The synthetic compound 2C-B produces a biphasic effect on movement in rats: initial inhibition followed by excitation, while amphetamine only causes hyperactivity. Both drugs disrupt prepulse inhibition of the acoustic startle reaction, a measure of sensory gating, but have opposite effects on the startle itself. 2C-B increases dopamine and decreases its metabolite DOPAC in the nucleus accumbens, a brain region linked to reward. Low doses of 2C-B reduce electrical brain activity and connectivity; a high dose first decreases then increases brain wave power and connectivity. Increases in theta and alpha brain waves correlate with heightened movement and dopamine levels. These results suggest 2C-B shares properties with hallucinogens, entactogens, and stimulants, and its dopamine effects may indicate psychotomimetic and addictive potential.
Research using non-competitive NMDA receptor antagonists—phencyclidine, ketamine, and dizocilpine—produces behavioral changes in humans and rats that resemble schizophrenia symptoms. Acute and chronic administration models show phenomenological validity and help test potential antipsychotic drugs. However, schizophrenia's pathophysiology remains unexplained. The neurodevelopmental model suggests that early-life NMDA receptor antagonism increases apoptosis or alters glutamatergic receptor function during central nervous system development, leading to psychosis that often emerges only in adulthood. Chronic antagonist administration triggers adaptation mechanisms that match findings in schizophrenia patients, making this model useful for studying the disease's pathophysiology.