Different effects of intracochlear sensory and neuronal injury stimulation on expression of synaptic N-methyl-D-aspartate receptors in the auditory cortex of rats in vivo.
CONCLUSIONS
The expression of synaptic N-methyl-D-aspartate (NMDA) receptors in the auditory cortex is dynamic and is bidirectionally regulated by auditory activity. Furthermore, the time course of changes in the level of NR2A protein differs after sensory and neuronal injury stimulation, which modulate different changes in synaptic plasticity.


OBJECTIVE
To examine the effects of different types of auditory activity on the expression of synaptic NMDA receptors (NMDARs) in the auditory cortex of rats.


METHODS
We prepared synaptosomes from the auditory cortices of postnatal Day 28 ototoxic-deafened Sprague-Dawley rats and postnatal Day 28 Sprague-Dawley rats subjected to noise trauma that were given various treatments and compared them to the synaptosomes of 1-6-week-old normal Sprague-Dawley rats. The expression of different NMDAR subunits in the synaptosomes was investigated by means of Western blotting.


RESULTS
Changes in NR1 and NR2B proteins were not significant during different types of auditory activity. The level of NR2A protein increased remarkably during postnatal development and as a result of electrical intracochlear stimulation, auditory deprivation and noise trauma. Seventy-two h after a 2-h period of sensory electrical intracochlear stimulation, the expression of NR2A protein returned to the level caused by auditory deprivation. Seventy-two h after a 3-h period of noise trauma, elevation of the level of NR2A protein was unchanged. We also confirmed that elevation of the level of synaptic NR2A protein was sensitive to protein synthesis inhibitor and NMDAR antagonist. However, transcription inhibitor had no effect on NR2A protein expression.
Wang
Zhengmin
Z
Otolaryngology Research Institute, EENT Hospital, Shanghai Medical College, Fudan University, 83 Feng Yang Road, Shanghai 200031, People's Republic of China. Shanghai_av@163.com
Ruan
Qingwei
Q
Wang
Dehui
D
D000818:Animals; D000831:Animals, Newborn; D001303:Auditory Cortex / Q000473:pathology*; D015153:Blotting, Western; D003056:Cochlear Nerve / Q000187:drug effects / Q000293:injuries / Q000473:pathology*; D003513:Cycloheximide / Q000633:toxicity; D003609:Dactinomycin / Q000633:toxicity; D004599:Electric Stimulation Therapy; D016057:Evoked Potentials, Auditory, Brain Stem / Q000235:genetics; D005260:Female; D006198:Hair Cells, Auditory / Q000187:drug effects* / Q000293:injuries* / Q000473:pathology; D006317:Hearing Loss, Noise-Induced / Q000473:pathology*; D008297:Male; D009473:Neuronal Plasticity / Q000235:genetics*; D010879:Piperazines / Q000633:toxicity; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics*; D012683:Sensory Deprivation / Q000502:physiology*; D013569:Synapses / Q000235:genetics*; D013574:Synaptosomes / Q000473:pathology*; D014158:Transcription, Genetic / Q000187:drug effects
D010879:Piperazines; D012333:RNA, Messenger; D016194:Receptors, N-Methyl-D-Aspartate; D003609:Dactinomycin; D003513:Cycloheximide; C050592:3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid