Resolving the contributions of anaesthesia, surgery, and nerve injury on brain derived neurotrophic factor expression in the medial prefrontal cortex of male rats in the CCI model of neuropathic pain

2017 ◽  
Vol 95 (12) ◽  
pp. 2376-2390 ◽  
Author(s):  
James W.M. Kang ◽  
Kevin A. Keay ◽  
David Mor
Keyword(s):  
Neuropathic Pain ◽  
Prefrontal Cortex ◽  
Nerve Injury ◽  
Medial Prefrontal Cortex ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Male Rats ◽  
Factor Expression ◽  
Cci Model

scholarly journals Recurrent Moderate Hypoglycemia Suppresses Brain-Derived Neurotrophic Factor Expression in the Prefrontal Cortex and Impairs Sensorimotor Gating in the Posthypoglycemic Period in Young Rats

2016 ◽  
Vol 38 (1) ◽  
pp. 74-82 ◽  
Author(s):  
Raghavendra Rao ◽  
Kathleen Ennis ◽  
Eugena P. Mitchell ◽  
Phu V. Tran ◽  
Jonathan C. Gewirtz
Keyword(s):  
Prefrontal Cortex ◽  
Prepulse Inhibition ◽  
Medial Prefrontal Cortex ◽  
Neurotrophic Factor ◽  
Sensorimotor Gating ◽  
Neuronal Injury ◽  
Brain Derived Neurotrophic Factor ◽  
Acoustic Startle Reflex ◽  
Fear Potentiated Startle ◽  
Recurrent Hypoglycemia

Recurrent hypoglycemia is common in infants and children. In developing rat models, recurrent moderate hypoglycemia leads to neuronal injury in the medial prefrontal cortex. To understand the effects beyond neuronal injury, 3-week-old male rats were subjected to 5 episodes of moderate hypoglycemia (blood glucose concentration, approx. 30 mg/dl for 90 min) once daily from postnatal day 24 to 28. Neuronal injury was determined using Fluoro-Jade B histochemistry on postnatal day 29. The effects on brain-derived neurotrophic factor (BDNF) and its cognate receptor, tyrosine kinase receptor B (TrkB) expression, which is critical for prefrontal cortex development, were determined on postnatal day 29 and at adulthood. The effects on prefrontal cortex-mediated function were determined by assessing the prepulse inhibition of the acoustic startle reflex on postnatal day 29 and 2 weeks later, and by testing for fear-potentiated startle at adulthood. Recurrent hypoglycemia led to neuronal injury confined primarily to the medial prefrontal cortex. BDNF/TrkB expression in the prefrontal cortex was suppressed on postnatal day 29 and was accompanied by lower prepulse inhibition, suggesting impaired sensorimotor gating. Following the cessation of recurrent hypoglycemia, the prepulse inhibition had recovered at 2 weeks. BDNF/TrkB expression in the prefrontal cortex had normalized and fear-potentiated startle was intact at adulthood. Recurrent moderate hypoglycemia during development has significant adverse effects on the prefrontal cortex in the posthypoglycemic period.

scholarly journals Human Plasma BDNF Is Associated With Amygdala-Prefrontal Cortex Functional Connectivity and Problem Drinking Behaviors

2019 ◽  
Vol 23 (1) ◽  
pp. 1-11
Author(s):  
Stephanie M Gorka ◽  
Tara Teppen ◽  
Milena Radoman ◽  
K Luan Phan ◽  
Subhash C Pandey
Keyword(s):  
Prefrontal Cortex ◽  
Individual Differences ◽  
Functional Connectivity ◽  
Alcohol Use ◽  
Medial Prefrontal Cortex ◽  
Neurotrophic Factor ◽  
Alcohol Use Disorder ◽  
Brain Derived Neurotrophic Factor ◽  
Drinking Behaviors ◽  
Threat Of Shock

Abstract Background Preclinical studies suggest that decreased levels of brain-derived neurotrophic factor in the amygdala play a role in anxiety and alcohol use disorder. The association between brain-derived neurotrophic factor levels and amygdala function in humans with alcohol use disorder is still unclear, although neuroimaging studies have also implicated the amygdala in alcohol use disorder and suggest that alcohol use disorder is associated with disrupted functional connectivity between the amygdala and prefrontal cortex during aversive states. Methods The current study investigated whether plasma brain-derived neurotrophic factor levels in individuals with and without alcohol use disorder (n = 57) were associated with individual differences in amygdala reactivity and amygdala-prefrontal cortex functional connectivity during 2 forms of aversive responding captured via functional magnetic resonance imaging: anxiety elicited by unpredictable threat of shock and fear elicited by predictable threat of shock. We also examined whether brain-derived neurotrophic factor and brain function were associated with binge drinking episodes and alcohol use disorder age of onset. Results During anxiety, but not fear, lower levels of plasma brain-derived neurotrophic factor were associated with less connectivity between the left amygdala and the medial prefrontal cortex and the inferior frontal gyrus. In addition, within individuals with alcohol use disorder (only), lower levels of brain-derived neurotrophic factor and amygdala-medial prefrontal cortex functional connectivity during anxiety were associated with more binge episodes within the past 60 days and a lower age of alcohol use disorder onset. There were no associations between brain-derived neurotrophic factor levels and focal amygdala task reactivity. Conclusions Together, the results indicate that plasma brain-derived neurotrophic factor levels are related to amygdala circuit functioning in humans, particularly during anxiety, and these individual differences may relate to drinking behaviors.

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