The purpose of the present study is to determine the effects of gallic acid (GA) on sodium arsenite (iAS)-induced behavior deficits and memory alteration in male rats. Thirty six animals were divided in to 6 groups (six animals in each) (i) saline+saline; (ii) saline+GA (50 mg/kg); (iii) saline+ GA (100 mg/kg) (iv) iAS + saline; (v) iAS + GA(50 mg/kg); (vi) iAS + GA (100 mg/kg). Animals were treated with iAS (2.5 mg/kg/ml); GA (50 and 100 mg/kg/ml) and saline (0.9%; 1 ml/kg) for 4 weeks. Repeated administration of iAS increases immobility time in forced swim test and decreases time spent in open arm (elevated plus maze) and light box (light dark activity box test) suggests depression like and anxiety-like symptoms respectively. On the other hand, animals treated with iAS + GA decreases immobility time and increases time spent in open arm and light box than saline+iAS treated animals suggests anxiolytic and antidepressant-like behavior of GA. Repeated administration of iAS also involves in memory impairment as observed in the Morris water maze test that is reversed by co-administration of GA, indicates that GA also involves in the enhancement of memory. Brain malondialdehyde (MDA) levels, antioxidant enzymes and acetylcholinesterase (AChE) activities also observed in the present study. Results show that iAS produces oxidative stress by increasing lipid peroxidation and decreasing antioxidant enzyme activity. Conversely co-administration of GA produces antioxidant effects by normalization of oxidative stress induced by iAS. Alteration in iAS induced AChE activity is also reversed by GA. It is suggested that GA via its antioxidant potential, has protective effects on iAS induced behavioral deficits and memory alteration. The findings have a strong implication on iAS induced neurological diseases, such as depression, anxiety, Alzheimer's disease and dementia etc.