A major goal in behavioral neuroscience is to identify the neural mechanisms underlying learning and memory. Fear conditioning models, including contextual and cued conditioning, are widely used to assess associative learning in rodents; however, commercially available systems for these experiments are often expensive (> $4000), limiting accessibility and reproducibility across laboratories. Here, we present a low-cost (about $100), modular fear conditioning platform for rodents that enables precise control of experimental parameters while maintaining compatibility with standard behavioral protocols. The fear conditioning system consists of conditioning chambers equipped with stainless-steel grid floors, a custom-built constant-current foot-shock generator, and an auditory cue delivery section, all synchronized with video-based behavioral recording. Shock intensity, duration, and timing are fully programmable, and the platform supports both contextual and cued fear conditioning paradigms.

Background: Cannabis is a widely used illicit drug with various threats of personality syndrome, and Nigella sativa has been widely implicated as having therapeutic efficacy in many neurological diseases. The present study investigates the ameliorative efficacy of Nigella sativa oil (NSO) on cannabis-induced moto-cognitive defects. Methods: Scopolamine (1 mg/kg i.p.) was given to induce dementia as a standard base line for cannabis (20 mg/kg)-induced cognitive impairment, followed by an oral administration of NSO (1 ml/kg) for 14 consecutive days. The Morris water maze (MWM) paradigm was used to assess the memory index, the elevated plus maze was used for anxiety-like behaviour, and the open field test was used for locomotor activities; thereafter, the rats were sacrificed and their brains were removed for histopathologic studies. Results: Cannabis-like Scopolamine caused memory impairment, delayed latency in the MWM, and anxiety-like behaviour, coupled with alterations in the cerebello-hippocampal neurons. The post-treatment of rats with NSO mitigated cannabis-induced cognitive dysfunction as with scopolamine and impaired anxiety-like behaviour by increasing open arm entry, line crossing, and histological changes. Conclusions: The observed ameliorative effects of NSO make it a promising agent against moto-cognitive dysfunction and cerebelo-hippocampal alterations induced by cannabis.