Epidemiological studies have linked developmental manganese (Mn) exposure to increased risk of ADHD and related symptoms in children and adolescents. Prior studies have shown that developmental Mn exposure causes lasting ADHD-like symptoms in a rat model, that these symptoms are accompanied by a hypofunctioning catecholaminergic system in fronto-cortical-striatal brain areas, and that methylphenidate, a DAT/NET antagonist, is efficacious in ameliorating the ADHD-like symptoms. However, stimulant medications such as methylphenidate do not lessen symptoms in 25-30% of children and adolescents diagnosed with ADHD, indicating the need for alternative ADHD medications. Guanfacine, a specific noradrenergic α2A receptor agonist, is an alternative non-stimulant ADHD medication, though currently there is no evidence whether it is efficacious in ameliorating the ADHD-like symptoms caused by developmental Mn exposure. Given this, we hypothesize that (1) guanfacine will ameliorate the lasting ADHD-like deficits caused by developmental Mn exposure, and (2) the guanfacine dose-response will differ in Mn vs control animals, providing further mechanistic support for noradrenergic dysfunction as a contributor to the Mn impairments. Male Long-Evans neonate rats were orally dosed with vehicle or Mn (50 mg/kg/d) from PND 1 – 21, and orally treated with guanfacine (0, 0.1, or 0.3 mg/kg/d) as adults during testing for attentional, impulse control, and sensorimotor function. Findings show that developmental Mn exposure causes lasting deficits in impulse control, attentional, and sensorimotor function, and that oral guanfacine was efficacious in ameliorating the Mn deficits, though efficacy depended upon the duration of guanfacine treatment and the functional domain of the Mn deficits. Moreover, guanfacine had little or no effect on impulse control, focused and selective attention, and sensorimotor function in control animals, or in Mn-exposed animals under trial conditions where Mn deficits did not emerge. These findings 1) demonstrate the efficacy of oral guanfacine, an alternative non-stimulant ADHD medication, to ameliorate the lasting ADHD-like symptoms caused by developmental Mn exposure, 2) support that hypofunctioning of the noradrenergic system in part mechanistically underlies the lasting Mn deficits, and 3) suggest that people with environmentally-induced ADHD, such as from elevated Mn exposure, may benefit from oral guanfacine treatment.