E. Friauf et al., Developmental expression of the glycine transporter GLYT2 in the auditory system of rats suggests involvement in synapse maturation, J COMP NEUR, 412(1), 1999, pp. 17-37
The synaptic action of many neurotransmitters is terminated by specific tra
nsporters that remove the molecules from the synaptic cleft and help to rep
lenish the transmitter supply. Here, we have investigated the spatiotempora
l distribution of the glycine transporter GLYT2 in the central auditory sys
tem of rats, where glycinergic synapses are abundant. In adult rats, GLYT2
immunoreactivity was found at all relay stations, except the auditory corte
x. Many immunoreactive puncta surrounded the neuronal somata in the cochlea
r nuclear complex, the superior olivary complex, and the nuclei of the late
ral lemniscus. In contrast, diffuse neuropil labeling was seen in the infer
ior colliculus and the medial geniculate body. The punctate perisomatic lab
eling and the diffuse neuropil labeling were very similar to the staining p
attern described previously with glycine antibodies in the auditory system,
suggesting that GLYT2 is a reliable marker for glycinergic synapses. Howev
er, there was a discrepancy between cytoplasmic GLYT2 and glycine labeling,
as not all neuron types previously identified with glycine antibodies disp
layed somatic GLYT2 immunoreactivity. During development, GLYT2 immunoreact
ivity appeared between embryonic days 18 and 20, i.e., shortly after the ti
me when the earliest functional synapses have been established in the audit
ory system. Labeling turned from a diffuse pattern to a clustered, punctate
appearance. The development was also characterized by an increase of the s
ignal intensity, which generally lasted until about postnatal day 10. There
after, a decrease occurred until about postnatal day 21, when the mature pa
ttern was established in most nuclei. Because of the perinatal onset of GLY
T2 immunoreactivity, we speculate that the transporter molecules participat
e in the process of early synapse maturation. (C) 1999 Wiley-Liss, Inc.