## 1 Introduction  
Atrazine is designed specifically to impair the physiology of weeds [1]; however, the physical and chemical properties of atrazine, such as its half-life, slow degradation [2], and solubility in different mediums, contribute to its persistence in the environment and, consequently, its contamination of ground, surface, and drinking water [3; 4; 5]. This suggests a constant presence of atrazine and its degradation products in the environment and, therefore, in drinking water and aquatic and terrestrial environments [3], with inevitable pathological consequences. The effects of atrazine exposure have been widely reported such as impaired development in fish [6] and perturbed immunology and growth in _Xenopus laevis_[7; 8]. However, most information on atrazine-induced effects in adult animal models have focused mostly on its endocrine-disrupting abilities, particularly in _Xenopus laevis_ gonadal morphology [9; 10; 11]. Furthermore, atrazine and its metabolites can bio-accumulate in aquatic microbiota with adverse aquatic ecosystem implications [12] and can induce several organ toxicities in non-target organisms. In organs such as the cerebellum, mostly physiological and biochemical effects of atrazine have been reported relative to perturbations of cerebellar pathophysiology and cerebral oxidative stress in quails and rats [13; 14; 15], as well as behavioral and neurotransmitter deficits in mice [16]. However, complementary reports on structural toxicity (histopathology) is lacking in the cerebellum, while atrazine cardiac toxicity in frogs has only been previously reported by us [17]. Furthermore, atrazine is widely known for its ability to disrupt estrogen and androgen receptors [18], but little is known about atrazine-induced effects on the histopathology of voltage-gated receptors (IP\({}_{3}\)Rs) in the heart (peripheral) and cerebellum (central) and the differential effects in both organs relative to their crucial functions. The frog heart and brain contain an abundance of excitable cells with voltage-gated channels on their membranes. Sodium, potassium, and calcium are physiologically important ions, and their homeostatic concentrations in human serum levels and frog heart tissue are vital for normal neuronal and cardiac function [19; 20]. In cardiomyocytes, each calcium ion released is accompanied by sodium transportation via sodium-potassium pumps [21; 22]. Additionally, calcium release is directly required for the initiation of cardiac excitation-contraction coupling and the activation of neuronal dendritic development, neuronal survival, and synaptic plasticity [23; 24]. Furthermore, cardiac cells and cerebellar neurons depend on IP\({}_{3}\)Rs for modulating calcium levels in response to external stimuli [25; 26]. Physiologically, myocytes and neurons are dependent on the efflux of calcium into the cytosol for excitation-contraction coupling and modulation of synaptic transmission, respectively, particularly cerebellar Purkinje cells, where IP\({}_{3}\)Rs are predominantly expressed [27]. Pathologically, the IP\({}_{3}\)Rs levels and genes in the heart and cerebellum have been associated with hypertrophy and spinocerebellar ataxia, respectively [28; 29]. However, histopathological evidence of atrazine IP\({}_{3}\)R toxicity in the _Xenopus_ frog cerebellum and heart is lacking. Hence, this study is directed at investigating the possible adverse impact of atrazine on the IP\({}_{3}\)Rs and its expression in the heart (peripherally located) and cerebellum (centrally located) of the adult _Xenopus_ frog at different concentrations of environmentally relevant levels of 0.01 ug/L, 200 ug/L [7; 30], and 500 ug/L, which has been reported in ambient surface water of sugarcane growing areas [31].