scholarly journals Hypothalamic-extended amygdala circuit regulates temporal discounting

2019 ◽  
Author(s):  
Mark A. Rossi ◽  
Haofang E. Li ◽  
Glenn W. Watson ◽  
H. Gregory Moore ◽  
Min Tong Cai ◽  
...  
Keyword(s):  
Choice Behavior ◽  
Arcuate Nucleus ◽  
Neural Circuit ◽  
Temporal Discounting ◽  
Neural Mechanisms ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Axon Terminals ◽  
First Time ◽  
Y Receptors

AbstractChoice behavior is characterized by temporal discounting, i.e., preference for immediate rewards over delayed rewards. Temporal discounting is often dysfunctional in psychiatric disorders, addiction, and eating disorders. However, the underlying neural mechanisms governing temporal discounting are still poorly understood. We found that food deprivation resulted in steep temporal discounting of food rewards, whereas satiation abolished discounting. In addition, optogenetic activation of AgRP-expressing neurons in the arcuate nucleus or their axon terminals in the posterior bed nucleus of stria terminalis (BNST) restored temporal discounting in sated mice. Activation of postsynaptic neuropeptide Y receptors (Y1Rs) within the BNST, which is influenced by neuropeptide released by AgRP neurons, was sufficient to restore temporal discounting. These results demonstrate for the first time a profound effect of motivational signals from hypothalamic feeding circuits on temporal discounting and reveal a novel neural circuit that regulates choice behavior.

scholarly journals Extended amygdala-parabrachial circuits alter threat assessment to regulate feeding

2020 ◽  
Author(s):  
Dionnet L. Bhatti ◽  
Andrew T. Luskin ◽  
Christian E. Pedersen ◽  
Bernard Mulvey ◽  
Hannah Oden-Brunson ◽  
...  
Keyword(s):  
Neural Circuit ◽  
Threat Assessment ◽  
Threat Detection ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Environmental Threats ◽  
Extended Amygdala ◽  
Evolutionarily Conserved ◽  
Evolutionary Success ◽  
Affective Information

AbstractAn animal’s evolutionary success depends on the ability to seek and consume foods while avoiding environmental threats. However, how evolutionarily conserved threat detection circuits modulate feeding is unknown. In mammals, feeding and threat assessment are strongly influenced by the parabrachial nucleus (PBN), a structure that responds to threats and inhibits feeding. Here, we report that the PBN receives dense inputs from the bed nucleus of the stria terminalis (BNST), an extended amygdala structure that encodes affective information. Using a series of complementary approaches, we identify opposing BNST-PBN circuits that modulate a genetically-defined population of PBN neurons to control feeding. This previously unrecognized neural circuit integrates threat assessment with the intrinsic drive to eat.

Renal denervation alters forebrain hexokinase activity in neurogenic hypertensive rats

1989 ◽  
Vol 256 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
J. K. Simon ◽  
T. X. Zhang ◽  
J. Ciriello
Keyword(s):  
Supraoptic Nucleus ◽  
Arcuate Nucleus ◽  
Medial Septum ◽  
Stria Terminalis ◽  
Nerve Transection ◽  
Preoptic Nucleus ◽  
Renal Nerve ◽  
Neurogenic Hypertension ◽  
Bed Nucleus ◽  
Aortic Depressor Nerve

The effect of afferent renal nerve transection (tARN) on the metabolic activity of forebrain structures the activity of which was altered after aortic depressor nerve transection (tADN) was studied using the hexokinase (HK) histochemical method in the rat. In tADN-sham (s) ARN rats, increases in HK activity were observed in the medial septum (MS), median preoptic nucleus (MnPO), subfornical organ, supraoptic nucleus, nucleus circularis (Nc), magnocellular, and dorsal and medial (mpPVH) parvocellular components of paraventricular nucleus, the anterior, lateral, and dorsomedial (DMH) hypothalamus, and in the central and medial nuclei of the amygdala. In addition, a decrease in HK activity was seen in the dorsal arcuate nucleus (dArc). Similarly, increases in HK activity were seen in sADN-tARN rats in all the above structures except MS, Nc, and DMH, where no changes were observed, and dArc, where an increase in HK activity was noted. The bed nucleus of the stria terminalis, lateral preoptic nucleus (POA), and ventral (v) Arc also showed elevated HK activity. In contrast, the increased HK activity after either tADN or tARN alone was returned to levels not different from sADN-sARN rats in all structures in the tADN-tARN rats, except MnPO, mpPVH, and dArc, where the level of HK activity was only attenuated, and MS, POA, and vArc, where it remained elevated. These data suggest that similar forebrain structure are associated with the hypertension after tADN and are involved in the integration of ARN information and that these sites of interaction are involved in the maintenance and the reversal of the neurogenic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Phasic signaling in the bed nucleus of the stria terminalis during fear learning predicts within- and across-session cued fear expression

2019 ◽  
Author(s):  
Max Bjorni ◽  
Natalie G. Rovero ◽  
Elissa R. Yang ◽  
Andrew Holmes ◽  
Lindsay R. Halladay
Keyword(s):  
Intertrial Interval ◽  
Cell Activity ◽  
Fear Learning ◽  
Neural Dynamics ◽  
Electrophysiological Recording ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Post Shock ◽  
First Time

AbstractWhile results from many past studies have implicated the bed nucleus of the stria terminalis (BNST) in mediating the expression of sustained negative affect, recent studies have highlighted a more complex role for BNST that includes aspects of fear learning in addition to defensive responding. As BNST is thought to encode ambiguous or unpredictable threat, it seems plausible that it may be involved in encoding early cued fear learning, especially immediately following a first tone-shock pairing when the CS-US contingency is not fully apparent. To investigate this, we conducted in vivo electrophysiological recording studies to examine neural dynamics of BNST units during cued fear acquisition and recall. We identified two functionally distinct subpopulations of BNST neurons that encode the intertrial interval (ITI) and seem to contribute to within- and across-session fear learning. “Ramping” cell activity during cued fear acquisition parallels the increase in freezing expression as mice learn the CS-US contingency, while “Phasic” cells encode post-shock (USpost) periods (30 s following encounter with footshock) only during early trials. Importantly, the magnitude of Phasic unit responsivity to the first USpost period predicted not only freezing expression in response to the subsequent CS during acquisition, but also CS freezing evoked 24 hr later during CS retrieval. These findings suggest for the first time that BNST activity may serve as an instructive signal during cued fear learning.

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