( k ) etamine - __________________________signal secret

K E T A M I N E

SYNTHESIZED IN 1962, HAS BEEN USED CLINICALLY AS AN INTRAVENOUS ANESTHETIC SINCE 1970.

KETAMINE HAS ALSO BEEN OBSERVED TO INDUCE
SYNAPTOGENESIS
—THE FORMATION OF NEW CONNECTIONS BETWEEN BRAIN CELLS

(...OR
NEUROGENESIS...)

THE FIRST RECOGNIZED PRIMARY MECHANISM OF ACTION OF KETAMINE IS INHIBITION OF NMDA RECEPTORS. THESE RECEPTORS ARE LOCATED AT SYNAPSES WHERE GLUTAMINE IS THE NEUROTRANSMITTER. THEY ARE INVOLVED IN LEARNING AND MEMORY [REZVANI, 2006].

INHIBITION OF NMDA RECEPTORS DECREASES EXCITATION IN SOME AREAS OF THE NERVOUS SYSTEM. IN THE CORTEX, THIS ALLOWS FOR INHIBITORY CIRCUITS TO HAVE A GREATER INFLUENCE. IN ADDITION, KETAMINE HAS BEEN SHOWN TO POTENTIATE CERTAIN FORMS OF THE GABAA RECEPTOR [HEVERS ET AL. 2008]. IT HAS BECOME CLEAR, HOWEVER, THAT KETAMINE HAS MANY OTHER EFFECTS AS A NEUROMODULATOR AND A MODULATOR FOR GENE EXPRESSION [SLEIGH ET AL. 2014]. IN THE SPINAL CORD, INHIBITION OF NMDA RECEPTORS LEADS TO DECREASED RELEASE OF ACETYLCHOLINE LEADING TO ANALGESIA [LYDIC AND BAGHDOYAN, 2002]. WHEN ABUSED AT SUBANESTHETIC DOSES, KETAMINE PRODUCES DISSOCIATIVE AND HALLUCINOGENIC EFFECTS.

IN FACT, LOW DOSES OF KETAMINE (1–4.5 MG/KG INTRAVENOUSLY OR 6.5–13 MG/KG INTRAMUSCULARLY) TAKE ABOUT 30–40 MIN TO SHOW MILD PSYCHOTOMIMETIC AND DISSOCIATIVE EFFECTS THAT THEN COMPLETELY DISSIPATE BY 80 MIN [ZARATE ET AL. 2006]. SOME OF THE SIDE EFFECTS OF KETAMINE INCLUDE PERCEPTUAL DISTURBANCES, CONFUSION, ELEVATIONS IN BLOOD PRESSURE, EUPHORIA, DIZZINESS, COGNITIVE AND MEMORY IMPAIRMENTS AND INCREASED LIBIDO [ZARATE ET AL. 2006]. HOWEVER, THE MAJORITY OF SIDE EFFECTS CEASE WITHIN 80 MIN AFTER THE INFUSION. ACTIVATING EFFECT ON MIDBRAIN DOPAMINERGIC CELL FIRING AND THE STIMULATION OF DOPAMINE RELEASE.

STUDIES THAT REVEAL HOW THE DRUG BEING HIGHLY REINFORCING
PARTICULARLY IN THE PREFRONTAL CORTEX.

IT INDUCES SYNAPTOGENESIS
(OR NEUROGENESIS)

_THE FORMATION OF NEW CONNECTIONS BETWEEN BRAIN CELLS____________________