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Evidence for transient perinatal glutamatergic innervation of globus pallidus
Insights
Transient glutamatergic innervation of the globus pallidus (GP) occurs during early development in mammals. This pathway may contribute to basal ganglia damage in conditions like cerebral palsy following perinatal hypoxia.
Area of Science:
- Neuroscience
- Developmental Biology
- Neurochemistry
Background:
- The globus pallidus (GP) in adult mammals is not known to receive glutamatergic innervation.
- Glutamate is a key excitatory neurotransmitter with excitotoxic potential.
Purpose of the Study:
- To investigate the presence and pattern of glutamatergic markers during postnatal development of the globus pallidus.
- To explore the potential role of transient glutamatergic pathways in perinatal brain injury.
Main Methods:
- Assessed presynaptic high-affinity glutamate uptake in rat globus pallidus (GP) during postnatal development.
- Measured postsynaptic Na+-independent glutamate receptor binding in rat GP and caudate-putamen (CPu) across development.
- Examined developmental patterns of pallidal glutamate binding in human brain tissue.
Main Results:
- Rat GP showed significant, transient increases in glutamate uptake and receptor binding post-birth, decreasing to adult levels over weeks.
- Human brains exhibited a similar developmental trajectory for pallidal glutamate binding.
- In contrast, the rat caudate-putamen (CPu) showed glutamate binding that increased post-birth and remained elevated into adulthood.
Conclusions:
- A transient glutamatergic pathway innervates the globus pallidus during the perinatal period.
- This developmental glutamatergic pathway in the GP may be implicated in basal ganglia damage associated with perinatal hypoxia/ischemia, potentially contributing to cerebral palsy.
Abstract:
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.