received funding by the Novartis Research Foundation, the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement no. 669582), by project grants from the Swiss National Science Foundation (SNSF), by a grant from the National Center of Competences in Research: ‘SYNAPSY  The Synaptic Bases of Mental Diseases’ (financed by the SNSF; all to AL), by the Heisenberg programme of the German Research Foundation (to PT), and

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