P.4.d.001 Involvement of 5-HT1A receptors of the basolateral amygdala in the anxiolytic effect of chronic imipramine administration

2012 ◽  
Vol 22 ◽  
pp. S372
Author(s):  
M. Vicente ◽  
C. Strauss ◽  
H. Zangrossi
Keyword(s):  
Basolateral Amygdala ◽  
Anxiolytic Effect ◽  
Chronic Imipramine

scholarly journals microRNA mir-598-3p mediates susceptibility to stress-enhancement of remote fear memory

2019 ◽  
Author(s):  
Meghan E Jones ◽  
Stephanie E. Sillivan ◽  
Sarah Jamieson ◽  
Gavin Rumbaugh ◽  
Courtney A. Miller
Keyword(s):  
Basolateral Amygdala ◽  
Differential Susceptibility ◽  
Anxiolytic Effect ◽  
Bioinformatic Analysis ◽  
Fear Memory ◽  
Fear Learning ◽  
Small Rna Sequencing ◽  
Female Mice ◽  
The Impact

ABSTRACTmicroRNAs (miRNAs) have emerged as potent regulators of learning, recent memory and extinction. However, our understanding of miRNAs directly involved in regulating complex psychiatric conditions perpetuated by aberrant memory, such as in posttraumatic stress disorder (PTSD), remains limited. To begin to address the role of miRNAs in persistent memory, we performed small-RNA sequencing on basolateral amygdala (BLA) tissue to identify miRNAs altered by auditory fear conditioning (FC) one month after training. mir-598-3p, a highly conserved miRNA previously unstudied in the brain, was downregulated in the BLA. Further decreasing BLA mir-598-3p levels did not alter the expression or extinction of the remote fear memory. Given that stress is a critical component in PTSD, we next assessed the impact of stress-enhanced fear learning (SEFL) on mir-598-3p levels, finding the miRNA is elevated in the BLA of male, but not female, mice susceptible to the effects of stress in SEFL. Accordingly, intra-BLA inhibition of mir-598-3p interfered with expression and extinction of the remote fear memory in male, but not female, mice. This effect could not be attributed to an anxiolytic effect of miRNA inhibition. Finally, bioinformatic analysis following quantitative proteomics on BLA tissue collected 30 days post-SEFL training identified putative mir-598-3p targets and related pathways mediating the differential susceptibility, with evidence for regulation of the actin cytoskeleton.

scholarly journals Targeting presynaptic H3 heteroreceptor in nucleus accumbens to improve anxiety and obsessive-compulsive-like behaviors

2020 ◽  
Vol 117 (50) ◽  
pp. 32155-32164
Author(s):  
Xiao-Yang Zhang ◽  
Shi-Yu Peng ◽  
Li-Ping Shen ◽  
Qian-Xing Zhuang ◽  
Bin Li ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Basolateral Amygdala ◽  
Anxiolytic Effect ◽  
Common Mechanism ◽  
Obsessive Compulsive ◽  
Compulsive Disorder ◽  
H3 Receptor ◽  
Neurobiological Substrates ◽  
Glutamatergic Pathways ◽  
Afferent Terminals

Anxiety commonly co‐occurs with obsessive-compulsive disorder (OCD). Both of them are closely related to stress. However, the shared neurobiological substrates and therapeutic targets remain unclear. Here we report an amelioration of both anxiety and OCD via the histamine presynaptic H3 heteroreceptor on glutamatergic afferent terminals from the prelimbic prefrontal cortex (PrL) to the nucleus accumbens (NAc) core, a vital node in the limbic loop. The NAc core receives direct hypothalamic histaminergic projections, and optogenetic activation of hypothalamic NAc core histaminergic afferents selectively suppresses glutamatergic rather than GABAergic synaptic transmission in the NAc core via the H3 receptor and thus produces an anxiolytic effect and improves anxiety- and obsessive-compulsive-like behaviors induced by restraint stress. Although the H3 receptor is expressed in glutamatergic afferent terminals from the PrL, basolateral amygdala (BLA), and ventral hippocampus (vHipp), rather than the thalamus, only the PrL– and not BLA– and vHipp–NAc core glutamatergic pathways among the glutamatergic afferent inputs to the NAc core is responsible for co-occurrence of anxiety- and obsessive-compulsive-like behaviors. Furthermore, activation of the H3 receptor ameliorates anxiety and obsessive-compulsive-like behaviors induced by optogenetic excitation of the PrL–NAc glutamatergic afferents. These results demonstrate a common mechanism regulating anxiety- and obsessive-compulsive-like behaviors and provide insight into the clinical treatment strategy for OCD with comorbid anxiety by targeting the histamine H3 receptor in the NAc core.

scholarly journals Posterior basolateral amygdala to ventral hippocampal CA1 drives approach behaviour to exert an anxiolytic effect

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Guilin Pi ◽  
Di Gao ◽  
Dongqin Wu ◽  
Yali Wang ◽  
Huiyang Lei ◽  
...  
Keyword(s):  
Basolateral Amygdala ◽  
Anxiolytic Effect ◽  
Superficial Layer ◽  
Dependent Manner ◽  
Maze Task ◽  
Model Of Alzheimer’S Disease ◽  
Hippocampal Ca1 ◽  
Plus Maze ◽  
Functionally Diverse ◽  
Anterior Posterior

AbstractThe basolateral amygdala (BLA) and ventral hippocampal CA1 (vCA1) are cellularly and functionally diverse along their anterior–posterior and superficial-deep axes. Here, we find that anterior BLA (aBLA) and posterior BLA (pBLA) innervate deep-layer calbindin1-negative (Calb1−) and superficial-layer calbindin1-positive neurons (Calb1+) in vCA1, respectively. Photostimulation of pBLA–vCA1 inputs has an anxiolytic effect in mice, promoting approach behaviours during conflict exploratory tasks. By contrast, stimulating aBLA–vCA1 inputs induces anxiety-like behaviour resulting in fewer approaches. During conflict stages of the elevated plus maze task vCA1Calb1+ neurons are preferentially activated at the open-to-closed arm transition, and photostimulation of vCA1Calb1+ neurons at decision-making zones promotes approach with fewer retreats. In the APP/PS1 mouse model of Alzheimer’s disease, which shows anxiety-like behaviour, photostimulating the pBLA–vCA1Calb1+ circuit ameliorates the anxiety in a Calb1-dependent manner. These findings suggest the pBLA–vCA1Calb1+ circuit from heterogeneous BLA–vCA1 connections drives approach behaviour to reduce anxiety-like behaviour.

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