For any organism to experience what is commonly defined as a high—a psychoactive alteration of mood or perception—a substance must interact with the central nervous system (CNS). This requires the drug molecule to cross the blood-brain barrier and bind to specific neuroreceptors, triggering a chemical cascade that results in an altered state of consciousness. While snakes possess the core neurological architecture to process foreign chemicals, their unique biology dictates the potential effects, making true recreational intoxication unlikely. Exposure to psychoactive compounds almost universally results in a state of severe distress or poisoning.
The Necessary Biological Mechanisms
Experiencing a psychoactive effect requires the presence of evolutionarily conserved neuroreceptor systems within the brain. In snakes, as in mammals, the central nervous system relies on neurotransmitters like dopamine, serotonin, and GABA to regulate mood, movement, and behavior. These systems are the targets for nearly all psychoactive substances. Research has confirmed that snakes possess functional dopaminergic pathways, including the D1 and D2 receptors, which are the same receptors targeted by stimulants in humans.
When substances like dopamine agonists or monoamine oxidase inhibitors—drugs known to modulate neurotransmitter levels—are administered, they cause measurable changes in snake behavior. These effects include alterations in tongue-flicking rate and climbing activity, demonstrating a functional response to psychoactive compounds. This confirms that the basic neurological machinery exists for an external chemical to influence the snake’s perception and motor control. However, the presence of the system only indicates the potential for an effect, not the capacity for a pleasurable, recreational experience.
Unique Metabolic Processing in Reptiles
A snake’s ectothermic, or cold-blooded, physiology profoundly influences how its body processes any foreign chemical. The speed and efficiency of detoxification are directly tied to the snake’s surrounding environmental temperature. This means that a snake’s metabolic rate is much slower and more variable than that of a warm-blooded mammal, leading to a prolonged duration of a substance’s presence in the body.
The liver is responsible for chemical breakdown, primarily utilizing a group of enzymes known as Cytochrome P450 (CYP450). Snakes possess multiple forms of these enzymes, including families related to the mammalian CYP1A and CYP2B, which are responsible for metabolizing many drugs and toxins. The slower reptilian metabolism means the body takes longer to deactivate or excrete a psychoactive substance. This extended exposure can compound the negative effects, meaning a dose that might produce a temporary high in a mammal instead results in prolonged, severe toxicity for the snake.
Distinguishing Intoxication from Toxicity
The effects observed when a snake encounters a foreign substance are almost always signs of toxicosis, not intoxication in the human sense of altered euphoria. When veterinarians treat captive snakes, accidental exposures to common chemicals or medications frequently result in severe neurological distress. For instance, toxicity from antiparasitic drugs like ivermectin or antibiotics like metronidazole can lead to distinct signs of central nervous system poisoning.
These symptoms often manifest as ataxia (a loss of full control of bodily movements), involuntary eye movements (nystagmus), tremors, or even seizures. Such clinical signs represent the body reacting to a poison that is disrupting normal neurological function, not an altered state of pleasure. The snake’s reaction is a fight for survival against a toxin overwhelming its system, a far cry from the voluntary, psychoactive experience implied by “getting high.”