Timing of Impulses From the Central Amygdala and Bed Nucleus of the Stria Terminalis to the Brain Stem

The amygdala and bed nucleus of the stria terminalis (BNST) are thought to subserve distinct functions, with the former mediating rapid fear responses to discrete sensory cues and the latter longer “anxiety-like” states in response to diffuse environmental contingencies. However, these structures are reciprocally connected and their projection sites overlap extensively. To shed light on the significance of BNST–amygdala connections, we compared the antidromic response latencies of BNST and central amygdala (CE) neurons to brain stem stimulation. Whereas the frequency distribution of latencies was unimodal in BNST neurons (∼10-ms mode), that of CE neurons was bimodal (∼10- and ∼30-ms modes). However, after stria terminalis (ST) lesions, only short-latency antidromic responses were observed, suggesting that CE axons with long conduction times course through the ST. Compared with the direct route, the ST greatly lengthens the path of CE axons to the brain stem, an apparently disadvantageous arrangement. Because BNST and CE share major excitatory basolateral amygdala (BL) inputs, lengthening the path of CE axons might allow synchronization of BNST and CE impulses to brain stem when activated by BL. To test this, we applied electrical BL stimuli and compared orthodromic response latencies in CE and BNST neurons. The latency difference between CE and BNST neurons to BL stimuli approximated that seen between the antidromic responses of BNST cells and CE neurons with long conduction times. These results point to a hitherto unsuspected level of temporal coordination between the inputs and outputs of CE and BNST neurons, supporting the idea of shared functions.

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Estradiol-17β-responsive A1 and A2 noradrenergic cells of the brain stem project to the bed nucleus of the stria terminalis in the ewe brain: A possible route for regulation of gonadotropin releasing hormone cells

Neuroscience ◽

10.1016/j.neuroscience.2009.10.027 ◽

2010 ◽

Vol 165 (3) ◽

pp. 758-773 ◽

Cited By ~ 9

Author(s):

A. Pereira ◽

J. Rawson ◽

A. Jakubowska ◽

I.J. Clarke

Keyword(s):

Brain Stem ◽

Gonadotropin Releasing Hormone ◽

Stria Terminalis ◽

Bed Nucleus ◽

Releasing Hormone ◽

The Brain ◽

Estradiol 17Β

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Optogenetic study of the projections from the bed nucleus of the stria terminalis to the central amygdala

Journal of Neurophysiology ◽

10.1152/jn.00677.2015 ◽

2015 ◽

Vol 114 (5) ◽

pp. 2903-2911 ◽

Cited By ~ 29

Author(s):

Nur Zeynep Gungor ◽

Ryo Yamamoto ◽

Denis Paré

Keyword(s):

Inhibitory Influence ◽

Stria Terminalis ◽

Evoked Responses ◽

Central Amygdala ◽

Bed Nucleus ◽

Long Duration ◽

Infected Cells ◽

Shed Light ◽

Conditioned Cues

It has been proposed that the central amygdala (CeA), particularly its medial sector (CeM), generates brief fear responses to discrete conditioned cues, whereas the bed nucleus of the stria terminalis (BNST) promotes long-lasting, anxiety-like states in response to more diffuse contingencies. Although it is believed that BNST-CeA interactions determine the transition between short- and long-duration responses, the nature of these interactions remains unknown. To shed light on this question, we used a double viral strategy to drive the expression of channelrhodopsin (ChR2) in BNST cells that project to CeA. Next, using patch-clamp recordings in vitro, we investigated the connectivity of infected cells to noninfected cells in BNST and compared the influence of BNST axons on neurons in the medial and lateral (CeL) parts of CeA. CeA-projecting BNST cells were concentrated in the anterolateral (AL) and anteroventral (AV) sectors of BNST. Dense plexuses of BNST axons were observed throughout CeA. In CeA and BNST, light-evoked excitatory postsynaptic potentials accounted for a minority of responses (0–9% of tested cells); inhibition prevailed. The incidence of inhibitory responses was higher in CeM than in CeL (66% and 43% of tested cells, respectively). Within BNST, the connections from CeA-projecting to non-CeA-targeting cells varied as a function of the BNST sector: 50% vs. 9% of tested cells exhibited light-evoked responses in BNST-AL vs. BNST-AV, respectively. Overall, these results suggest that via its projection to CeA, BNST exerts an inhibitory influence over cued fear and that BNST neurons projecting to CeA form contrasting connections in different BNST subnuclei.

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Repeated exposure with short-term behavioral stress resolves pre-existing stress-induced depressive-like behavior in mice

Nature Communications ◽

10.1038/s41467-021-26968-4 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Eun-Hwa Lee ◽

Jin-Young Park ◽

Hye-Jin Kwon ◽

Pyung-Lim Han

Keyword(s):

Basolateral Amygdala ◽

Expression Profiles ◽

Gene Expression Profiles ◽

Repeated Exposure ◽

Repeated Injection ◽

Stria Terminalis ◽

Prelimbic Cortex ◽

Short Term ◽

Bed Nucleus ◽

The Brain

AbstractChronic stress induces adaptive changes in the brain via the cumulative action of glucocorticoids, which is associated with mood disorders. Here we show that repeated daily five-minute restraint resolves pre-existing stress-induced depressive-like behavior in mice. Repeated injection of glucocorticoids in low doses mimics the anti-depressive effects of short-term stress. Repeated exposure to short-term stress and injection of glucocorticoids activate neurons in largely overlapping regions of the brain, as shown by c-Fos staining, and reverse distinct stress-induced gene expression profiles. Chemogenetic inhibition of neurons in the prelimbic cortex projecting to the nucleus accumbens, basolateral amygdala, or bed nucleus of the stria terminalis results in anti-depressive effects similarly to short-term stress exposure, while only inhibition of neurons in the prelimbic cortex projecting to the bed nucleus of the stria terminalis rescues defective glucocorticoid release. In summary, we show that short-term stress can reverse adaptively altered stress gains and resolve stress-induced depressive-like behavior.

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GABA and NMDA receptors in CRF neurons have opposing effects in fear acquisition and anxiety in central amygdala vs. bed nucleus of the stria terminalis

Hormones and Behavior ◽

10.1016/j.yhbeh.2015.04.001 ◽

2015 ◽

Vol 76 ◽

pp. 136-142 ◽

Cited By ~ 25

Author(s):

Georgette M. Gafford ◽

Kerry J. Ressler

Keyword(s):

Nmda Receptors ◽

Stria Terminalis ◽

Central Amygdala ◽

Bed Nucleus ◽

Opposing Effects ◽

Crf Neurons

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Dopamine D2 receptor-mediated circuit from the central amygdala to the bed nucleus of the stria terminalis regulates impulsive behavior

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1811664115 ◽

2018 ◽

Vol 115 (45) ◽

pp. E10730-E10739 ◽

Cited By ~ 6

Author(s):

Bokyeong Kim ◽

Sehyoun Yoon ◽

Ryuichi Nakajima ◽

Hyo Jin Lee ◽

Hee Jeong Lim ◽

...

Keyword(s):

Dopamine D2 Receptor ◽

D2 Receptor ◽

Inhibitory Neurons ◽

Stria Terminalis ◽

Neural Pathways ◽

Impulsive Behavior ◽

Central Amygdala ◽

Dopamine System ◽

Addictive Disorders ◽

Bed Nucleus

Impulsivity is closely associated with addictive disorders, and changes in the brain dopamine system have been proposed to affect impulse control in reward-related behaviors. However, the central neural pathways through which the dopamine system controls impulsive behavior are still unclear. We found that the absence of the D2 dopamine receptor (D2R) increased impulsive behavior in mice, whereas restoration of D2R expression specifically in the central amygdala (CeA) of D2R knockout mice (Drd2−/−)normalized their enhanced impulsivity. Inhibitory synaptic output from D2R-expressing neurons in the CeA underlies modulation of impulsive behavior because optogenetic activation of D2R-positive inhibitory neurons that project from the CeA to the bed nucleus of the stria terminalis (BNST) attenuate such behavior. Our identification of the key contribution of D2R-expressing neurons in the CeA → BNST circuit to the control of impulsive behavior reveals a pathway that could serve as a target for approaches to the management of neuropsychiatric disorders associated with impulsivity.

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Transsexualism

Oxford Textbook of Endocrinology and Diabetes ◽

10.1093/med/9780199235292.003.9134 ◽

2011 ◽

pp. 1463-1468

Author(s):

Louis J. G. Gooren

Keyword(s):

Sexual Differentiation ◽

External Genitalia ◽

The Other ◽

Stria Terminalis ◽

Bed Nucleus ◽

Psychological Phenomenon ◽

Opposite Sex ◽

Male To Female ◽

The Brain

Transsexualism is the condition in which a person with apparently normal somatic sexual differentiation is convinced that he/she is actually a member of the opposite sex. It is associated with an irresistible urge to be hormonally and surgically adapted to that sex. Traditionally transsexualism has been conceptualized as a purely psychological phenomenon, but research on the brains of male-to-female transsexuals has found that the sexual differentiation of the brain—the bed nucleus of the stria terminalis (BSTC) and the hypothalamic uncinate nucleus—had followed a female pattern (1). This finding may lead to a concept of transsexualism as a form of intersex, where the sexual differentiation of the brain (which in mammals also undergoes sexual differentiation) is not consistent with the other variables of sex, such as chromosomal pattern, nature of the gonad and nature of internal/external genitalia. Thus it can be argued that transsexualism is a sexual differentiation disorder.

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