L10 Flashcards
What are the main types of neurotransmitters, and how do they function?
Fast neurotransmitters (e.g., glutamate, GABA) act on ligand-gated ion channels. Slow neurotransmitters (e.g., dopamine, serotonin) act on G-protein-coupled receptors (GPCRs).
What is the role of GABA in the brain?
GABA is the main inhibitory neurotransmitter, reducing excitability by increasing chloride influx through ligand-gated channels.
How does the NMDA receptor function, and why is it significant?
NMDA receptors are calcium-permeable channels requiring glutamate and glycine binding to open. They are involved in learning and memory but can cause excitotoxicity if overstimulated.
What is the mechanism of action of benzodiazepines on GABA receptors?
Benzodiazepines, like diazepam, enhance the action of GABA by increasing its affinity for the GABAA receptor, leading to sedation.
What is the relationship between dopamine and Parkinson’s disease?
Parkinson’s disease is caused by the loss of dopamine neurons. L-DOPA is used to increase dopamine levels for treatment.
How do SSRIs work to treat depression?
SSRIs, such as fluoxetine, inhibit the serotonin transporter, increasing the availability of serotonin in the synaptic cleft to enhance mood.
What is the role of glycine in the CNS, and how can its inhibition affect the body?
Glycine acts as an inhibitory neurotransmitter in the spinal cord. Inhibition (e.g., by strychnine) can cause hyperexcitability and spasms.
What are the effects of NMDA receptor antagonists like ketamine?
Ketamine blocks NMDA receptors, acting as an anesthetic and reducing excitotoxicity.
How do serotonin receptors differ in their actions in the CNS?
Serotonin receptors include GPCRs like 5-HT1 (inhibitory) and 5-HT2 (excitatory), and 5-HT3, a ligand-gated ion channel affecting nausea.
What role do astrocytes play in glutamate regulation?
Astrocytes convert excess glutamate into glutamine, preventing excitotoxicity.
Explain the mechanisms of excitotoxicity caused by glutamate and its implications for brain health.
Excitotoxicity occurs when excessive glutamate overstimulates NMDA and AMPA receptors, leading to calcium overload in neurons. This activates enzymes like proteases and lipases, causing membrane damage, nitric oxide overproduction, and neurotoxicity. It is associated with stroke, trauma, and neurodegenerative diseases.
Compare the GABAA and GABAB receptors, including their structure and pharmacological modulation.
GABAA receptors are ligand-gated chloride channels mediating fast inhibition. Drugs like benzodiazepines enhance their action. GABAB receptors are GPCRs mediating slow inhibition via potassium channels. They reduce excitability and are less commonly targeted therapeutically.
Discuss the role of serotonin (5-HT) in mood regulation and the mechanisms of drugs targeting serotonin receptors.
Serotonin affects mood, behavior, and sensory processing. SSRIs block serotonin reuptake, increasing availability at synapses to alleviate depression. Agonists like sumatriptan target 5-HT1 for migraine relief, while 5-HT3 antagonists like ondansetron treat nausea.
What are the therapeutic and toxicological implications of dopamine in the CNS?
Dopamine regulates motor control, reward, and behavior. Its depletion causes Parkinson’s disease, treated with L-DOPA. Excess dopamine is linked to schizophrenia, managed with dopamine antagonists. Drugs targeting dopamine pathways can lead to addiction and side effects like dyskinesia.
Describe how drugs targeting NMDA receptors can be both beneficial and harmful.
NMDA receptor antagonists (e.g., ketamine) reduce excitotoxicity, benefiting conditions like Alzheimer’s disease and stroke. However, blocking these receptors can impair learning and memory and cause psychotic effects, as seen with high doses of ketamine.
