Class Notes (835,872)
New Zealand (288)
Psychology (68)
PSYC476 (18)
Lecture

4. CNS depressants.docx

13 Pages
151 Views
Unlock Document

Department
Psychology
Course
PSYC476
Professor
Kristin Hillman
Semester
Fall

Description
CNS Depressants – Week 4 8/23/2013 2:23:00 PM Quiz next week – starts 9am 20mins test Why use a CNS depressant? (class brainstorm)  E.g. valium, Xanax, ambien, rohypnol, GHB  Counter stress  Reduce anxiety  Sedative (sleepy/drowsiness)  Recreational (e.g. Xanax = happiness effects)  [Weaning for addiction] = valium  there are more specific drugs for this  Insomnia  Date rape (e.g. rohypnol)  Unintentional consumption  [Schizophrenia] = valium  there are more specific drugs for this Primary uses:  4 primary uses for CNS depressants: o 1. To reduce anxiety o 2. To facilitate sleep (i.e. sedative/counter insomnia) o 3. To reduce awareness/consciousness  therapeutic = anesthesia  malicious intent  4. To reduce muscle spasms or associated pain o Talked about last week  Oral muscle relaxers (also CNS depressants) 1. To reduce stress: What is anxiety?  Defined by dictionary = o 1. Distress or uneasiness of mind o 2. State of apprehension and psychic tension  It is essentially “nervous energy” o Everyone experiences it…  What causes it? o Anxiety is a natural response to certain situations o Acuity it is ok to be anxious  Some argue beneficial (when you are anxious it cognitively primes you to do things such as study for exam or something…it drives performance)  Can help memory…but when it goes on a long time it can impair it o Chronic anxiety becomes problematic  Get mood changes  Impairs memory (not good)  Get sick more  Irritability, pessimism, dysphoria, lack of concentration, physiological effects  Drug that reduces it?  Anxiolytic History of CNS depressants/anxiolytics:  CNS depressants have been used throughout civilization…  Can we think of any drugs that people have used to chill out and reduce tension? o Apiates o Alcohol o Cannabis o Psychedelics (e.g. scopolamine) o Tobacco (e.g. nicotine) o All of these give some contented euphoria  People have been using drugs for a long time to reduce stress  1850s – 2000s What is a CNS depressant?  It‟s a drug that depressed your CNS activity  CNS functions to: o 1. Receive info from PNS (the outside world) o 2. Integrate and understand info o 3. Initiate appropriate response  When you take a CNS depressant you start to decrease all of these functions.  CNS and PNS systems work but talking to each other, neurons need to be excitable  these  Pharmacology angles for depressants:  Decrease excitation – how? o By dercrasing glutamatergic tone  Glutamate (Glu)  Increase inhibition – how? o By increasing GABAergic tone o Main approach – CNS depressants by and large increase GABAergic tone in the CNS  (GABA) Glu and GABA:  You don‟t want too much inhibition or hyperexcitation o It‟s a very fine balance that your brain has to try and keep – use Glu and GABA to do that  These are primary neurotransmitters  For many years, these chemicals were not accepted as neurotransimtters  Neurotransmitter system criteria: o They were figured out later that they do fit the criteria o They are amino acids and derivatives Glutamate (Glu)  Synthesis: o Derived from glucose or glutamine  change that to glutamate  Storage and release: o Loaded via vesicular glutamate transporters  Postsynaptic Glutamate receptors: o 4 different subtypes:  NMDA – ionotropic (i.e. excite the cell)  Kainate – ionotropic  AMPA – ionotropic  mGlu – metabotropic (i.e. inhibit the cell)  Note: mGluRs (of Gi variety) can be presynaptic  Need to get rid of it so it doesn‟t excite the cell constantly, Clearance:  Reuptake via high-affinity glucose transporter (which is called GLUT) – o can also have EAAT (excitatory amino acid transporter) type of transporter – picks up more general things GABA:  Synthesis: o Derived from glutamate  Need GAD and B6  Receptors:  GABA (A)  GABA (B)  GABA ©  Clearance:  Depolarizing  Important role of glial If whole goal is to get more GABA in your system, why don’t you just drink some GABA?  No – GABA doesn‟t cross the BBB o BBB can stop things coming in, but also stops things going out (stops GABA from going out which is good,  Think about synapse because that‟s where all out drug targets are.  What are the alternative approaches? o synthesis o release o post-synaptic receptor activity o clearance and metabolism CNS Depressant Mode of Action:  If keep increasing the GABAergic tone  (it is dose dependent, if you have too much in the system you will reach death)  Think of it as a scale: o Anxiolysis o Sedation o Sleep o Unconsciousness o surgical anaesthesia …..  A lot of the time we talk about CNS depressants as sedatives, or sometimes tranquilizers (terminology) History:  CNS depressants have been used throughout civilization…  Bromides first widely used sedative o half life, take on the half life = these drugs had a very high toxicity effect (remember graph that goes up and up…that‟s what happens here)  Chloral hydrate was the next widely marked sedative  Mickey Finn o Used to date-rape people by dropping this into girls drinks o nowadays, known as "slip someone a Mickey" o can actually find this still being used  typically in rest homes, in age-related dimensia cases so that people don‟t get up in the middle of the night etc. Barbiturates introduced:  Don‟t remember all  Should be able to give ONE example of this…memorize one of the names o e.g. Phenobarbital = first used  120 hours half life (take every 5 days) – not that convenient so making drugs with shorted half lives were good  The way they work =  They depress motor cognitive and behavioural functioning o DOSE-DEPENDANT effects  Can lead to death if a lot is taken – refer to spectrum before…  there were thousands of deaths from taking these - not good drugs, safety profile wise...  They facilitate the GABA (A) receptor opening  Site of Action  GABA drugs can work everywhere in your system  they act throughout the CNS  when you start to depress activity in the brainstem, you also depress your heart rate and your respiratory rate drops off- this is how it can kill you.  Side effects??  Your reaction time  cognition - learning and memory is impaired  biggest side effect is death Barbituates:  they exhbit a lot of tolerance o there are 2 types of tolerance:  1. Pharmacodynamics tolerance  2. Pharmacokinetics tolerance  activity of enzymes upregulate, so it increases the own drugs metabolism (have to keep taking more to get effects)  Can exhibit abuse and dependence  Have physiological effects = mostly sleep related = major sleep disturbances) o when go off drugs can affect sleep  Also have psychological effects = desire for effect  Therapeutic window  Small window, therefore quite quickly you start to go into toxicity range  Mainstay of sedative prescription up until 1960s, but today not readily prescribed as anxiolytics due to safety issues.  still around today used for: o anticonvulsant for epilepsy o operative sedation/anesthesia o death o truth sera?  Is there a drug that can make you tell the truth? o Some believe truth serums will come back – David Brown, Washington Post 2006 Truth Serum?  Why would you take such as drug? Who would use it?  Court of law to maybe get a confession  In a psychiatric sense  Military for interrogation purposes  For sports – get a confession for drug-taking instead of spending all this money on testing  Are there any truth sera available today?  Potential compounds that have been investigated in the past o Alcohol? o Sodium Amytal? o Scopolamine? – from reading o Oxytocin? o LSD/mescaline  Is it ethical to administer such a drug to another person?  Maybe if you sign consent to it…it could prove innocence etc?  Could it be used in a malicious way?  Interrogation etc  Could it be used in a positive way?  Life/death reasons?? – e.g. kidnapped child  Do we have a truth serum today = NO  Clinical records for narcoanalysis found in psychiatry:  1930s – William Bleckwenn demonstrated potential for amytal to treat catatonic mutism (e.g. stuttering etc)  1940s  Today - very contentious amongst medical professionals  There has also been this military drive to use this in prisoners of war etc.  At early stages of CNS depression, many people do become more talkative  does this mean they are telling the truth (filter goes away when you get drunk, but that doesn‟t imply truth) – need to think about this. Meprobamate (Miltown):  1950s  One of the most first prescription drugs to be widely marketed, with targeted campaigns towar
More Less

Related notes for PSYC476

Log In


OR

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


OR

By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.


Submit