TRANSIENT MOLECULAR VISUALIZATION OF OCULAR DOMINANCE COLUMNS (ODCS) IN NORMAL ADULT MARMOSETS DESPITE THE DESEGREGATED TERMINATION OF THE RETINO-GENICULO-CORTICAL PATHWAYS
U. Markstahler et al., TRANSIENT MOLECULAR VISUALIZATION OF OCULAR DOMINANCE COLUMNS (ODCS) IN NORMAL ADULT MARMOSETS DESPITE THE DESEGREGATED TERMINATION OF THE RETINO-GENICULO-CORTICAL PATHWAYS, Journal of comparative neurology, 393(1), 1998, pp. 118-134
The activity-dependent immediate early gene protein Krox-24, expressed
in the neocortex at high basal levels, decreases rapidly upon neurona
l deactivation (Chaudhuri et al. [1995] Vis. Neurosci. 12:35-50). In i
nfant marmosets, as in most primates, the geniculo-cortical terminatio
ns segregate into eye-specific anatomical ocular dominance columns (OD
Cs), which disappear, however, during adolescence (Spatz [1989] Brain
Res. 488:376-380), resulting in balanced inputs from the two eyes (Sen
gpiel et al. [1996] Vis. Neurosci. 13:145-160). Nevertheless, we found
, in adult marmosets, 24 hours after monocular retinal activity blocka
de by tetrodotoxin, distinct alternating compartments of potentiated a
nd depressed Krox-24-like immunoreactivity (Krox-IR) in layer IV of ar
ea 17. This pattern of Krox-IR disappeared at 10 days of retinal silen
cing, but was still present at this survival time in stains for cytoch
rome oxidase or NADPH-diaphorase. After 20 days of retinal silencing,
the pattern was not demonstrable with any of the three stains. We term
these compartments physiological ODCs, in contrast to the anatomical
ODCs of most primates. If the anatomical ODCs of infant marmosets disa
ppear by collateral sprouting into the inappropriate ODCs, then the co
llateral geniculo-cortical synapses might differ slightly in their pro
perties from the original ones. We silenced the sets of original and c
ollateral synapses of the one ocularity. This apparently transiently i
nitiated, at the synapses driven by the intact eye, two different comp
lex processes leading to molecular potentiation at the original synaps
es and to molecular depression at the collateral synapses. J. Comp. Ne
urol. 393:118-134, 1998. (C) 1998 Wiley-Liss, Inc.