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Physio Psych > Exam 1 - Neurotransmitters and Pharmacology > Flashcards

Exam 1 - Neurotransmitters and Pharmacology Flashcards

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1
Q

Synaptic transmission steps

A
  1. NT synthesis and storage
  2. NT release
  3. Receptor action
  4. Inactivation
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2
Q

What does synaptic transmission produce?

A

Postsynaptic potentials which are brief, hyperpolarizations or depolarizations that increase or decrease the firing rate of the postsynaptic axon

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3
Q

Neurotransmitter (NT)

A

the chemical released from the synaptic axon terminal that serves as the basis of communication between neurons

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4
Q

Neuromodulator (NM)

A

acts like an NT, but NOT restricted to the synaptic cleft and diffuses throughout extracellular fluid. They can be excitatory (EPSP) or inhibitory (IPSP). Almost all drugs work by altering synaptic transmission and use NMs

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5
Q

7 Classes of NTs

A

amino acids
acetylcholine
monoamines
peptides
lipids
nucleosides
soluble gases

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6
Q

Amino acids (AA)

A

responsible for most synaptic communication in the brain. The 3 most common are glutamate, GABA, and Glycine

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7
Q

Glutamate (Glu)

A

(type of AA), main excitatory NT in the CNS. Binds to MANY receptors (ionotropic and metabotropic receptors). Drugs that affect Glu do so by interacting with its receptors. Glu released from presynaptic neuron and is removed from synapse by excitatory AA transporters and broken up by enzyme so never taken back to presynaptic neuron. Too much Glu can lead to prolonged over excitation in neurons and cause damage like irregular heartbeat and high blood pressure

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8
Q

How many types of ionotropic receptors and metabotropic receptors does Glu bind to?

A

3 ionotropic - NMDA, AMPA, Kainate. 1metabotropic - metabotropic Glu receptor

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9
Q

GABA - Gamma-aminobutyric acid

A

(type of AA) main inhibitory NT widely distributed throughout CNS. Reduction of GABA (ex. abnormality of GABA secreting neurons or GABA receptors) contributes to likelihood of seizures. Has MANY receptors that drugs interact with (Ex. Xanax and Vial mimic GABA to produce calming effect)

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10
Q

Acetylcholine (Ach)

A

Neurons that release Ach are found in specific pathways in CNS. Functions: role in REM sleep, facilitates learning, modulates formation of memories. Secreted in PNS –> muscle contraction. Binds to ionotropic receptors and metabotropic receptors.

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11
Q

What types of ionotropic receptors and metabotropic receptors does Ach bind to?

A

Ionotropic receptors like Nicotinic are stimulated by nicotine (drug from tobacco leaves). Metabotropic receptors like muscarinic are stimulated by muscarine (drug from poison mushroom)

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12
Q

Monoamines

A

most somas located in the brain stem, allow a lot of terminal buttons to be distributed throughout many regions of the brain. Involved in activating/deactivating several regions of the brain. classified into 3 categories –> catecholamines, indolamine, ethylamine

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13
Q

Dopamine (DA)

A

(type of Monoamine - catecholamines) produces both EPSPs and IPSPs, depending on the receptor. Functions: movement, attention, learning, reinforcement (pleasure, satisfaction, motivation). Pathophysiology –> Parkinson’s disease and schizophrenia. Several drugs stimulate or block specific DA receptors. Antipsychotics block dopamine

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14
Q

Norepinephrine (NE) aka noradrenaline AND epinephrine aka adrenaline

A

(type of Monoamine - catecholamines), part of fight or flight response, increase vigilance, increase and maintain blood pressure, increase energy use by the body.
Norepinephrine affects the blood vessels.
Epinephrine affects the heart. Secreted by adrenal medulla

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15
Q

Serotonin (5-HT)

A

(type of Monoamine - Indolamine). Functions: mood regulation, eating, sleep, arousal, regulation of pain. Drugs that inhibit reuptake of 5-HT are commonly used in treatment of mental illness

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16
Q

Histamine

A

(type of Monoamine - ethylamine). Functions: wakefulness, digestive system, immune system. Antihistamines are drugs that block histamine receptors cause drowsiness Ex. Benadryl

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16
Q

Peptides

A

2 or more amino acids that are linked together. They are created in the soma of the neuron and transported down the axon. All peptides are destroyed by enzymes so there is no reuptake. The main family is the “endogenous opioids.” Opioid drugs stimulate opioid neurons Ex. heroin, oxycodone, morphine. Functions: emotions, pain, appetite, reinforcement

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17
Q

Lipids

A

They appear to be synthesized on demand (only produced and released as needed and not stored in synaptic vessels). Endocannabinoids are the most important. Natural ligands for the receptors are responsible for the physiological effects of marijuana. Functions: appetite regulation, produces analgesia (absence of feeling pain), cognitive effects

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18
Q

Nucleosides

A

compound of a sugar molecule bound with a purine or pyrimidine base. Ex. adenosine - neuromodulator, released by astrocytes when a neuron in the CNS needs extra oxygen or energy, involved in dilation of blood vessels. Adenosine receptors open potassium channels and produce an inhibitory effect

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19
Q

Soluble Gases

A

used for interneuron communication Ex. nitric oxide dilates blood vessels, near metabolically active parts of the brain, possible role in learning (facilitation neural changes) Ex. carbon monoxide

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20
Q

Neurotransmitters have what 2 effects

A

They can be excitatory (EPSP) or inhibitory (IPSP).

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21
Q

Autoreceptors

A

receptors on the presynaptic neuron that regulate the production and release of NT, They are mainly inhibitory

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22
Q

Agonists

A

facilitate post synaptic effects. Bind with proteins and directly triggers release NT, causing another Act Pot. Ex. Black widow spider venom causes release of Ach (muscle contraction).

23
Q

Antagonists

A

inhibit or block post synaptic effects. Drugs can block vesicle NT transporters by binding to the transporter and making it inactive. Ex. Reserpine blocks vesicle transporters for monoamine NT system. Drugs can prevent release of NT from terminal button, deactivating the proteins that cause docked synaptic vesicles to fuse with the presynaptic membrane. Ex. Botulinum toxin (botox) prevents release of Ach

24
Q

Effects of Drugs on Receptors

A

Receptors are ligand-gated channels. 2 types of binding - competitive and noncompetitive

25
Q

Types of Competitive and Noncompetitive binding

A

Competitive binding - DIRECT agonist and direct antagonist. Noncompetitive binding - INDIRECT agonist and indirect antagonist

26
Q

Competitive binding (direct)

A

drug binds where the NT normally does. (like ionotropic receptors)

27
Q

direct agonist

A

binds and mimics NT effects Ex. nicotine (mimics Ach by increasing attention, reinforcing effects)

28
Q

Direct antagonist

A

binds and blocks NT from binding by covering up the receptor Ex. Botox (blocks Ach receptors and prevents muscle contraction)

29
Q

Noncompetitive binding (indirect)

A

receptors have 2 binding sites, drug binds to the 2nd binding site and either facilitates or inhibits the channel opening. (like metabotropic receptor bc extra step)

30
Q

Indirect agonist

A

facilitates opening of ion channel Ex. diazepam (valium): requires NT GABA to bind to have an calming effect

31
Q

indirect antagonist

A

inhibits opening of ion channel Ec. Phencyclidine (PCP) attached to Glu receptor and blocks calcium ions from entering, which causes hallucinatory effects

32
Q

Effect of Drugs on Deactivation

A

Reuptake (after binding, NT is taken back to the terminal button in presynaptic neuron) or deactivated by enzyme
Agonist effects of drugs –> block reuptake or deactivate enzymes in the area. Ex. cocaine blocks reuptake of DA

33
Q

drug

A

an exogenous chemical not necessary for normal functioning that considerably alters the functions of certain cells of the body when taken in relatively low doses

34
Q

drug effects

A

changes we can observe in an individual’s physiological processes and behavior

35
Q

sites of action

A

points at which molecules of the drug interact with molecules located on or in cells of the body, affecting some biochemical processes of these cells

36
Q

pharmacokinetics

A

movement of drugs, including processes by which drugs are absorbed, distributed, metabolized, and excreted

37
Q

life cycle of drugs

A

absorption, distribution, metabolism, excretion

38
Q

absorption

A

drug is administered and absorbed through tissues Ex. intramuscular injection

39
Q

distribution

A

drug is distributed throughout the body and blood

40
Q

metabolism

A

drug is changed to an inactive form by enzymes that are usually in the liver.
drugs are metabolized and deactivated by enzymes (enzymes are mainly in liver but also blood and brain)
Enzymes may destroy or transform molecules of a drug. The transformed molecule may be more active than the original, which allows the drug to last longer

41
Q

excretion

A

drug is excreted (removed from the body) as kidneys filter and excrete drugs and their metabolites in urine

42
Q

absorption –> routes of administration

A

route of administration determines the amount of drug that reaches the brain and its speed to act. Types: injection, oral, inhalation, topical, intracerebral

43
Q

injection (route of administration)

A

Intravenous (IV) - substance suspended in liquid and injected through hypodermic needle, very fast method (maybe fastest?)
intramuscular (IM) - into muscle
subcutaneous (SC) - into space beneath skin

44
Q

oral (route of administration)

A

administered into mouth to be swallowed. must be able to survive stomach acid. Ex. pills

45
Q

inhalation (route of administration)

A

administration of vaporous substance into the lungs, the route from the lungs to the brain is short, rapid effects (fastest)

46
Q

topical (route of administration)

A

directly onto skin or mucous membrane

47
Q

intracerebral (route of administration)

A

administration directly into the brain or CSF. Some substances cannot cross the blood brain barrier

48
Q

Factors that affect drug effectiveness

A

affinity and the location of the site of action. (Drugs have multiple effects and diff sites of action)

49
Q

affinity

A

readiness with which 2 molecules (the drug and its binding site attach) join together at the site of action.
High affinity - low concentration of drug will produce effects Ex. tylenol
Low affinity - high concentration/dose of drug must be administered to feel effects

50
Q

location of the site of action

A

Oxycodone and aspirin are the most desirable drugs that have a high affinity for sites of action for therapeutic effects and low affinity for sites of action that produce toxic effects. Both have effect of diminishing pain but diff site of action (oxycodone - brain, aspirin - blocks pain receptors)

51
Q

placebo effect

A

placebo - a harmless substance with no physiological effect. based on person’s belief, it can manifest an effect. Ex. telling person a placebo is a stimulant results in increased heart rate and blood pressure

52
Q

repeated administration (drug effectiveness)

A

can lead to sensitization or withdrawal

53
Q

Tolerance (drug effectiveness)

A

effects of drug diminish. more needs to be taken to produce the same effects.
There is a decrease in effectiveness of the drug binding to receptors (receptors are become less sensitive and the affinity decreases or the amounts of receptors decrease) or the coupling of receptors to ion channels production of 2nd messengers becomes less effective

54
Q

sensitization

A

repeated doses produce greater effects. Ex. repeated injections of cocaine are more likely to produce movement disorders and seizures

55
Q

withdrawal

A

causes the opposite of the effects of the drug. Most systems in the body are regulated so they stay optimal. Ex. heroin produces euphoria but withdrawal from it produces dysphoria and agitation. Physical dependence - when stopping the usage of a drug causes withdrawal

Physio Psych (5 decks)

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