Phantasmidine

Phantasmidine is a nicotinic agonist that acts at acetylcholine receptors. It mimics the effects of acetylcholine on the body's neuronal-based nervous systems (both the central nervous system [CNS] and the peripheral nervous system [PNS]) and the muscle-based nervous system (the somatic nervous system).

Nicotinic acetylcholine receptors in general comprise a sub-section of the family of ligand-gated ion channels, of which ions such as Ca⁺², Na⁺, and K⁺ are permeable to the barrier.[7] Phantasmidine is selective for nicotinic acetylcholine receptors (nAChR) containing ß4 subunits; however, responses in neuromuscular nAChR (such as ß1-containing receptors) and ß2-containing neuronal receptors (such as K-177 cells) are also elicited, albeit to a lesser degree (Fitch et al. 331-337).

Studies conducted in mice have proven useful in showing the interaction and relationship of nAChR α- and ß- subunits to the body's processes and interaction with this toxin. In particular, α3 and ß4 nAChR subunits have shown to play a role in ganglionic transmission, indicating they play a role in the stimulation of either the parasympathetic nervous system (as an agonist) or the sympathetic nervous system.

• When the ß4 subunit was eliminated in mice, the mice were resistant to nicotine-induced seizures and displayed reduced nicotine withdrawal (when compared with wild mice) (Fitch et al. 331-337).
• α4 subunits have been proven to play an important role in preserving the body's nociceptive response (Zhou 120 – 123); when the body experiences pain, the receptors involved in this pathway will signal the autonomic nervous system and create a subsequent sensation of pain. Due to the continuous influx of positive charge (as a result of the depolarization of the cell), the cell will continue to send action potentials, causing the brain to receive constant pain signals.
• ß2 subunits have been indicated to play a role in the body's learning, memory, and addiction pathways (Zhou 120 – 123).

The table provided below[8][9] summarizes the types of cells that phantasmidine affects as well as the resultant behavior exhibited in the listed species. The depolarization of a cell results from the activation of a cation-permeable membrane, which causes an influx of Ca⁺² into the cell. This influx of positive charge induces the release of acetylcholine into the body to interact with the parasympathetic nervous system. This, in turn, causes the inhibitory responses exhibited.

Not much about the exact toxicity of phantasmidine is known; however, epibatidines in general are 200 times more potent than morphine (Riley 21). Phantasmidine interacts with the body's stimulation of the parasympathetic nervous system, making it a dangerous inhibitory poison. Symptoms of phantasmidine poisoning may include decreased heart rate, continuous sensations of pain, coma, and (in larger doses) death.

A plausible antidote for phantasmidine poisoning would be mecamylamine, a nAChR antagonist (Zhou 120 – 123). Other nAChR antagonists may serve as effective antidotes for this particular type of poisoning, as they would block nAChR to prevent the acetylcholine agonist from binding to the acetylcholine receptors.

Nicotinic agonists in general have proven useful analgesics in treating disorders that respond to nAChR (Fitch et al. 1-17) (Zhou 120-123). For example, phantasmidine or phantasmidine-derivatives are being tested for their potential use as short-acting muscle relaxants. They are also currently being researched as a potential analgesic for the treatment of:

• Neurodegenerative disorders (such as dementia caused by Alzheimer's disease)
• Myasthenia Gravis
• Tobacco dependence
• Glaucoma
• Tourette syndrome
• Cardiovascular disorders (such as hypertension)
• Psychiatric disorders (such as schizophrenia)
• Pain
• Epilepsy

Such treatments can be administered parenterally (intravenously, intradermally, intramuscularly) or through inhalation of a pharmaceutically-composed aerosol.