Extended Amygdala-Parabrachial Circuits Alter Threat Perception to Control Feeding
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ABSTRACT:
PROVIDER: PRJNA551593 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9610560.fastq.gz | Fastqsanger.gz | |||
| SRR9610561.fastq.gz | Fastqsanger.gz | |||
| SRR9610562.fastq.gz | Fastqsanger.gz | |||
| SRR9610563.fastq.gz | Fastqsanger.gz | |||
| SRR9610564.fastq.gz | Fastqsanger.gz |
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Project description:Anxiety is elicited by excessive apprehension about unpredictable threats. However, the neural circuit governing unpredictable threat induced anxiety remains unclear. Here, we found ventral bed nucleus of the stria terminalis (vBNST) GABAergic neurons displayed selective activation to unpredictable threats by means ofthrough coordinated excitatory input from insular cortex (IC) glutamergic neurons and inhibitory input from lateral nucleus of the amygdala (CeL) somatostatin (SOM) neurons. Using activity-dependent neuronal tagging technology, we found that unpredictable threat responsive cells in vBNST drive freezing and anxiety via projections to ventral lateral periaqueductal grey (vlPAG) and median nucleus of the amygdala (CeM) respectively. Finally, we identified KCNQ3 plays an essential role in hyperactivity of vBNST GABAergic neurons and induced anxiety. These data identified a forward inhibitory circuit that determine the selective activation of vBNST in unpredictable threat and anxiety, and suggest that Kcnq3 KCNQ3 channel acts as a promising target in treatment of anxiety disorder following unpredictable stress.
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Project description:Dynamic Patterns of Threat-associated Gene Expression in the Amygdala and Blood
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Project description:Purpose: Identification the biological response to fear and stress in both brain and blood is vital for investigators performing peripheral studies of psychiatric traits. The goal of this study was to determine genes responsive to fear conditioning (FC), a well-characterized rodent model of threat-exposure, in the presence or absence of prior stress history, providing insight into the physiological processes underlying traumatic memory formation and trauma-related disorders such as PTSD. Methods: RNA sequencing was performed in blood and amygdala from mice that underwent fear conditioning (FC) with and without prior immobilization stress history (Immo+FC), or untreated animals (home cage HC). Libraries were prepared using the Illumina TruSeq™ RNA kit as per manufacturer’s instructions. Libraries were normalized and 8 samples were multiplexed in each lane of the flowcell. PhiX was used as an internal control on each lane to monitor the error statistics. Cluster generation was performed on the V3 flowcell on the Illumina cBot. The clustered flowcell was then sequenced on the Illumina HiSeq1000 system employing a single-end 101 cycles run. Alignment to the mm10 UCSC Mouse Assembly was performed using STAR version 2.3 (Dobin et al, 2013); parameters were set using the annotation as a splice junction reference. Sample reads were assembled into transcript models using cufflinks (v2.1.1) which were then merged and processed with cuffdiff v2.1.1, (Trapnell et al, 2012) to produce per sample FPKM expression levels and estimate differential expression between the sample groups. Results: In the amygdala, 607 genes associated with FC vs. HC (FDR<.05). In the same tissue, 516 genes showed different expression in response of immobilization (Immo+FC) compared to the FC group (FDR<.05). In the blood of the same animals, 468 genes had distinct changes in expression (Immo+FC vs FC; FDR<.05) and were enriched for biological processes such as inflammation and cytokine signaling. Conclusions: This study identified genes and pathways that respond to threat in the amygdala and blood of animals with and without a prior stress history. Future studies will be needed to examine the necessity, function and relevance of these regulated genes in human clinical stress and trauma-related disorders including.
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Project description:Both the amygdala and the bed nucleus of the stria terminalis (BNST) have been implicated in maladaptive anxiety characteristic of anxiety disorders. However, the underlying circuit and cellular mechanisms have remained elusive. Here we show that mice with Erbb4 gene deficiency in somatostatin-expressing (SOM+) neurons exhibit heightened anxiety as measured in the elevated plus maze test and the open field test, two assays commonly used to assess anxiety-related behaviors in rodents. Using a combination of electrophysiological, molecular, genetic and pharmacological techniques we demonstrate that the abnormal anxiety in the mutant mice is caused by enhanced excitatory synaptic inputs onto SOM+ neurons in the central amygdala (CeA), and the resulting reduction in inhibition onto downstream SOM+ neurons in the BNST. Notably, our results indicate that an increase in dynorphin signaling in SOM+ CeA neurons mediates the paradoxical reduction in inhibition onto SOM+ BNST neurons, and that the consequent enhanced activity of SOM+ BNST neurons is both necessary for and sufficient to drive the elevated anxiety. Finally, we show that the elevated anxiety and the associated synaptic dysfunctions and increased dynorphin signaling in the CeA-BNST circuit of the Erbb4 mutant mice can be recapitulated by stress in wild-type mice. Together, our results unravel previously unknown circuit and cellular processes in the central extended amygdala that can cause maladaptive anxiety.
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Project description:The co-morbidity of anxiety and dysfunctional reward processing in illnesses such as addiction and depression suggests that common neural circuitry contributes to these disparate neuropsychiatric symptoms. The extended amygdala, including the bed nucleus of the stria terminalis (BNST), modulates fear and anxiety, but also projects to the ventral tegmental area (VTA), a region implicated in reward and aversion, thus providing a candidate neural substrate for integrating diverse emotional states. However, the precise functional connectivity between distinct BNST projection neurons and their postsynaptic targets in the VTA, as well as the role of this circuit in controlling motivational states, have not been described. Here we record and manipulate the activity of genetically and neurochemically identified VTA-projecting BNST neurons in freely behaving mice. Collectively, aversive stimuli exposure produced heterogeneous firing patterns in VTA-projecting BNST neurons. By contrast, in vivo optically identified glutamatergic projection neurons displayed a net enhancement of activity to aversive stimuli, whereas the firing rate of identified GABAergic (?-aminobutyric acid-containing) projection neurons was suppressed. Channelrhodopsin-2-assisted circuit mapping revealed that both BNST glutamatergic and GABAergic projections preferentially innervate postsynaptic non-dopaminergic VTA neurons, thus providing a mechanistic framework for in vivo circuit perturbations. In vivo photostimulation of BNST glutamatergic projections resulted in aversive and anxiogenic behavioural phenotypes. Conversely, activation of BNST GABAergic projections produced rewarding and anxiolytic phenotypes, which were also recapitulated by direct inhibition of VTA GABAergic neurons. These data demonstrate that functionally opposing BNST to VTA circuits regulate rewarding and aversive motivational states, and may serve as a crucial circuit node for bidirectionally normalizing maladaptive behaviours.
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