**1. Introduction**

Understanding brain and nerve poisons have been a long-standing tradition dating back to ancient times. By the turn of the twentieth century, contemporary physiological and biochemical investigations had elucidated a few of these poisons' mechanisms of action. *Neurotoxicity* is defined as any unfavorable effect on the central or peripheral nervous systems' chemistry, structure, or function induced by chemical or physical agents either at maturity or during development. Any impairment of normal function or adaptability to the surrounding environment is regarded as a side effect. Thus, even if functional and structural changes are minimal or reversible, the most prevalent morphological abnormalities, such as neurons, axonopathy, or myelinopathy, may be unfavorable [1].

Additionally, neurochemical alterations should be regarded as harmful even if they are reversible and transient and cause dysfunction. Neurotoxicity can also arise due to indirect effects, such as harm to the cardiovascular or hepatic systems or changes in the endocrine system. Numerous compounds function in various ways and can directly or indirectly affect the neurological system [2].

The nervous tissue present in the brain, spinal cord, and periphery includes an extraordinarily complex biological system that generally describes many of the original traits of individuals. However, as with any profoundly complex system, even minor disturbances to its environment can result in significant functional disturbances. Factors leading to the vulnerability of nervous tissue include a large surface area of neurons, a high lipid content that retains lipophilic toxins, high blood flow to the brain inducing increased effective toxin exposure, and persistence of neurons through an individual's lifetime, leading to the compounding of damages**.**

As the nervous system is more vulnerable to toxins, several mechanisms are designed to protect it from internal and external hazards, including the blood–brain barrier. The blood–brain barrier (BBB) and choroid plexus that provide a layer of protection against toxin absorption in the brain. The choroid plexuses are vascularized layers of tissue found in the brain's third, fourth, and lateral ventricles, which through the function of their ependymal cells, are responsible for the synthesis of cerebrospinal fluid (CSF). Importantly, through the selective passage of ions and nutrients and trapping heavy metals such as lead [1–3].

#### **2. Mechanism of action in neurotoxicity**

Many neurotoxicants function by inhibiting the GABAA receptor, resulting in prolonged closure of the chloride channel and excess nerve excitation (**Figure 1**). Cyclodiene, the organochlorine insecticide lindane, and some pyrethroid insecticides prove acute neurotoxicity, at least partly through this mechanism. Symptoms of GABA inhibition include dizziness, headache, nausea, vomiting, tremors, convulsions, and death. Other some acts via Na channel inhibitors (tetrodotoxin), K channel inhibitors (tetraethylammonium), Cl channel inhibitors (chlorotoxin), Ca channel inhibitors (conotoxin), inhibitors of synaptic vesicle release (botulinum toxin, tetanus toxin), receptor inhibitors (bungarotoxin), blood–brain barrier inhibitors (aluminum mercury), Ca-mediated cytotoxicity (lead), and toxins with multiple effects (ethanol). In some cases, the hemostasis of energy can be affected [2].

#### **Figure 1.**

*The neurotoxins block the receptors, thus preventing the maintenance of proper physiological function.*
