Schizophrenia Pharmacology and Neurochemical Abnormalities

Flashcards covering the neurochemical abnormalities, dopamine pathways, biological changes, and animal models associated with schizophrenia pharmacology.

L-DOPA/DA

Substances that increase dopamine function and can mimic the positive symptoms of schizophrenia.

Amphetamine

A drug that exacerbates symptoms in schizophrenia patients at lower doses and can cause schizophrenia-like positive symptoms.

D2 receptors

Dopamine receptors for which all antipsychotics have a common affinity.

D1/D2 ratio

Imaging studies show an abnormal ratio of these receptors, including high D1 density in cortical areas, which can disrupt information processing.

5-HT2A receptor agonists

Psychomimetic substances that provoke mystical states, synesthesia, and schizophrenia-like symptoms or hallucinations.

Second generation antipsychotics (SGA)

Antipsychotics that typically block 5-HT2A receptors.

5-HT1A receptors

Receptors that some antipsychotics interact with, possibly leading to beneficial cognitive effects.

Glutamate-driven excitotoxicity

A hypothesis suggesting this process could underlie the reduction in gray matter volume observed in schizophrenia.

NMDA receptors

Glutamate receptors whose hypofunction is associated with abnormal brain neurodevelopment; they require glycine (D-serine) binding for activation and are blocked by magnesium.

Non-competitive NMDA antagonists

Substances like PCP and ketamine that can induce behavioral changes similar to positive and negative symptoms and cause cognitive impairment.

PCP (angel dust)

A street drug and non-competitive NMDA antagonist that can exacerbate or cause symptoms of schizophrenia.

Ketamine

An anaesthetic and street drug that acts as a strong inhibitor at a non-competitive binding site on the NMDA receptor.

Memantine

A drug that acts as a weak NMDA antagonist and cognition enhancer, typically given for Alzheimer's Disease (AD).

Mesolimbic VTA pathways

Dopamine pathways involved in motivation and pleasure that are hyperactive in schizophrenia, leading to positive symptoms.

Mesocortical VTA pathways

Dopamine pathways involved in emotion and cognition that are underactive in schizophrenia, leading to cognitive impairment and negative symptoms.

Nigrostriatal SNC pathways

Dopamine pathways responsible for the control of movements.

Synaptic pruning

A process that may become excessive in schizophrenia due to abnormalities in microglia.

Antibodies against NMDA receptors

Found in $2-5\%$ of patients who are resistant to antipsychotics; this condition can be treated with selective plasma filtration.

Chronic neonatal administration of PCP

An animal model that induces lasting cognitive deficits and increases in putative equivalents of positive symptoms.

D-amphetamine (animal model)

A model used to induce excessive motor activity involving the activation of dopamine D2 receptors in the limbic pathway.

Drug-induced catalepsy

A test used to evaluate the ability of a drug to cause motor side effects.

GABA chandelier neurons

Neurons in the prefrontal areas whose involvement is hypothesized in brain neuronal abnormalities of schizophrenia.