Slow IPSC kinetics, low levels of alpha 1 subunit expression and paired-pulse depression are distinct properties of neonatal inhibitory GABAergic synaptic connections in the mouse superior colliculus
R. Juttner et al., Slow IPSC kinetics, low levels of alpha 1 subunit expression and paired-pulse depression are distinct properties of neonatal inhibitory GABAergic synaptic connections in the mouse superior colliculus, EUR J NEURO, 13(11), 2001, pp. 2088-2098
Remodelling of visual maps in the superior colliculus (SC) depends on neuro
nal activity. Synaptic inhibition could contribute to this process because
spontaneous spike discharge in the SC was modulated by GABA(A) receptor act
ivation at postnatal days (P) 1-3. To investigate the functional capacity o
f GABAergic synaptic transmission at this early stage of development, whole
-cell patch-clamp recordings were made from wide field neurons (WFNs) in ho
rizontal slices comprising the superficial grey layer of the SC. Focal stim
ulation in the vicinity of WFNs evoked tetrodotoxin-sensitive stimulus-lock
ed inhibitory postsynaptic currents (eIPSCs). The failure rate of eIPSCs wa
s low (approximate to 0.2), and the maximal amplitude of evoked unitary eIP
SCs exceeded the amplitude of average miniature IPSCs (mIPSCs) by a factor
of 4-5, suggesting that action potential-mediated GABA release was more eff
ective than spontaneous release. Some of the properties of GABAergjc synapt
ic transmission in the neonatal SC were age-specific. In contrast with eIPS
Cs in the more mature SC at P20-22, neonatal eIPSCs decayed more slowly, pr
eferentially fluctuated in duration, not amplitude, and mostly lacked tempo
ral summation, due to depression at shorter intervals. The paired-pulse rat
io (eIPSC(2):eIPSC(1)) was inversely related to the duration of eIPSCs. PCR
analysis showed, in addition, that the ratio of alpha1: alpha3 subunit exp
ression was lower in the neonatal SC. Together, these results suggest that,
at a young age, efficacy of GABAergic synaptic transmission is primarily c
onstrained by the slow kinetics and the saturation of postsynaptic GABA(A)
receptors.