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Lecture Four

CNS Depressants

Why use a CNS Depressant? * Therapeutic reasons:for anxiety or anxiety-ridden depression, for motor problems (PD, motor spasms&rigidity), help insomnia. Behavioural reasons:get high (recreational), maliciously (roofies), to get sedated for sleep but not prescribed. Addictive reasons
Recall the FOUR Primary uses for CNS Depressants! (from first page of lecture notes) *
A drug that reduces anxiety is called what? * Anxiolytic
What is an anxiolytic? * A drug that reduces anxiety
What are some drugs historically used to relax/sleep/anaesthetise/dull the pain? * Alcohol, Opium, Nicotine, Marijuana/Cannabis
What is the definition of a CNS Depressant? A drug that depresses/dampens activity in the CNS
In general terms, how do you decrease excitatory tone or increase inhibitory tone? You target neurotransmitters
Glutamate is excitatory or inhibitory? Excitatory - excites neurons
GABA is excitatory or inhibitory? Inhibitory - inhibits neurons
Why is Glucose so important? How does it relate to the important of eating food regularly? * You have to eat food regularly because it is how the brain gets Glucose and without Glucose the brain suffers.
Name the four receptors for Glutamate (Glu) * NMDA, Kainate, AMPA, mGlu
Which of the four receptors for Glutamate are ionotropic? NMDA, Kainate, AMPA
Which of the four receptors for Glutamate are metabotropic? mGlu
What is the simple difference between ionotropic receptors and metabotropic receptors? * Ionotropic receptors can open or close a channel while Metabotropic receptors do not have a channel that opens or closes, instead they are linked to another small chemical called a G-protein.
How does the Glutamate receptor do clearance? * Reuptake occurs via Glutamate transporters.
What is an Autoreceptor? * A receptor that slows down or stops further neurotransmitters releasing by binding with a presynaptic receptor. (it is inhibitory, control mechanism)
Specifically, how would you get a CNS depressant to decrease excitation? * Would target the Glutamatergic system to decrease the Glutamatergic tone
Specifically, how would you get a CNS depressant to increase inhibition? * Would target the GABAergic system to increase the GABAergic tone.
Which one is more common form of CNS depressant? (decrease excitation or increase inhibition?) * increase inhibition by targeting the GABAergic system to increase the GABAergic tone.
Could you just drink GABA? * No, because the GABA molecule cannot pass the the Blood-Brain-Barrier so wont work if you drink it. Instead gave to try other approaches.
With an CNS depressant involving GABA, what is the end goal? In the post-synaptic cell we want as much GABAergic tone/ GABA activity as possible.
What is Bromides? * A type of CNS depressant
Why was Bromide banned? * Because of its toxicity due to is high half life of 12 which means that the drug would be in the body for 72 days. When Bromide is taken again, the drug previously taken would still be in the system.
Name an example of a Barbiturate. State its half life and generic * Butisol. Generic: butabarbital. Half life: 30-40 hours
What is the mode of action of Phenobarbital and other barbiturates widespread? CNS depressant: depress motor, cognitive and behavioural functioning.
What is meant by "dose-dependent effects" of Phenobarbital and other barbiturates widespread. * It is used as an anxiolytic or as a sedative so using the spectrum you can chose what you want it to do and take the dose for that
Why is there so much fatality caused by Phenobarbital and other widespread barbiturates? * People get addicted to it, and the spectrum comes into play where the more you take the further down the spectrum you go.
What is the mode of action of Barbiturates? * Depress motor, cognitive and behavioural functioning.
What is the mechanism of action of Barbiturates? * To facilitate GABA(A) receptor opening
What is the site of action for Barbiturates? Act throughout the CNS, noted depression of neuronal activity in the brain stem.
What are the three side effects of Barbiturates? * Since site of GABA receptors are everywhere, even brainstem, they can effect breathing machinery and cause coma/death. Cause behavioural effects of slowing and drowsiness so shouldn't drive. Cause cognitive slowing so bad memory.
Barbiturates exhibit tolerance. What is tolerance? * When you need more and more to get the same effect
Barbiturates can exhibit abuse and dependence. What is dependence? * Cessation of the drug results in physiological effects.
Barbiturates have a narrow therapeutic window. What is this? * ...? look back on previous lecture notes on therapeutic window
Describe negative reinforcement. * Say a person goes off a Barbiturates for insomnia and find they have lots of nightmares (due to more REM periods) so this acts as a neg. reinforcer for them to go back on the drug. So is when use drug reg., stop using, have withdrawal, go back on
In terms of Truth Serums, Why would you take such a drug? And who would use it? * Mainly for interrogations, to disinhibit suppressed memory, to be able to own up to something. Police, Military.
In terms of Truth Serums, Are there any truth sera available today? * Possibly alcohol, Pentathal, LSD (Psychodylic drugs) or Oxytocin (most promising)
In terms of Truth Serums, Is it ethical to administer such a drug to another person? * No if they agree to it. Yes if they unknowlingly take it.
In terms of Truth Serums, could it be used in a malicious way? * Yes for interrogations or to make someone trust you so you can take advantage (Oxytocin)
In terms of Truth Serums, could it be used in a positive way? * Yes, to solve crime, to prove someone's innocence.
How did CNS depressant Amytal effect soldiers who came back from war? How was this seen as a possible truth serum? * Soldiers were closed and canatonic. Amytal caused them to open up, talk fluidly, without studdering. So saw it as a possible truth sera.
Milton (Meprobamate) was one of the first Rx drugs to be widely marketed with targeted campaigns towards women and kids. How were they promoted to women and kids? * Promoted to help woman's stress of being a mother and wife and going through menopause. For pregnant women under financial stress and changing body. For children who had tantrums.
Milton (Meprobamate) was one of the first Rx drugs to be widely marketed with targeted campaigns towards women and kids. Describe the shifts in marketing/Rx drug culture. * Societal: incr. acceptance of psychoactive drugs, opened purchasing power, recogn. efficacy of drug - that a little pill can change your life. Clinical: physician lobbying. Industry: Seen as a big business!
Go over what a placebo effect is. Give an example * So with pill you think of it as a drug and that it will effect you.
Go over Expectation effect. Give an example * "Sleeping Pill" So you think it will make you sleepy - that is your expectation.
Go over Contextual effect. Give an example * With Sleeping pill, if you go into a dark bedroom, in pyjamas this will make you sleepy
what is the advantage of Benzodiazepines from all the Barbiturates? * It is much safer - has a ceiling effect! Doesn't go all the way down the effect spectrum. Stops at sleep. So you cant die, coma, be unconscious etc with this drug alone.
What is different about the mechanism of action for Benziodiazepine compared with that of Barbiturates? * Benzodiazepines only facilitate the GABA(A) receptor rather than opening it. So a more moderate effect.
Any sedative should not be combined with another sedative. Why? * Because it creates a lot of inhibition in the brain so can cause death, be very fatal!
Benzodiazepines exhibit the same potential for abuse and dependence as Barbiturates. Recall what this is * - Physical sleep disturbances (from more REM sleep). - Psychological desire for effect (like the chilled out feel)
Second Generation Anxiolytics have a prominent hypnotic effect, not anxiolytic. So prescribed to induce physiological sleep pattern. What is an example of a receptor for them? its generic and half life? * Ambien, Generic: zolpidem. Half life: 2 hours.
What is the mechanism of action for Second Generation Anxiolytics? * They facilitate activity of the GABA(Aalpha1) receptor - so more specific utilising the alpha1. More selectivity.
With Second Generation Anxiolytics, they have minimal to no residual daytime sedation. Why? * Because hey have short half-lives of 2, 1 or 6 hours.
What is the definition of General Anaesthetic? * Global but reversible CNS depression resulting in loss of sensation and perception.
General Anaesthetics have varied Mechanisms of Action (MOA). What are they? * Inhalational agents e.g. nitrous oxide. Or Intravenous agents e.g thiopental
To achieve a surgical plane of anaesthesia, usually a combination of four things are used: memorise form lecture notes!! *
Why are Chloral Hydrate, Flunitrazepam (Rohypnol) and Y-hydroxybutyrate often mixed with alcohol? * Cos they are often daterape drugs so the person is already drinking alcohol & therefore expects to feel weird so does not notice the extra CNS depressant compared to if they were drinking water. Also pushes them down the spectrum(synegent CNS depressant)
How could a CNS depressant be a euphoriant?? * (3 things could be going on) 1) Placebo, Expectation & Contextual effects. 2) Behavioural disinhibition. 3)Disinhibition/dyscontrol reaction
What do we mean by Behavioural disinhibition? * Normally we have a filter so don't act crazy or say crazy things. Perhaps GHB depresses these filters that you normally have.
What do we mean by Disinhibition/Dyscontrol Reaction? * It is to do with the individuality of how our brains are wired. In the lab they generalize the effects but for some people it might actually excite them as they have different phenotypes.
Disinhibition/dyscontrol reactions are more common in who? * Children and the elderly
Describe Propofol and its primary reasons for use * A non-barbiturate sedative. Mechanism of action: mostly GABA(A) receptor facilitator. Therapeutic use for surgical sedation/anaesthesia. Recreational use is a potential segway into addiction e.g. micheal jackson used to sleep.
Created by: alice476