scholarly journals β-Adrenoceptor Blockade in the Basolateral Amygdala, But Not the Medial Prefrontal Cortex, Rescues the Immediate Extinction Deficit

2017 ◽  
Vol 42 (13) ◽  
pp. 2537-2544 ◽  
Author(s):  
Thomas F Giustino ◽  
Jocelyn R Seemann ◽  
Gillian M Acca ◽  
Travis D Goode ◽  
Paul J Fitzgerald ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Basolateral Amygdala

scholarly journals Basolateral amygdala input to the medial prefrontal cortex controls obsessive-compulsive disorder-like checking behavior

2019 ◽  
Vol 116 (9) ◽  
pp. 3799-3804 ◽  
Author(s):  
Tingting Sun ◽  
Zihua Song ◽  
Yanghua Tian ◽  
Wenbo Tian ◽  
Chunyan Zhu ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Obsessive Compulsive Disorder ◽  
Medial Prefrontal Cortex ◽  
Basolateral Amygdala ◽  
Obsessive Compulsive ◽  
Neuronal Tracing ◽  
Compulsive Disorder ◽  
Glutamatergic Neurons ◽  
Fmri Study ◽  
Checking Behavior

Obsessive-compulsive disorder (OCD) affects ∼1 to 3% of the world’s population. However, the neural mechanisms underlying the excessive checking symptoms in OCD are not fully understood. Using viral neuronal tracing in mice, we found that glutamatergic neurons from the basolateral amygdala (BLAGlu) project onto both medial prefrontal cortex glutamate (mPFCGlu) and GABA (mPFCGABA) neurons that locally innervate mPFCGlu neurons. Next, we developed an OCD checking mouse model with quinpirole-induced repetitive checking behaviors. This model demonstrated decreased glutamatergic mPFC microcircuit activity regulated by enhanced BLAGlu inputs. Optical or chemogenetic manipulations of this maladaptive circuitry restored the behavioral response. These findings were verified in a mouse functional magnetic resonance imaging (fMRI) study, in which the BLA–mPFC functional connectivity was increased in OCD mice. Together, these findings define a unique BLAGlu→mPFCGABA→Glu circuit that controls the checking symptoms of OCD.

scholarly journals Synaptic Modulation via Basolateral Amygdala on the Rat Hippocampus–Medial Prefrontal Cortex Pathway in Fear Extinction

2013 ◽  
Vol 123 (3) ◽  
pp. 267-278 ◽  
Author(s):  
Sumitaka Inoue ◽  
Hidekazu Kamiyama ◽  
Machiko Matsumoto ◽  
Yoshiki Yanagawa ◽  
Sachiko Hiraide ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Basolateral Amygdala ◽  
Fear Extinction ◽  
Rat Hippocampus ◽  
Synaptic Modulation

scholarly journals Morphine selectively promotes glutamate release from glutamatergic terminals of projection neurons from medial prefrontal cortex to dopamine neurons of ventral tegmental area

2017 ◽  
Author(s):  
Li Yang ◽  
Ming Chen ◽  
Ping Zheng
Keyword(s):  
Prefrontal Cortex ◽  
Locomotor Activity ◽  
Ventral Tegmental Area ◽  
Medial Prefrontal Cortex ◽  
Lateral Hypothalamus ◽  
Basolateral Amygdala ◽  
Glutamate Release ◽  
Dopamine Neurons ◽  
Projection Neurons ◽  
Ventral Tegmental

AbstractRecently, we found that morphine promoted presynaptic glutamate release of dopamine (DA) neurons in the ventral tegmental area (VTA), which constituted the main mechanism for morphine-induced increase in VTA-DA neuron firing and related behaviors (Chen et al., 2015). However, what source of presynaptic glutamate release of DA neurons in the VTA is promoted by morphine remains unknown. To address this question, we used optogenetic strategy to selectively activate glutamatergic inputs from different projection neurons and then observed the effect of morphine on them. The result shows that morphine promotes glutamate release from glutamatergic terminals of projection neurons from the medial prefrontal cortex (mPFC) to VTA DA neurons, but has no effect on that from the basolateral amygdala (BLA) or the lateral hypothalamus (LH) to VTA DA neurons, and the inhibition of glutamatergic projection neurons from the mPFC to the VTA significantly reduces morphine-induced increase in locomotor activity of mice.

scholarly journals Rostral and caudal BLA engage distinct circuits in the prelimbic and infralimbic PFC

2021 ◽  
Author(s):  
Kasra Manoocheri ◽  
Adam G Carter
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Basolateral Amygdala ◽  
Pyramidal Tract ◽  
Ex Vivo ◽  
Layer 2 ◽  
Deep Layers ◽  
Local Circuits ◽  
Whole Cell Recordings

Connections from the basolateral amygdala (BLA) to medial prefrontal cortex (PFC) regulate memory and emotion and become disrupted in neuropsychiatric disorders. We hypothesized that the diverse roles attributed to interactions between the BLA and PFC reflect multiple circuits nested within a wider network. To assess these circuits, we first used anatomy to show that the rostral BLA (rBLA) and caudal BLA (cBLA) differentially project to prelimbic (PL) and infralimbic (IL) subregions of the PFC, respectively. We then combined in vivo silicon probe recordings and optogenetics to show that rBLA primarily engages PL, whereas cBLA mainly influences IL. Using ex vivo whole-cell recordings and optogenetics, we then assessed which neuronal subtypes are targeted, showing that rBLA preferentially drives layer 2 (L2) cortico-amygdalar (CA) neurons in PL, whereas cBLA drives layer 5 (L5) pyramidal tract (PT) cells in IL. Lastly, we used soma-tagged optogenetics to explore the local circuits linking superficial and deep layers of PL, showing how rBLA can also impact L5 PT cells. Together, our findings delineate how subregions of the BLA target distinct networks within the PFC to have different influence on prefrontal output.

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