scholarly journals Increased hippocampal GABAergic inhibition after long-term high-intensity sound exposure

PLoS ONE ◽  
2019 ◽  
Vol 14 (5) ◽  
pp. e0210451 ◽  
Author(s):  
Alexandra O. S. Cunha ◽  
Junia L. de Deus ◽  
Cesar C. Ceballos ◽  
Ricardo M. Leão
Keyword(s):  
High Intensity ◽  
Gabaergic Inhibition ◽  
Sound Exposure

scholarly journals Mechanisms of high-intensity sound exposure on inhibiting hippocampal long-term potentiation: role of brain-derived neurotrophic factor

2019 ◽  
Author(s):  
Júnia L. de Deus ◽  
Mateus R. Amorim ◽  
Aline B. Ribeiro ◽  
Procópio C. G. Barcellos-Filho ◽  
César C. Ceballos ◽  
...  
Keyword(s):  
Emotional Disorders ◽  
Neurotrophic Factor ◽  
High Intensity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Brain Derived Neurotrophic Factor ◽  
Sound Stimulation ◽  
Sound Exposure ◽  
Term Potentiation

AbstractExposure to humans and experimental animals to loud noises produce cognitive and emotional disorders and recent studies have shown that hippocampal neuronal function is affected by auditory stimulation or deprivation. We have found previously that in the hippocampus of rats exposed to high-intensity sound (110 dB) for one-minute the Schaffer-CA1 long-term potentiation (LTP) is strongly inhibited. Here we investigated possible mechanisms involved in this effect. We found, using c-fos expression, that exposure to 110 dB sound-activated neurons in the CA1 and CA3 hippocampal region. Using electrophysiological recordings in hippocampal slices, we found that both GABAergic and glutamatergic neurotransmission were unaffected by high-intensity sound stimulation. However, hippocampal brain-derived neurotrophic factor (BDNF), which is involved in promoting hippocampal synaptic plasticity, presented decreased levels in sound-stimulated animals. Perfusion of slices with BDNF revert the inhibition of LTP after a single sound stimulus in comparison to sham-stimulated rats. Furthermore, the perfusion with LM 22A4, a TrkB receptor agonist also rescued LTP from sound-stimulated animals. Our results strongly suggest that the exposure to high-intensity sound inhibits the BDNF production in the hippocampus, which could be a possible mechanism of the inhibition of LTP by high-intensity sound exposure.

scholarly journals Increased hippocampal GABAergic inhibition after long-term high-intensity sound exposure

2018 ◽  
Author(s):  
Alexandra Siqueira Cunha ◽  
Junia lara de Deus ◽  
Cesar Celis Ceballos ◽  
Ricardo Mauricio Leao
Keyword(s):  
High Intensity ◽  
Pyramidal Neurons ◽  
Prolonged Exposure ◽  
Long Term Potentiation ◽  
Gabaergic Neurotransmission ◽  
Sound Exposure ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Synaptic Level

Exposure to loud sounds has been related to deleterious mental and systemic effects in addition to auditory maladies. Hippocampal function has been shown to be affected to either high intensity sound exposure or long-term sound deprivation. Hippocampal long-term potentiation (LTP) is inhibited after 10 days of daily exposure to 2 minutes of high-intensity noise (110 dB), in the hippocampi of Wistar rats. He we investigate how the glutamatergic and GABAergic neurotransmission mediated by ionotropic receptors is affected by the same protocol of high intensity sound exposure. We found that while the glutamatergic transmission both by AMPA/kainite and NMDA receptors in the Schaffer-CA1 synapses is largely unaffected by long-term exposure to high intensity sound, the amplitude of the inhibitory GABAergic currents is potentiated, but not the frequency of the both spontaneous and miniature currents. We conclude that GABAergic transmission is potentiated at the post-synaptic level in the hippocampal CA1 pyramidal neurons after a prolonged exposure to short periods of high-intensity sound. This effect could be an important factor for the reduced LTP in the hippocampi of these animals after high intensity sound exposure, and demonstrated that prolonged exposure to high- intensity sound can affect hippocampal inhibitory transmission and consequently its function.

scholarly journals Decrease in regional body fat after long-term high-intensity interval training

2017 ◽  
Vol 6 (2) ◽  
pp. 103-110 ◽  
Author(s):  
Koichiro Azuma ◽  
Yusuke Osawa ◽  
Shogo Tabata ◽  
Fuminori Katsukawa ◽  
Hiroyuki Ishida ◽  
...  
Keyword(s):  
Body Fat ◽  
High Intensity ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
Regional Body Fat ◽  
High Intensity Interval

Effect of Infrasound and Low Frequency Sound Exposure at Intensities below 100 dB(SPL) on the Rota-Rod Treadmill Performance of Guinea Pigs

1983 ◽  
Vol 2 (3) ◽  
pp. 37-41 ◽  
Author(s):  
Naoki Maehara ◽  
Reiko Kishi ◽  
Terukazu Sadamoto ◽  
Izumi Harabuchi ◽  
Kohtaroh Yamamura
Keyword(s):  
Guinea Pigs ◽  
Motor Coordination ◽  
Low Frequency ◽  
Vestibular Function ◽  
Moderate Intensity ◽  
Endurance Time ◽  
Frequency Sound ◽  
Sound Exposure ◽  
Preliminary Study

A preliminary study to investigate whether or not long-term exposure to very low frequency sound at a moderate intensity below 100 dB(SPL) affects the vestibular function and/or motor coordination in guinea pigs was carried out. At first, optimal conditions of Rota-Rod Treadmill performance for guinea pigs were determined. Then, 20 and 40 Hz-low frequency sound at 80–90 dB(SPL) exposure was used for 150 minutes and measurement of the endurance time on the Rota-Rod Treadmill was carried out at rotation speeds of 8 rpm or 10 rpm. At 10 rpm rotation speed, and 20 Hz, 90 dB(SPL) stimulus, the endurance time was significantly reduced at 150 minutes, compared with that of the control, whereas no significant reduction in endurance time was obtained at 85 dB(SPL).

scholarly journals Lactate and BDNF: Key Mediators of Exercise Induced Neuroplasticity?

2020 ◽  
Vol 9 (4) ◽  
pp. 1136 ◽  
Author(s):  
Patrick Müller ◽  
Yves Duderstadt ◽  
Volkmar Lessmann ◽  
Notger G. Müller
Keyword(s):  
Physical Exercise ◽  
High Intensity ◽  
Long Term Potentiation ◽  
Potential Mediator ◽  
Term Potentiation ◽  
Lactate Levels ◽  
Exercise Induced ◽  
Lactate Infusion ◽  
Relationship Of

Accumulating evidence from animal and human studies supports the notion that physical exercise can enhance neuroplasticity and thus reduce the risk of several neurodegenerative diseases (e.g., dementia). However, the underlying neurobiological mechanisms of exercise induced neuroplasticity are still largely unknown. One potential mediator of exercise effects is the neurotrophin BDNF, which enhances neuroplasticity via different pathways (e.g., synaptogenesis, neurogenesis, long-term potentiation). Current research has shown that (i) increased peripheral lactate levels (following high intensity exercise) are associated with increased peripheral BDNF levels, (ii) lactate infusion at rest can increase peripheral and central BDNF levels and (iii) lactate plays a very complex role in the brain’s metabolism. In this review, we summarize the role and relationship of lactate and BDNF in exercise induced neuroplasticity.

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