Activation of brain‐derived neurotrophic factor signaling in the basal forebrain reverses acute sleep deprivation‐induced fear memory impairments

Autor: Yitian Yang, Qiang Fu, Zhipeng Xu, Yan Lu, Ying-Ying Wang, Ma Tao, Guanhua Li, Weidong Mi, Wei Wang, Hao Zhang
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Male
medicine.medical_specialty
Basal Forebrain
fear memory
Tropomyosin receptor kinase B
050105 experimental psychology
lcsh:RC321-571
03 medical and health sciences
Behavioral Neuroscience
0302 clinical medicine
Neurotrophic factors
Internal medicine
medicine
Animals
Receptor
trkB
0501 psychology and cognitive sciences
Phosphorylation
Rats
Wistar
lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry
Microinjection
Original Research
Brain-derived neurotrophic factor
Basal forebrain
brain‐derived neurotrophic factor
Memory Disorders
business.industry
Brain-Derived Neurotrophic Factor
05 social sciences
Azepines
Fear
Sleep in non-human animals
sleep deprivation
Rats
Sleep deprivation
Endocrinology
Treatment Outcome
nervous system
Benzamides
medicine.symptom
Signal transduction
business
Sleep
030217 neurology & neurosurgery
Signal Transduction
Zdroj: Brain and Behavior
Brain and Behavior, Vol 10, Iss 4, Pp n/a-n/a (2020)
ISSN: 2162-3279
Popis: Introduction The mechanisms underlying sleep deprivation‐induced memory impairments and relevant compensatory signaling pathways remain elusive. We tested the hypothesis that increased brain‐derived neurotrophic factor (BDNF) expression in the basal forebrain following acute sleep deprivation was a compensatory mechanism to maintain fear memory performance. Methods Adult male Wistar rats were deprived of 6‐hr total sleep from the beginning of the light cycle. The effects of sleep deprivation on BDNF protein expression and activation of downstream tropomyosin receptor kinase B (TrkB)/phospholipase C‐γ1 (PLCγ1) signaling in the basal forebrain and fear memory consolidation were examined. BDNF or selective downstream TrkB receptor antagonist ANA‐12 was further injected into the basal forebrain bilaterally to observe the changes in fear memory consolidation in response to modulation of the BDNF/TrkB signaling. Results Six hours of sleep deprivation‐induced both short‐ and long‐term fear memory impairments. Increased BDNF protein expression and TrkB and PLCγ1 phosphorylation in the basal forebrain were observed after sleep deprivation. Microinjection of BDNF into the basal forebrain partly reversed fear memory deficits caused by sleep deprivation, which were accompanied by increased BDNF protein levels and TrkB/PLCγ1 activation. After ANA‐12 microinjection, sleep deprivation‐induced activation of the BDNF/TrkB pathway was inhibited and impairments of fear memory consolidation were further aggravated. Conclusions Acute sleep deprivation induces compensatory increase of BDNF expression in the basal forebrain. Microinjection of BDNF into the basal forebrain mitigates the fear memory impairments caused by sleep deprivation by activating TrkB/PLCγ1 signaling.
We found that acute sleep deprivation could increase BDNF protein expression and downstream TrkB/PLCγ1 activation robustly in the basal forebrain area. Microinjection of BDNF into basal forebrain could further activate TrkB/PLCγ1 signaling and reverse the decline in fear memory consolidation. Moreover, microinjection of TrkB receptor antagonist ANA‐12 could aggravate sleep deprivation‐induced memory impairments.
Databáze: OpenAIRE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje