TY - JOUR
T1 - Evidence for transient perinatal glutamatergic innervation of globus pallidus
AU - Greenamyre, Timothy
AU - Penney, John B.
AU - Young, Anne B.
AU - Hudson, Christopher
AU - Silverstein, Faye S.
AU - Johnston, Michael V.
PY - 1987
Y1 - 1987
N2 - There is no known glutamatergic innervation of globus pallidus (GP) in adult mammals, but we report that during postnatal development of the GP there are large, transient increases in both presynaptic high-affinity glutamate uptake and postsynaptic Na+-independent glutamate receptor binding. These glutamatergic markers increase rapidly in rat GP after birth and then decrease to adult levels over a period of weeks. A similar developmental pattern of pallidal glutamate binding was found in human brains. In contrast, binding in rat caudate-putamen (CPu) increases after birth, reaches a peak, and remains constant into adulthood. The results suggest that a glutamatergic pathway transiently innervates the globus pallidus during the perinatal period. Because glutamate is an excitotoxin, this pathway may account, in part, for the basal ganglia damage seen in some forms of cerebral palsy after perinatal hypoxia/ischemia.
AB - There is no known glutamatergic innervation of globus pallidus (GP) in adult mammals, but we report that during postnatal development of the GP there are large, transient increases in both presynaptic high-affinity glutamate uptake and postsynaptic Na+-independent glutamate receptor binding. These glutamatergic markers increase rapidly in rat GP after birth and then decrease to adult levels over a period of weeks. A similar developmental pattern of pallidal glutamate binding was found in human brains. In contrast, binding in rat caudate-putamen (CPu) increases after birth, reaches a peak, and remains constant into adulthood. The results suggest that a glutamatergic pathway transiently innervates the globus pallidus during the perinatal period. Because glutamate is an excitotoxin, this pathway may account, in part, for the basal ganglia damage seen in some forms of cerebral palsy after perinatal hypoxia/ischemia.
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U2 - 10.1523/jneurosci.07-04-01022.1987
DO - 10.1523/jneurosci.07-04-01022.1987
M3 - Article
C2 - 2883265
AN - SCOPUS:0023136512
SN - 0270-6474
VL - 7
SP - 1022
EP - 1030
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 4
ER -