Differential efferent projections of GABAergic Neurons in the Basolateral and Central Nucleus of Amygdala in mice

Emotions arise from activations of specialized neuronal populations in several parts of the cerebral cortex, notably the anterior cingulate, insula, ventromedial prefrontal, and subcortical structures, such as the amygdala, ventral striatum, putamen, caudate nucleus, and ventral tegmental area. Feelings are conscious, emotional experiences of these activations that contribute to neuronal networks mediating thoughts, language, and behavior, thus enhancing the ability to predict, learn, and reappraise stimuli and situations in the environment based on previous experiences. Contemporary theories of emotion converge around the key role of the amygdala as the central subcortical emotional brain structure that constantly evaluates and integrates a variety of sensory information from the surroundings and assigns them appropriate values of emotional dimensions, such as valence, intensity, and approachability. The amygdala participates in the regulation of autonomic and endocrine functions, decision-making and adaptations of instinctive and motivational behaviors to changes in the environment through implicit associative learning, changes in short- and long-term synaptic plasticity, and activation of the fight-or-flight response via efferent projections from its central nucleus to cortical and subcortical structures.

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Activity dynamics of amygdala GABAergic neurons during cataplexy of narcolepsy

eLife ◽

10.7554/elife.48311 ◽

2019 ◽

Vol 8 ◽

Cited By ~ 1

Author(s):

Ying Sun ◽

Carlos Blanco-Centurion ◽

Emmaline Bendell ◽

Aurelio Vidal-Ortiz ◽

Siwei Luo ◽

...

Keyword(s):

Calcium Imaging ◽

Direct Evidence ◽

Calcium Transient ◽

Gabaergic Neurons ◽

Predator Odor ◽

Central Nucleus ◽

Time Dynamic ◽

Imaging Tool ◽

Neuronal Groups ◽

Deep Brain

Recent studies showed activation of the GABAergic neurons in the central nucleus of the amygdala (CeA) triggered cataplexy of sleep disorder narcolepsy. However, there is still no direct evidence on CeA GABAergic neurons’ real-time dynamic during cataplexy. We used a deep brain calcium imaging tool to image the intrinsic calcium transient as a marker of neuronal activity changes in the narcoleptic VGAT-Cre mice by expressing the calcium sensor GCaMP6 into genetically defined CeA GABAergic neurons. Two distinct GABAergic neuronal groups involved in cataplexy were identified: spontaneous cataplexy-ON and predator odor-induced cataplexy-ON neurons. Majority in the latter group were inactive during regular sleep/wake cycles but were specifically activated by predator odor and continued their intense activities into succeeding cataplexy bouts. Furthermore, we found that CeA GABAergic neurons became highly synchronized during predator odor-induced cataplexy. We suggest that the abnormal activation and synchronization of CeA GABAergic neurons may trigger emotion-induced cataplexy.

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Modulation of Neuronal Activity on Intercalated Neurons of Amygdala Might Underlie Anxiolytic Activity of a Standardized Extract of Centella asiatica ECa233

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2018/3853147 ◽

2018 ◽

Vol 2018 ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

Aree Wanasuntronwong ◽

Oraphan Wanakhachornkrai ◽

Penphimon Phongphanphanee ◽

Tadashi Isa ◽

Boonyong Tantisira ◽

...

Keyword(s):

Ampa Receptors ◽

Brain Slices ◽

Centella Asiatica ◽

Gabaergic Neurons ◽

Anxiolytic Activity ◽

Central Nucleus ◽

Electrophysiological Properties ◽

Whole Cell Patch Clamp ◽

External Capsule ◽

Excitatory Synaptic Input

GABAergic intercalated neurons of amygdala (ITCs) have recently been shown to be important in the suppression of fear-like behavior. Effects of ECa233 (a standardized extract of Centella asiatica), previously demonstrated anxiolytic activity, were then investigated on ITCs. Cluster of GABAergic neurons expressing fluorescence of GFP was identified in GAD67-GFP knock-in mice. We found that neurons of medial paracapsular ITC were GABAergic neurons exhibiting certain intrinsic electrophysiological properties similar to those demonstrated by ITC neurons at the same location in C57BL/6J mice. Therefore, we conducted experiments in both C57BL/6J mice and GAD67-GFP knock-in mice. Excitatory postsynaptic currents (EPSCs) were evoked by stimulation of the external capsule during the whole cell patch-clamp recordings from ITC neurons in brain slices. ECa233 was found to increase the EPSC peak amplitude in the ITC neurons by about 120%. The EPSCs in ITC neurons were completely abolished by the application of an AMPA receptor antagonist. Morphological assessment of the ITC neurons with biocytin demonstrated that most axons of the recorded neurons innervated the central nucleus of the amygdala (CeA). Therefore, it is highly likely that anxiolytic activity of ECa233 was mediated by increasing activation, via AMPA receptors, of excitatory synaptic input to the GABAergic ITC leading to depression of CeA neurons.

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The efferent projections of the central nucleus and the pericentral nucleus of the inferior collculus in the cat

The Journal of Comparative Neurology ◽

10.1002/cne.901940311 ◽

1980 ◽

Vol 194 (3) ◽

pp. 649-662 ◽

Cited By ~ 150

Author(s):

Richard A. Anderse ◽

G. Linn Roth ◽

Lindsay M. Aitkin ◽

Michael M. Merzenich

Keyword(s):

Central Nucleus ◽

Efferent Projections

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A Central Amygdala–Ventrolateral Periaqueductal Gray Matter Pathway for Pain in a Mouse Model of Depression-like Behavior

Anesthesiology ◽

10.1097/aln.0000000000003133 ◽

2020 ◽

Vol 132 (5) ◽

pp. 1175-1196

Author(s):

Weiwei Yin ◽

Lisheng Mei ◽

Tingting Sun ◽

Yuping Wang ◽

Jie Li ◽

...

Keyword(s):

Mouse Model ◽

Restraint Stress ◽

Periaqueductal Gray ◽

Gabaergic Neurons ◽

Central Nucleus ◽

Gabaergic Interneurons ◽

Chronic Restraint Stress ◽

Central Amygdala ◽

Glutamatergic Neurons ◽

Pain Symptoms

Abstract Background The mechanisms underlying depression-associated pain remain poorly understood. Using a mouse model of depression, the authors hypothesized that the central amygdala–periaqueductal gray circuitry is involved in pathologic nociception associated with depressive states. Methods The authors used chronic restraint stress to create a mouse model of nociception with depressive-like behaviors. They then used retrograde tracing strategies to dissect the pathway from the central nucleus of the amygdala to the ventrolateral periaqueductal gray. The authors performed optogenetic and chemogenetic experiments to manipulate the activity of this pathway to explore its roles for nociception. Results The authors found that γ-aminobutyric acid–mediated (GABAergic) neurons from the central amygdala project onto GABAergic neurons of the ventrolateral periaqueductal gray, which, in turn, locally innervate their adjacent glutamatergic neurons. After chronic restraint stress, male mice displayed reliable nociception (control, mean ± SD: 0.34 ± 0.11 g, n = 7 mice; chronic restraint stress, 0.18 ± 0.11 g, n = 9 mice, P = 0.011). Comparable nociception phenotypes were observed in female mice. After chronic restraint stress, increased circuit activity was generated by disinhibition of glutamatergic neurons of the ventrolateral periaqueductal gray by local GABAergic interneurons via receiving enhanced central amygdala GABAergic inputs. Inhibition of this circuit increased nociception in chronic restraint stress mice (median [25th, 75th percentiles]: 0.16 [0.16, 0.16] g to 0.07 [0.04, 0.16] g, n = 7 mice per group, P < 0.001). In contrast, activation of this pathway reduced nociception (mean ± SD: 0.16 ± 0.08 g to 0.34 ± 0.13 g, n = 7 mice per group, P < 0.001). Conclusions These findings indicate that the central amygdala–ventrolateral periaqueductal gray pathway may mediate some aspects of pain symptoms under depression conditions. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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