Loss of Brain-Derived Neurotrophic Factor Mediates Inhibition of Hippocampal Long-Term Potentiation by High-Intensity Sound

• Published in: Cellular and molecular neurobiology Vol. 41; no. 4; pp. 751 - 763
• Main Authors: de Deus, Júnia L., Amorim, Mateus R., Ribeiro, Aline B., Barcellos-Filho, Procópio C. G., Ceballos, César C., Branco, Luiz Guilherme S., Cunha, Alexandra O. S., Leão, Ricardo M.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-05-2021; Springer Nature B.V
• Subjects: Animals; Biomedical and Life Sciences; Biomedicine; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - deficiency; Brain-Derived Neurotrophic Factor - metabolism; c-Fos protein; CA1 Region, Hippocampal - physiology; Cell Biology; Cognitive ability; gamma-Aminobutyric Acid - metabolism; Glutamatergic transmission; Glutamic Acid - metabolism; Hippocampal plasticity; Hippocampus; Hippocampus - physiology; Long-term potentiation; Long-Term Potentiation - physiology; Male; Neurobiology; Neurosciences; Neurotransmission; Noise; Original Research; Perfusion; Proto-Oncogene Proteins c-fos - metabolism; Pyramidal Cells - metabolism; Rats; Rats, Wistar; Sound; Synapses - physiology; Synaptic plasticity; Synaptic Transmission; TrkB receptors; γ-Aminobutyric acid; LTP; BDNF; High-intensity sound; Hippocampus
• ISSN: 0272-4340; 1573-6830; 1573-6830
• DOI: 10.1007/s10571-020-00881-8

Exposure to noise produces cognitive and emotional disorders, and recent studies have shown that auditory stimulation or deprivation affects hippocampal function. Previously, we showed that exposure to high-intensity sound (110 dB, 1 min) strongly inhibits Schaffer-CA1 long-term potentiation (LTP). Here we investigated possible mechanisms involved in this effect. We found that exposure to 110 dB sound activates c-fos expression in hippocampal CA1 and CA3 neurons. Although sound stimulation did not affect glutamatergic or GABAergic neurotransmission in CA1, it did depress the level of brain-derived neurotrophic factor (BDNF), which is involved in promoting hippocampal synaptic plasticity. Moreover, perfusion of slices with BDNF rescued LTP in animals exposed to sound stimulation, whereas BDNF did not affect LTP in sham-stimulated rats. Furthermore, LM22A4, a TrkB receptor agonist, also rescued LTP from sound-stimulated animals. Our results indicate that depression of hippocampal BDNF mediates the inhibition of LTP produced by high-intensity sound stimulation.