6331- Psychopharmacology

What are the four parts of a neuron?

soma, dendrites, axon, terminal buttons

describe each of the four parts

soma is the cell body, dendrites are the branches that receive messages through multiple receptors, axon is a long tube that carries messages from the soma to the tb, terminal buttons are at the end of the axon and are small sacs or vesicles that hold NTs and transfers them through a synapse

two ways terminal buttons transfers neurotransmitters

between the terminal button of one neuron to the dendrite of another neuron OR between the terminal button of one neuron to the soma of another

Label all the parts

a. axon

b. dendrites

c. soma

d. terminal buttons

in the grand scheme of things where does neural communication take place and what are the two ways that neurons communicate

in the central nervous system, neurons communicate chemically or electrically

what can activate neurons in the cns, in what two ways

all drugs and substances; endogenous is from within the body (endorphins, insulin, adrenaline) or exogenous which from outside the body and introduced to the body in the same way (caffeine, vitamins, herbs, medications)

Process of neural communication

1. receptors are stimulated by nt

2. action potential occurs if enough receptors are stimulated at once and this travels along axon to the tb

3. At the tb nt is released

4. travels across synapse from pre to postsynaptic membrane of dendrite where it might interact with receptors

5. receptors receive signal and activate postsynaptic cell, allowing for retransmission

another name for action potential

electrical impulse

Label the parts

a. neurotransmitters

b. receptor sites

c. electrical impulse (action potential)

d. presynaptic

e. postsynaptic

ions

electrically charged particles that facilitate the electrical properties of neural transmission (most neurons are slightly electrically charged)

resting potential

the difference between intracellular and extracellular ion concentration, typically -70 mV (outside is more negative than inside)

threshold potential

-55 mV

TRUE OR FALSE: some drugs can affect various phases of action potential

true

extracellular space primarily contain

intracellular spaces primarily contain

sodium (Na⁺) and chloride (Cl^-)

potassium (K⁺)

How many stages does action potential occur in

4 stages: stimulation, rising phase, peak and falling phase, undershoot and refractory period

membrane potential

the potential difference between inside and outside the cell

what is the stimulation phase'

how does this happen

action potential starts when the membrane potential is reduced to the threshold potential

this happens when a receptor is activated by a neurotransmitter which sends excitatory or inhibitory messages

what do excitatory messages do to a cell

depolarize- allows Na⁺ to flow in - reducing membrane potential and increasing chances of threshold potential

what do inhibitory messages do to a cell

hyperpolarize- allows Cl^- to flow in- increasing membrane potential and decreasing the chances of threshold potential

Which actional potentials are expressed

how often do cell receive messages

what size are aps and what cause a stronger behavioral repsonse

the ones that outnumber the other; if there are more inhibitory messages than excitatory messages an ap will not be expressed

neurons receive inhibitory and excitatory messages constantly

all aps are the same size, however the number of aps express a stronger behavioral response

explain runaway and an example

voltage-gated sodium channels openings; tetrodotoxin in pufferfish can cause paralysis by blocking these channels

Rising phase

when ap is triggered and threshold potential is reached, runaway occurs which results in rapid depolarization until +40mV (peak) is reached

the cell tries to compensate for all of the sodium

by taking K⁺ out by opening channels by they open more slowly at first

peak and falling phase

example of this

K+ eventually catches up to peak and inactivates sodium from flowing in by a small protein blocking the voltage-gate sodium channel opening

potassium overpowers sodium and the voltage drops rapidly

ex: alpha toxins in a scorpion sting can block sodium inactivation this results in a prolong ap that doesn’t have a traditional falling phase and can lead to ataxia or muscle lock

undershoot and refractory period phase

After hyperpolarization the voltage is often lower than the resting potential this begins the refractory period

ion exchangers move Na⁺ back out and K⁺ in, this can last as long as an ap however reset is necessary before another ap can happen

when ap or electrical impulse reaches the nerve terminal, neurotransmitters are released by exocytosis

this is helped by calcium (Ca⁺⁺) ions in the terminal buttons moving neurotransmitters inside of these vesicles to release to the synapse by binding to the cell wall

the nts diffuse across the synapse to the postsynaptic membrane where receptors are activated by ion channels and de or hyperpolarize that neuron

this signaling is over when there are no longer nts present in the synapse, reuptake can occur

Neurotransmitter and receptor sites analogy

are like a key and lock

receptors are specific proteins of amino acid made to be unique

signal transduction process occurs when a nt binds to a receptor…

1. through ligand-gated ion channel receptors

2. inducing chemical changes within the cell (many are G-protein-linked receptors because they bind guanine nucleotides these are dopamine, glutamate, gamma aminobutyric or GABA)

And changes it’s physical shape

1. some receptor sites are g-protein-linked receptors (bind guanine nucleotides these are dopamine, glutamate, gamma aminobutyric or GABA) and the bindings actuate the second messenger which is cyclic adenosine monophosphate or cyclic AMP

2. cyclic AMP actuate other molecules or enzymes that excite or inhibit other chemicals and it results in protein kinases

3. protein kinases changes the physical shape of the protein and that controls the opening of ligand-gated ion channel receptors

3 main nts of emotion and behaviors? what are the differences?

monoamines: two catecholamines (dopamine and norepinephrine) and one indolamine (serotonin); the difference between the two is based on the chemical structure

What are other nt that attribute to emotion and behavior

Amino acids: GABA, glycine, glutamine

Neuropeptides (chains of aa): substance P and endorphins

Dopamine and Norepinephrine are synthesized from what? how is it absorbed

Tyrosine

amino acid that comes from diet (meat, poultry, seafood, beans, tofu, lentils) and can be synthesized for purchase

enzyme DOPA decarboxylase converts tyrosine into L-DOPA and dopamine

dopamine from here can turn into norepinephrine by enzyme dopamine B-hydroxylase

Norepinephrine function

regulation of sleep-wake cycles, sustained attention, alertness, biological responses to new stimuli

noradrenaline function

mediate anxiety, fear, stress, and responses, thus plays role in mood and anxiety disorder with low levels

Serotonin aka… Comes from…

5-hydroxytryptamine (5-HTP) is synthesized from tryptophan by the enzyme tryptophan hydroxylase

comes from milk, sunflower seeds, bananas

serotonin function… low levels of this are asoociated with what?

brian functioning including mood, anxiety, arousal, irritability, tranquilitu, cognition, appetite, sleep-wake cycles, and obsessions

(low levels of serotonin are associated with anxiety, mood and psychotic disorders)

Agonists

increase the availability or action of nt by binding to receptors and acting

antagonists

decrease the availability of neural communication by binding to receptors and blocking

Acetylcholine: excitatory or inhibitory/ cns or pns

affects memory, learning, behavioral arousal, attention, mood, and REM sleep in CNS

found at synapses where nerve terminals meet the skeletal muscles causing excitation leading to muscle contractions in PNS

what is another name for epinephrine? explain where it is found and what it does

adrenaline

more active and is secreted by adrenal glands (small endocrine glands above the kidney) in PNS

regulates flight or fight responses

Norepinephrine: excitatory or inhibitory/ pns or cns

primarily an excitatory nt, has axons in the brainstem that project into the limbic system and frontal lobes in the CNS

regulates wakefulness and alertness

dopamine: excitatory or inhibitory

regulates behavior, movement, learning, mood and attention'; may have excitatory and inhibitory effects in the brain

overactivity or oversensitivity may play a role in schizophrenia

drugs of abuse directly activate dopamine receptors

serotonin: excitatory or inhibitory

key nt in homeostasis in the brain and involves inhibition of activity and behavior

regulates mood, appetite, sleep and arousal, pain

projects into almost the same areas as norepinephrine (limbic and frontal lobes)

Other neurotransmitters that affect mood and behavior and their functions ( 3 G’s excitatory or inhibitory)

GABA makes brain more stable by dec neural transmissions; benzodiazepines and barbiturates increase levels of GABA

glycine inhibits amino acids neurotransmissions mostly in the spinal cord; when glycine receptors are activated the cell becomes hyperpolarized and less likely to transmit signals; strychnine is a toxin that blocks receptors this leads to overexcitation and possibly death

glutamate is an aa nt that is excitatory and lowers the threshold; found Asian food in the form og monosodium glutamate (MSG) which excites the taste buds

Psychodynamics

study of how drugs affect receptor sites, send signals, and cause some neuro chemicals; at the synapse

Pharmacokinetics

administration, absorption, distribution, metabolism and elimination of a drug inside the body

Routes of administration (other names for them)

orally, subcutaneously (deep tissue injection), intramuscularly (IM or muscle injection); intradermally (dermal injection), intranasally; inhalational, sublingually, transdermally, (skin absorption), intravenously (IV)

Which route is most common? quickest? used in hospital or clinic settings to control behavior or in long-acting forms for more chronically ill patients?

oral; inhalation; intramuscular

What are soltabs? What are some examples

orally disolved tablets

olanzepine (Zyprexa Zydis)

mirtazapine (Rameron Soltabs)

risperidone (Risperdal M-tab)

Clonzepam (Klonopin Wafers)

Which routes are absorbed the fastest

intramuscular, intravenous, etc are absorbed faster than oral drugs and oral liquids are faster than capsules or tablets

What are the benefits of slower or extended release tablets

they allow for fewer doses and in turn cause fewer side effects because there is a slower rate of absorption

the process of how oral drugs are absorbed

• starts in the stomach and duodenum (first segment of the small intestines), into the venous system, and delivered through the circulatory system

• the liver is the first organ to receive oral drugs, it breaks it down into actives and non actives during first-pass metabolism and into the bloodstream

Can certain diseases and their treatment affect absorption

yes, gastrointestinal diseases and their treatment can affect absorption and example of this are antacids interfere with some antibiotics

After the liver breaks down the drug what do they turn into and where do they go? What is this process called

active metabolites that can be readily absorb are sent to their target organs via the bloodstream and non-active metabolites are expelled. This process is called first-pass metabolism

What is the target for psychotropic drugs after first pass metabolism

the central nervous system

What are some examples of intramuscular or IM drugs

haloperidol (Haldol Decanoate

fluphenazine (Prolixin Decanoate)

Risperidone (Risperdal Consta)

what factors affect absorption

protein binding, drug half-life, lipid solubility

what is protein binding? what is an example and purpose?

when a drug binds tightly to plasma protein

example is albumin in the bloodstream

this determines how much of the drug is available to act on the brain by hindering the drug’s metabolism and excretion causing it to remain in the circulatory system longer

what is drug half-life? what’s an example? how many half-lives are needed for a drug to completed be eliminated

the average amount of time required to eliminates one half of the drug’s concentration

Xanax has a half like of 11 hours, after 11 hours it’s concentration in the body is reduced to 50%, after 22 hours it’s concentration is reduced to 75%, after 33 hours it’s concentration is reduced to 87.5%, after 44 hours- 93.8%, after 55 hours- 96.9%

5 half-lives

what is lipid solubility? What are lipophilic drugs and what happens to drugs that arent lipophilic? what is it also called?

how easily a drug crosses a cell membrane

drugs that are more likely to cross over the blood-brain barrier and extert their effect, other drugs don’t cross the blood-brain barrier and do not get to exert their effect on the central nervous system

fat solubility

drugs are metabolized by what enzyme… what happens because of this

the 9450 enzyme family

drugs compete for the same pathways and drug interact because of this

regarding decreased liver enzymes what should you look out for… are all drugs metabolized by the liver

geriatric patients have dec liver enzumes, so their doses need to be reduced to avoid toxicity

medical conditions such as viral hepatitis and liver cirrhosis may also dec metabolism

some medication arent metabolized by the liver and are excreted unchanged by the kidneys in urine (ex: lithium or Lithobid)

What makes up the therapeutic index? explain

the ration of therapeutic dose and the toxic does makes up the therapeutic index

a toxic dose is when a drug concentration produces mild or severe side effects

a therapeutic dose is when a drug concentration gives a desired response

high versus low therapeutic index and example of low

high therapeutic index are desiriable drugs because the ratio is far from each other

low therapeutic index is risky because the margin is slim (lithium)

dose-response curve

considered when determining a therapeutic dose

when a drug is introduced, there is a slow titration upwards and that usually corresponds with an increasing response

at certain point the drugs levels off and increasing the dose at this point would only increase the risk of side effects and toxicity

loading doses

higher dose to obtain a certain response; seldom adjustments are needed

tolerance and tolerance with alcohol

needs greater amounts of drug over time to produce desired effect

this develops over time with alcohol

withdrawal and withdrawal with alcohol

set of characteristic symptoms that emerge when a drug is abruptly discontinued after heavy and prolonged use

if alcoholic suddenly stops drinking, it throws the body in a state of shoch which can cause tremors, agitation, insomnia, hallucination, and even seizures

discontinuation syndrome and example drugs

not medically dangerous like withdrawals

paroxetine (Paxil) or venlafaxine (Effexor XR) may cause malaise or flulike symptoms when patients missed a does or stops medication

potentiation

when one drug may enhance the effect of a second drug

synergism

when one drug may enhance the effec of a drug significantly more than expected

alcohol and benzodiazepines

placebo response and noceno

when the brain acts as if the drug was present even though it isent

when it causes negative effect

label all of the parts

a. increasing dose

b. range of maximum effect

c. range of increasing effect with increasing dose

d. threshold

e. range of no effect

f. increasing response

Latin Abbreviation and meanings

1. a.c.

2. b.i.d.

3. cap.

4. c with bar on top ( c )

5. h.

6. hs

7. p.c.

8. p.o.

9. p.r.n.

10. q4h

11. q6h

12. qd*

13. q.i.d.

14. q.o.d.*

15. Rx

16. stat.

17. tab.

18. t.i.d.

1. before food

2. twice a day

3. capsule

4. with

5. hour

6. at bedtime

7. after food

8. by mouth

9. as needed

10. every 4 hours

11. every 6 hours

12. every day

13. four times a day

14. every other day

15. prescription

16. immediately

17. tablet

18. three times a day

Latin Abbreviation and names

1. a.c.

2. b.i.d.

3. cap.

4. c with bar on top ( c )

5. h.

6. hs

7. p.c.

8. p.o.

9. p.r.

10. q4h

11. q6h

12. qd*

13. q.i.d.

14. q.o.d.*

15. Rx

16. stat.

17. tab.

18. t.i.d.

1. ante cibum

2. bis in die

3. capula

4. cum

5. hora

6. hora somni

7. post cibum

8. per os

9. pro re nata

10. quaque 4 hora

11. quaque 6 hora

12. quaque 1 die

13. quarter in die

14. quaque altera die

15. recipere

16. statim

17. tabella

18. ter in die