Cholinergic, monoaminergic and glutamatergic changes following perinatal asphyxia in the rat

Perinatal asphyxia (PA) is considered to lead to a variety of brain disorde rs including spasticity, epilepsy, mental retardation, and minimal brain di sorder syndromes and may form the basis for psychiatric and neurodegenerati ve diseases later in life. We examined markers for neuronal transmission in volved in the pathomechanisms of PA and candidates as mediators for long-te rm sequelae. We tested tyrosine hydroxylase (TH) and the vesicular monoamin e transporter (VMAT) representing the monoaminergic system, the vesicular a cetylcholine transporter (VAChT), and the excitatory amino acid carrier 1 ( EAAC1), a neuronal subtype or the glutamate transporter, using immunohistoc hemistry on brain sections of rats subjected to graded PA. Three months fol lowing the asphyxiant insult immunoreactive (IR)-TH was decreased in striat um, hippocampus, thalamus, frontal cortex, and cerebellum, IR-VMAT was incr eased, and IR-VAChT was decreased in striatum. IR-EAAC1 glutamate transport er was increased in frontal cortex. The cholinergic, monoaminergic, and glu tamatergic changes, still observed 3 months after the asphyxiant insult: ma y reflect their involvement in the pathomechanisms of PA and indicate mecha nisms leading to long-term complications of PA. The variable consequences o n the individual markers in several brain regions may be explained by speci fic susceptibility of cholinergic, monoaminergic, and glutamatergic neurons to the asphyxiant insult.