Neuronally modulated transcription of a glycine transporter in rat dorsal cochlear nucleus and nucleus of the medial trapezoid body

✍ Scribed by Barmack, N.H.; Guo, H.; Kim, H.J.; Qian, H.; Qian, Z.-Y.

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 779 KB
• Volume: 415
• Category: Article
• ISSN: 0021-9967
• DOI: 10.1002/(sici)1096-9861(19991213)415:2<175::aid-cne3>3.0.co;2-u

✦ Synopsis

Neurotransmitter transporters limit transmitter concentration at the postsynaptic membrane by removing neurotransmitters from the synaptic cleft. Not only do neurotransmitter transporters contribute to the regulation of synaptic transmission, but they themselves might be dynamically regulated by neuronal activity of the neurons in which they are expressed. In this experiment, we investigated the question of whether the transcription of two different glycine transporters, Glyt1 and Glyt2, is influenced by neuronal activity. These transporters are found in the dorsal cochlear nucleus (DCN) and medial nucleus of the trapezoid body. Glyt1 and Glyt2 mRNA were measured by using hybridization histochemistry and a semiquantitative reverse transcription polymerase chain reaction. Decreases in auditory primary afferent activity, caused by either unilateral labyrinthectomy or disruption of the middle ear ossicles, caused a reduction in Glyt2, but not Glyt1 mRNA in the ipsilateral DCN and in the contralateral medial nucleus of the trapezoid body. Acoustic stimulation at either 10 kHz or 40 kHz was used to provide controlled increases in primary afferent activity, evoking localized increases in Glyt2 mRNA in clusters of neurons in the DCN. The location of these clusters corresponded to the regions of the auditory tonotopic map devoted to these frequencies. The duration of changes in Glyt2 mRNA evoked by unilateral labyrinthectomy, measured with the reverse transcription polymerase chain reaction, was 5-10 days. These data provide the first example of in vivo regulation of transporter transcription by neuronal activity.