Aim and Objective <p>Stress has become an integral part of life, often triggering various biological systems involved in maintaining homeostasis and causing a range of physiological and pathological changes depending on the type and duration of the stress. Further, environmental chemical significantly contributes to intensify the stress.</p> Methods <p>This study investigated how prior exposure to chronic psychological stress (immobilization stress, IMS) or physical stress (forced swim stress, FSS) modifies lambda-cyhalothrin (LCT)-induced dopaminergic and neurobehavioral impairments.Neither IMS (one session, 15 min/day in restrainer for 28 days), FSS (one session,3 min/day for 28 days), nor LCT alone (3.0 mg/kg body weight, p.o. for 3 days on days 26–28) produced significant changes in motor activity, rotarod performance, or DA-D2 receptor in the corpus striatum brain region as compared with controls. These treatments alone caused only marginal alterations in tyrosine hydroxylase (TH) mRNA expression, TH immunoreactivity, and Nissl staining in the striatum region. However, pre-exposure to IMS or FSS for 28 days followed by LCT treatment distinctly impaired motor activity and rotarod performance. Exhibit changes in striatal dopamine receptor binding, TH mRNA expression and immunoreactivity and altered Nissl staining compared with IMS, FSS, or LCT alone.</p> Conclusion <p>These findings suggest that chronic psychological or physical stressors enhance the brain's susceptibility to LCT-induced dopaminergic impairments, leading to measurable neurobehavioral deficits.</p> Graphical abstract <p>Enhanced vulnerability to lambda-cyhalothrin induced neurotoxicity in rats pre-exposed to stress.</p>