Chapter 5 - Chapter 5: Barbiturates, General Anesthetics,...

Info iconThis preview shows pages 1–2. Sign up to view the full content.

View Full Document Right Arrow Icon
Chapter 5: Barbiturates, General Anesthetics, Gamma Hydroxybutyrate (GHB), and Antiepileptic Drugs (Julien, pp. 140-163) Background -Like alcohol, these are drugs that depress CNS function Sites and Mechanisms of Action (complex and controversial) -Barbiturates, benzodiapezines and other sedatives reduce electrical activity and whole- brain glucose metabolism in the brain -Is the cause reduced excitatory activity or increased inhibitory activity? Amnestic Properties -Several studies have found that sedatives attenuate glutamate neurotransmission -Hypothesis: amnestic properties of sedative drugs result from glutamate antagonism, as memory is highly dependent on the activity of glutamate neurons Anesthetic Properties -Barbs, benzos, anesthetics, and similar “depressant” drugs bind to the GABA-A receptor and facilitate binding of GABA to its receptor, and this plays a major role in knocking people out Increased Toxicity of Barbiturates -Unlike other depressants, barbs are capable of opening chloride channels independently of GABA availability—this increases the risk of overdose with barbs Sedative-Induced Brain Dysfunction -Any sedative, in high doses, can produce amnesia and a state of dementia -The elderly who already have some loss of nerve cell function are adversely affected by
Background image of page 1

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full DocumentRight Arrow Icon
Image of page 2
This is the end of the preview. Sign up to access the rest of the document.

This document was uploaded on 04/06/2011.

Page1 / 3

Chapter 5 - Chapter 5: Barbiturates, General Anesthetics,...

This preview shows document pages 1 - 2. Sign up to view the full document.

View Full Document Right Arrow Icon
Ask a homework question - tutors are online