UW BIOL UNIT 4 DEPRESSANTS REVIEW

Unit 4 – Depressants  Study Guide 

I.  VOCABULARY  

• Analgesia – stopping pain 

• Analgesic – drug that stops pain 

• Prostaglandin – lipid that is produced as a result of pain/stress 

• Substance P – Protein that is released when pain is detected  

• Opiate – depressant from the poppy plant  

• Acetyl group – methyl group + carbon group, easier to cross BBB 

• Methyl group – a group of ch3 that tells how of a potent group 

• HYPERPOLARIZATION – neuron inside becomes more negative 

• GABA – inhibitory NT (opens CI- channels) 

• chloride GABA receptor – gaba binds and chloride flows in (neuron more neg inside) 

• chloride channel – chloride goes in/out (biophysics) 

• Endorphin – reduces the pain by binding to opiate receptors (ligand) 

• opiate receptor – protein where endorphins and opiates bind to cause depressed/pain relief 

• Alcohol/ethanol - depressant; alcohol is type of ethanol 

• Methanol – a type of ethanol, dont drink it 

• Isopropanol – a type of ethanol, disinfectant  

• Cirrhosis – severe liver damage can be from lots of drinking  

• Fetal Alcohol syndrome (FAS) - drinking alcohol during pregnancy (deformed face, growth delay, memory, attention, etc) 

•  Vasodilation – constriction of the blood vessel making it harder to pump blood 

•  Diuretic – makes the body pee 

•  lipid bilayer (membrane) - the thing that molecules cross the membrane 

• Channel – protein that lets molecules move through the membrane freely 

• action potential – electrical signal (high pos) 

•  D2DR – dopamine d2 receptor  

• Aldehyde – carbonyl group, in formaldehyde  

•  aldehyde dehydrogenase – enzyme that breaks down acealhyde to acetate 

•  Marijuana - (weed, cannabis), depressant 

•  Cannabinoid – interacts w/ cannabinoid receptors 

•  cannabinoid receptor (CB1 and CB2) - where cannabinoid bind 

•  Endogenous cannabinoid (=endocannabinoid) -  ligand cannabinoid 

•  Anandamide – endocannabinoid (binds to CB1 usually) 

•  Phytocannabinoid – cannabinoids from plants 

•  Placebo – thinking an effect is happening but nothing really has changed 

•  Hippocampus - memory 

•  brain stem – non thinking functions (breath, hr, etc) 

• Cerebellum – balance, fine movements 

• cerebral cortex – all the lobes 

II. Depressants  

A. Fill in your table for depressants with a focus on addiction, side effects, and medicinal use. 

B. How is it true that you react to pain before your brain knows what happened? What receptors are involved? What are important stops along the way where the signal transfers from one neuron to another? 

Yeah, the pain hits quickly, and the reflex tells you to respond becore it hits. Nociceptor, spinal cord, brain, muscle, etc. 

C.    Why does opiate and ethanol abuse result in tolerance and dependency?  What are some symptoms of withdrawal? 

You make more enzymes, less receptors, and brain gets marinated from ethanol. pain feels more severe, aches, constipation, pupil constriction, dec breathing, dec HR 

D.  Be able to identify one opiate agonist and one opiate antagonist.  Why would each be used? 

Antagonist – Nalaxone (blocks opiod receptors so opiates can’t bind reverses ODs) 

Agonist – Methadone (binds to opiate receptors, works SLOWLYY) 

E. What is shock? How are substance P and endorphins doing a “balancing act” when you get hurt? 

Shock – too much pain; substance P signals pain by sending the NTs out and endorphins try to dampen the pain when you get hurt  

F.   Know a bit about the half-life and or TI differences among the depressants.  Which would you consider to be relatively safe?  There are many right answers to this question. It’s how you DEFEND your answer that matters.  Which are most dangerous? 

Opiates  

• Half life: Morphine: 2-3 hr, Heroin→ 10 min, Oxycodone→ 4-5 hr, Fent (fat sol) → 2-4 hr 

• TI: Varies by opiate 

Ethanol 

• Half life: 3-4hrs, then 20-30 mins  

G.  What's the one drug you should be most cautious about combining with others?  Why? 

Opiates they slow down the breathing and depress veryyy quickly and combined with other depressants is dangerous 

H.  Could you make an argument for considering ethanol or cannabis as a “medicinal” drug?  Under what circumstances? 

Ethanol can be used an antiseptic, cannabis can help with pain, seizures, etc 

I. What is retrograde signaling? Explain at the level of detail we reviewed in class. Why is this a useful system for neurons? 

Retrograde signaling is working the release backwards (post to pre), so nts are released in the postsynaptic neuron and bind to the receptors on the presynaptic neuron to produce an effect. Regulates the amount of NTs released  

J.  How many opiate receptors are there? What are they called and what are they responsible for?  

• Mu → sedation, analgesia, sedation, euphoria abuse 

• Kappa → dysphoria, not an euphoria analgelesia 

• Delta → emotion regulation, analgesia 

K. How many cannabinoid receptors are there? What are they called and what are they responsible for? 

• CB1 - pain, excitation, memories, appetite 

• CB2 - inflammation 

L. Where does/does ethanol bind? What proteins are most impacted by ethanol? 

GABA receptors (enhancing; more CI- flows into the cell, making the cell more negative), GABA receptors mainly 

 1.  Complete the table. 

2.  Which medical condition would make depressant use particularly ill-advised?  Check all that apply. 

1. Hypertension (high blood pressure) 

2. Narcolepsy  

3. Anorexia 

4. Anxiety  

5. Depression 

3.  Draw an action potential.  Your axes are time vs. voltage. 

1. Upon this drawing, label RESTING potential 

2. Upon this drawing, label depolarization and which ion moves during depolarization 

3. Make a second line that represents a neuron which is hyperpolarized at rest. It is best to use a different color for this line so it can be distinguished from the other.    

4.  Cannabis is an unusual depressant for two key reasons.  Explain how cannabis differs from others with regard to: 

1. Heart rate – inc hr quickly and depressants normally supress hr 

2. Toxicity – cannabis doesnt have an LD50 and most depressants do, so its harder to die from cannabis toxicity 

5.  If you encounter someone who tells you that cannabis makes people crazy, formulate a evidence based rebuttal. 

Although cannabis can alter the person mentally due to some genetic factors, the altering is temporary and recoverable and does not show permante changes that could show that someone is crazy 

6.  Look up (online) how many infants in the US are born with fetal alcohol syndrome.   

~1-3 in 1000 

1. How much ethanol did a mother have to drink for this condition to be seen? 

Its not very known the exact number of drinks, but the dosage is overall on the high end 

2. Why is the fetus particularly vulnerable to ethanol (it is true, but not enough, to say that she is vulnerable because she is developing/growing). 

The ethanol travels through to the placenta easily, and the fetus’ liver cannot digest ethanol 

7.  Your friend is in pain (sorry).  Help him understand his medication choices by completing the following chart. 

8.  Name 1-2 depressants (some categories have only one answer, but try to find two) that:  

1. Effects potassium and calcium channels: opiates, cannabis  

2. Open chloride channels: alcohol, benzodiaphines  

3. Have endogenous receptors on neurons: opiates, cannabis  

4. Potency is influenced by an acetyl group: heroin 

5. Potency is influence by a methyl group: meth 

9.  During pregnancy, endorphin production climbs, topping out 10 days prior to delivery.  How might this down-swing in endorphins be related to post-partum depression? 

The increase of endorphins that reduce the amount of pain increasing through the pregnancy gives the mother happiness and pleasure without heavy pain and if 10 days prior to delivery of the bay the endorphins are suddenly cut down from what the mother typically has an expects, the mother will withdrawals and won’t have the happy feeling anymore, ultimately having the opposite (withdrawal effect) of sadness or in this case, post-partum depression.  

10.  Choose two depressants and for each, describe why that depressant is unwise to use if you are hoping to raise your GPA. 

Alcohol – messes with your memory, and if you can’t remember anything that you have learned, you can’t pass your exams and raise your grades/GPA 

Cannabis – messes with your motivation and intellectual functioning, and if don’t want to do the work, you can’t raise your GPA with not work done