NEVER forget: negative emotional valence enhances recapitulation DOI Open Access
Holly J. Bowen, Sarah M. Kark, Elizabeth A. Kensinger

et al.

Psychonomic Bulletin & Review, Journal Year: 2017, Volume and Issue: 25(3), P. 870 - 891

Published: July 10, 2017

Language: Английский

Anxiety Cells in a Hippocampal-Hypothalamic Circuit DOI Creative Commons
Jessica C. Jimenez, Katy Su, Alexander Goldberg

et al.

Neuron, Journal Year: 2018, Volume and Issue: 97(3), P. 670 - 683.e6

Published: Jan. 31, 2018

Language: Английский

Citations

552

Striatal circuits for reward learning and decision-making DOI
Julia Cox, Ilana B. Witten

Nature reviews. Neuroscience, Journal Year: 2019, Volume and Issue: 20(8), P. 482 - 494

Published: June 6, 2019

Language: Английский

Citations

486

A competitive inhibitory circuit for selection of active and passive fear responses DOI
Jonathan P. Fadok, Sabine Krabbe, Milica Marković

et al.

Nature, Journal Year: 2017, Volume and Issue: 542(7639), P. 96 - 100

Published: Jan. 25, 2017

Language: Английский

Citations

470

Neurobiological links between stress and anxiety DOI Creative Commons
Núria Daviu, Michael R. Bruchas, Bita Moghaddam

et al.

Neurobiology of Stress, Journal Year: 2019, Volume and Issue: 11, P. 100191 - 100191

Published: Aug. 13, 2019

Stress and anxiety have intertwined behavioral neural underpinnings. These commonalities are critical for understanding each state, as well their mutual interactions. Grasping the mechanisms underlying this bidirectional relationship will major clinical implications managing a wide range of psychopathologies. After briefly defining key concepts study stress in pre-clinical models, we present circuit, cellular molecular involved either or both anxiety. First, review studies on divergent circuits basolateral amygdala (BLA) emotional valence processing anxiety-like behaviors, how norepinephrine inputs from locus coeruleus (LC) to BLA responsible acute-stress induced We then describe recent revealing new role mitochondrial function within nucleus accumbens (NAc), individual trait rodents, participating link between Next, report findings impact reward encoding through alteration circuit dynamic synchronicity. Finally, work unravelling hypothalamic corticotropin-releasing hormone (CRH) neurons controlling stress-induce behaviors. Altogether, research reviewed here reveals sharing subcortical nodes Understanding overlap these two psychobiological states, might provide alternative strategies manage disorders such post-traumatic disorder (PTSD).

Language: Английский

Citations

382

Development of the emotional brain DOI

B. J. Casey,

Aaron S. Heller, Dylan G. Gee

et al.

Neuroscience Letters, Journal Year: 2017, Volume and Issue: 693, P. 29 - 34

Published: Dec. 2, 2017

Language: Английский

Citations

355

Identification of a prefrontal cortex-to-amygdala pathway for chronic stress-induced anxiety DOI Creative Commons
Wei-Zhu Liu, Wen-Hua Zhang, Zhi-Heng Zheng

et al.

Nature Communications, Journal Year: 2020, Volume and Issue: 11(1)

Published: May 6, 2020

Abstract Dysregulated prefrontal control over amygdala is engaged in the pathogenesis of psychiatric diseases including depression and anxiety disorders. Here we show that, a rodent model induced by chronic restraint stress (CRS), dysregulation occurs basolateral projection neurons receiving mono-directional inputs from dorsomedial cortex (dmPFC→BLA PNs) rather than those reciprocally connected with dmPFC (dmPFC↔BLA PNs). Specifically, CRS shifts dmPFC-driven excitatory-inhibitory balance towards excitation former, but not latter population. Such specificity preferential to connections made dmPFC, caused enhanced presynaptic glutamate release, highly correlated increased anxiety-like behavior stressed mice. Importantly, low-frequency optogenetic stimulation afferents BLA normalizes release onto dmPFC→BLA PNs lastingly attenuates CRS-induced increase behavior. Our findings thus reveal target cell-based mPFC-to-amygdala transmission for stress-induced anxiety.

Language: Английский

Citations

325

Behavioral and neurobiological mechanisms of pavlovian and instrumental extinction learning DOI
Mark E. Bouton, Stephen Maren, Gavan P. McNally

et al.

Physiological Reviews, Journal Year: 2020, Volume and Issue: 101(2), P. 611 - 681

Published: Sept. 24, 2020

This article reviews the behavioral neuroscience of extinction, phenomenon in which a behavior that has been acquired through Pavlovian or instrumental (operant) learning decreases strength when outcome reinforced it is removed. Behavioral research indicates neither nor operant extinction depends substantially on erasure original but instead new inhibitory primarily expressed context learned, as exemplified by renewal effect. Although nature inhibition may differ and either case decline responding depend both generalization decrement correction prediction error. At neural level, requires tripartite circuit involving amygdala, prefrontal cortex, hippocampus. Synaptic plasticity amygdala essential for learning, cortical neurons encoding fear memories involved retrieval. Hippocampal-prefrontal circuits mediate relapse phenomena, including renewal. Instrumental involves distinct ensembles corticostriatal, striatopallidal, striatohypothalamic well their thalamic returns (extinction) excitatory (renewal other phenomena) control over responding. The field made significant progress recent decades, although fully integrated biobehavioral understanding still awaits.

Language: Английский

Citations

296

Amygdala inputs to prefrontal cortex guide behavior amid conflicting cues of reward and punishment DOI
Anthony Burgos-Robles,

Eyal Y. Kimchi,

Ehsan M. Izadmehr

et al.

Nature Neuroscience, Journal Year: 2017, Volume and Issue: 20(6), P. 824 - 835

Published: April 24, 2017

Language: Английский

Citations

283

Dopamine enhances signal-to-noise ratio in cortical-brainstem encoding of aversive stimuli DOI

Caitlin M. Vander Weele,

Cody A. Siciliano,

Gillian A. Matthews

et al.

Nature, Journal Year: 2018, Volume and Issue: 563(7731), P. 397 - 401

Published: Nov. 1, 2018

Language: Английский

Citations

277

Locus coeruleus to basolateral amygdala noradrenergic projections promote anxiety-like behavior DOI Creative Commons
Jordan G. McCall,

Edward R. Siuda,

Dionnet L. Bhatti

et al.

eLife, Journal Year: 2017, Volume and Issue: 6

Published: July 14, 2017

Increased tonic activity of locus coeruleus noradrenergic (LC-NE) neurons induces anxiety-like and aversive behavior. While some information is known about the afferent circuitry that endogenously drives this neural behavior, downstream receptors anatomical projections mediate these acute risk behavioral states via LC-NE system remain unresolved. Here we use a combination retrograde tracing, fast-scan cyclic voltammetry, electrophysiology, in vivo optogenetics with localized pharmacology to identify substrates increased mice. We demonstrate photostimulation fibers BLA evokes norepinephrine release basolateral amygdala (BLA), alters neuronal activity, conditions aversion, increases Additionally, report β-adrenergic phenotype NE BLA. These studies begin illustrate how complex efferent selectively mediates behavior through distinct receptor projection-selective mechanisms.

Language: Английский

Citations

276