Cocaine (COC) [BSA]

In 1855, German chemist Friedrich first extracted anesthetic ingredients from coca leaves and named it Erythroxylon. In 1859, Austrian chemist Neumann refined a higher purity substance and named it cocaine. This compound is also known as cocaine. In medicine, it is used as a local anesthetic or vasoconstrictor. Due to its good anesthetic effect and strong penetration, it is mainly used for surface anesthesia, but due to its strong toxicity, it is not suitable for injection. At the same time, it can be used as a strong natural central nervous system stimulant, but it is also abused due to its excitatory effect on the central nervous system. Since 1985, it has become one of the world's major drugs, mostly in America and Europe.

Figure 1. Cocaine causes transcription-dependent neuroplasticity in the reward pathway.(Sources: Rogge GA, et al. 2013)

Studies have shown that cocaine can cause damage to the human digestive system, immune system, cardiovascular system and genitourinary system. In addition, cocaine acts as a dose-dependent hepatotoxin, which can cause hepatocyte necrosis. Research has found that using a small amount of cocaine-like substances can eliminate fatigue and improve mood. This is because it can block the body's nerve conduction, produce local anesthesia, and stimulate the cerebral cortex and the central nervous system by enhancing the activity of chemical substances in the body. Users show high emotions, restlessness, and even aggressive tendencies. Cocaine is a tropane alkaloid with a molecular formula of C₁₇H₂₁NO₄. Its structural study found that cocaine is a colorless, odorless, monoclinic crystal with a melting point of 98°C. Cocaine is almost insoluble in water, but soluble in organic solvents such as ethanol and ether, but its hydrochloride is easily soluble in water. Cocaine is an ester. When hydrolyzed with acid or alkali, it produces benzoic acid, methanol, and L-ecgonine. This reaction is reversible.

Cocaine is a stimulant that directly affects neurons in the brain that are related to pleasure transmission. These neurons use the neurotransmitter dopamine to transmit pleasure and excitement. Studies have shown that under normal physiological conditions, excitation signals are transmitted from the axon terminals in the form of electrical signals. Afterwards, the electrical signal stimulates the calcium ion channels of the presynaptic membrane, allowing calcium ions outside the membrane to enter the synaptic vesicles inside the membrane through the calcium ion channels. This process stimulates the synaptic vesicles to move to the presynaptic membrane and fuse with it, and finally release neurotransmitters. Neurotransmitters reach the postsynaptic membrane through free diffusion in the tissue fluid, bind to the relevant receptors on the postsynaptic membrane, and exert their effects, changing the permeability of the postsynaptic membrane to ions and triggering changes in the postsynaptic membrane potential. In this way, the excitation signal is transmitted from one neuron to the next neuron in the form of electrical signal-chemical signal-electrical signal. After the neurotransmitter takes effect, it separates from the receptor and is quickly explained or recycled into the cell to prevent it from continuing to act. When a person takes cocaine, cocaine enters the human body through the respiratory system and shuts down the transporter that recycles dopamine on the presynaptic membrane, so dopamine stays in the synaptic cleft and continues to act. The cell cannot accept long-term stimulation, so the nervous system will adjust to reduce the dopamine receptors on the postsynaptic membrane. After the effect of cocaine is lost, the dopamine receptors have been reduced. When dopamine is released again, the normal excitement level of the body is weakened. In order to maintain the normal excitement intensity, drug addicts will take drugs again, thus forming a vicious cycle and making people addicted. Similarly, some stimulants and antidepressants have the same mechanism, which occurs in the synaptic structure and inhibits the recycling of neurotransmitters by the presynaptic membrane through some chemical drugs.

COC