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PsychoPharm > Midterm#1 - Units 2-7 > Flashcards

Midterm#1 - Units 2-7 Flashcards

1
Q

What are oligodendrocytes

A

Glial cells that extend their membranes around axons to provide myelin (which serves to facilitate the movement of elstrical impulses to the axon terminals) - a single oligo can provide myelin to multiple axons.

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2
Q

What are Schwann cells

A

They serve the same purpose as oligodendrocytes but in the PNS, and one can only myelinate a single axon.

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3
Q

what are astrocytes? how do they work in the BBB?

A

Glial cells that help form the blood brain barrier, facilitate neuronal functioning and respond to injury.
They force endothelial cells more tightly together around viens.

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4
Q

what does the axon hillock do?

A

it is the site of initiation of an action potential - summation occurs here as integration of multiple signals occurs here

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5
Q

The PNS and its adjacents

A

The PNS is the system located outside of the skull ad spine; it encompasses the somatic NS (which contains spinal and cranial nerves) and the autonomic NS (which includes sympathetic and parasympathetic divisions)

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6
Q

Function and structure of sympathetic NS

A
  • prepares the body for activity
  • pre-ganglionic cell releases ACh on post-ganglionic neurons
  • then, post ganglionic cell releases norepinephrine, epinephrine, or dopamine on target organs
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7
Q

structure and function of the parasympathetic NS

A
  • dominant during relaxed states

- both pre and post ganglionic neurons release ACh on their targets

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8
Q

Forebrain structures

A
  • Cerebral cortex
  • Basal ganglia
  • Thalamus
  • Hypothalamus
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9
Q

Hindbrain and general role

A
  • Cerebellum, pons, and medulla. Controls critical autonomic functions such as breathing and heart rate
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10
Q

What are the divisions of the CNS

A
  • forebrain
  • Midbrain
  • hindbrain
  • spinal cord
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11
Q

What is Basal Ganglia/Striatum

A

Subcortical structure important for motor control, reward and habits.
One part of system is Ventral striatum which contains nucc acc (key role in reward pathway)
One part of system is Dorsal Striatum, containing the caudate and putamen, important for habit formation

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12
Q

Describe the Limbic system and involved structures

A
  • subcortical network important for learning motivation and emotional responses
  • consists of a series of structures that together form a ring around the thalamus and hypothalamus
  • Includes cingulate gyrus, hippocampus(learning), amygdala(fear), olfactory bulb and hypothalamus
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13
Q

What are the four cortical lobes and what they do?

A
  • Frontal lobe; critical for decision making, sensory integration, and signaling movement production(where signal to produce movement occurs). Also contains the motor cortex.
  • Parietal Lobe; contains somatosensory cortex which processes the sensation of touch sent from the body, also analyzes visual information that contains movement
  • Temporal lobe; critical for processing auditory information as well as lang. production and comprehension
  • Occipital lobe; critical for processing of visual stimuli
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14
Q

What is the basal ganglia, and how does substantia nigra affect it

A

Structure that acts to stabilize voluntary movement
- substantia nigra regulates activity in the BG, primary symptoms of Parkinson’s disease occurs from the destruction of substantia nigra neurons that go to the basal ganglia

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15
Q

What is the nucleus accumbens

A

facilitates rewarding effects, called the reward center.

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16
Q

What is the hypothalamus

A

structure that maintains physiological processes by motivating behavior (like when the body needs food, hypo triggers feelings of hunger)

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17
Q

What is the thalamus

A

The sensory relay center - routes sensory information from the body to appropriate lobes.

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18
Q

Directional terms

A
  • Anterior/Rostral: front of brain
  • Posterior/Caudal: Back of brain
  • Superior/Dorsal: top of brain
  • Inferior/Ventral: bottom of brain
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19
Q

Describe the membrane potential of a neuron at rest including the dist. of ions inside an outside cell

A

At rest, mp is -60mV, membrane polarized,

-inside: lots of K+ ions, some organic anions- and few Na+ and Cl- ions

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20
Q

What happens to membrane potential when Na+ channels open

A

Depolarization occurs (decrease in diff between charges in and out), positive charge within the cell increases as Na+ ions flow into cell. -40mV

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21
Q

What happens to membrane potential when K+ channels open

A

Hyperpolarization occurs(increase in difference between charge in and out) as K+ ions flow out of cell, -90mV

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22
Q

What happens to membrane potential when Cl- channel opens

A

Hyperpolarization occurs as Cl- flows into the cell.

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23
Q

What is a ligand-gated ion channel and where are they located

A

A channel activated in response to a ligand becoming attached, located on dendrites, soma, or on axon terminal as autoreceptor

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24
Q

What is a volatge-gated ion channel? Where are they located?

A

A channel that is activated by the change in electrical charge of membrane. Located along axon

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25
Q

What is summation?

A

The addition of ipsp’s or epsp’s occuring within a neuron in response to input from afferent neurons.

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26
Q

When do voltage gated Na+ channels open and close?

A

Opens when membrane potential reaches -40mV, closes when reaches +40mV

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27
Q

When do voltage gated K+ channels open?

A

Open when mp is +40mV

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28
Q

Steps of synaptic transmission

A
  1. Depolarization of pre-synaptic neuron causes voltage gated calcium channels to open and let Ca into the cell
  2. Calcium helps bind vesicles containing NT to membrane, releasing NT into synaptic cleft
  3. NT bind to receptors on post-synaptic cell, causing either ipsp’s or epsp’s in post synaptic cell.
  4. Transmission is terminated through degradation or re-uptake of NT, autoreceptors on pre-synaptic cell also facilitate this by triggering negative feedback loop where cell is hyperpolarized leading to CaV channels being closed.
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29
Q

What is an ionotropic receptor?

A

Ligand gated ion channel

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30
Q

What is a metabotropic receptor?

A
  • NOT an ion channel
  • G-protein coupled receptors where when NT binds it causes activation of G-protein which then activates nearby G-protein gated ion channel or effector enzyme which acts as a second-messenger which can cause longer-term changes within cell and cell membrane.
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31
Q

Describe ACh and receptors

A

2 types of receptors

  • nAChR’s: ionotropic receptor, found througout CNS and PNS and muscles; ligand gated Na+ channels and therefore excitatory
  • mAChR’s: metabotropic receptors, can be excitatory or inhibitory, are primary ACh receptors on parasymp. tagret organs.
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32
Q

Steps in ACh transmission

A
  • ACh packaged by VAT into vesicles for release in cleft
  • ACh then binds to nAChR’s or mAChR’s on post-cell
  • Transmission terminated by degradation via AChE enzyme, or re-uptake into pre-cell
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33
Q

Cholinergic neurons in the PNS and CNS

A
  • CNS: located in number of brain regions and neurons project to variety of targets; Basal forebrain chol. neur project through cortex; Hippocampal chol. neur. project within hippocampus; Midbrain chol. neur. project to reward pathway
  • PNS: in both symp and para divisions, but particularly important for para division; All spinal motor neurons cholinergic; nAChR’s on muscles and mAChR’s on target organs
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34
Q

(Amino Acid NT) Glutamate and receptors; Packaging, transmission and degradation

A
  1. Receptors mostly excitatory
    - Three ionotropic receptors: NMDA, AMPA and Kainate (all excitatory ligand gated Na+ channels)
    - Three metabotropic receptors: called mGluR’s and are a mixture of excitatory and inhibitory
  2. Packaged by VGLUT, termination via re-uptake into axon terminal or astrocytes via EAAT’s
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35
Q

(Amino Acid NT) GABA and receptors, packaging and termination

A
  1. GABA receptors all inhibitory
    - GABAa receptors ionotropic ligand gates Cl- channels
    - GABAb receptors metabotropic
  2. Packaged by VGAT, terminated by re-uptake into axon terminals or astrocytes via GAT1-3
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36
Q

Anatomy of Amino acid NT’s and receptors

A
  • Glu most abundant NT in NS, GABA is second.
  • Most neurons in brain gluatamatergic, pyrimidal neurons which are majority of cortical neurons are glutamatergic
  • Also lots of GABAergic neurons thru brain
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37
Q

What is neuronal excitotoxicity and how does it happen?

A

The death of neurons due to high exposure of glutamate, causing too much calcium to accumulate in the neuron which is lethal.

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38
Q

(Monoamine NT) Dopamine receptors, packaging and termination

A
  • DA receptors are all metabotropic; D1 family are excitatory and D2 family inhibitory
  • Packaged by VMAT, transmission terminated by degradation via MAO or COMT, or re-uptake by DAT
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39
Q

What are the DA pathways in the brain?

A
  • Mesocortical: cell bodies in (midbrain) VTA and axons project to cortex (mainly frontal)
  • Mesolimbic: cell bodies in VTA and axons project to nucleus accumbens, pleasure/addiction pathway
  • Substantianigra: cell bodies in sub.nigra that project to basal ganglia, significant for drug effects on movement
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40
Q

(Monoamine NT) Norepinephrine receptors (adrenoceptors), packaging and termination, and location in brain

A
  • All metabotropic, most (but not all) excitatory; both alpha and beta adrenoceptors.
  • Packaged by VMAT, termination via degradation via MAO or COMT, or re-uptake by NET
  • Variety of targets, but cell bodies located in locus coeruleus; In PNS NE is key NT for symp division
41
Q

(Monoamine NT) Serotonin (5-HT) receptors, packaging and termination, location

A
  • Mostly metabotropic neurons, one ionotropic. Mixture of excitatory and inhibitory, 7 subtypes.
  • Packaged by VMAT, terminated by degradation via MAO, or reuptake by SERT
  • Wide variety of targets, cell bodies located in Raphe nuclei
42
Q

What is pharmacokinetics?

A

study of the factors that influence bioavailability of a drug (ability of drug to reach site of action)

43
Q

What is pharmacodynamics?

A

the interaction of the drug with a target

44
Q

What is absorption and How does absorption affect bioavailability?

A

Absorption is the passage of a drug from site of administration to bloodstream.
- Speed and effectiveness of absorption affected by route of admin and properties of the drug: Smaller, lipid soluble molecules absorbed more easily (environment can affect lipid solubility-nonionized better, ionized worse, and properties of drug determine what enviro for prime absorption)
Route of admin determines length of journey and thefore how quickly and effectively drug is absorbed.

45
Q

What is first pass metabolism?

A

Drug saturated blood collected from stomach and small intestine goes directly to liver for metabolism before circulation to rest of body.

46
Q

What is distribution and what are the main obstacles to it?

A

Dist. involves the drug getting to target site. The BBB and non-specific binding are obstacles:

  • BBB; capillaries in brain more tightly sealed, so drug has harder time crossing from blood to extracellular fluid in brain where target sites are located, passive diffusion of drugs requires molecules to be very small and lipid soluble.
  • Non-specific binding; some drugs bind to inactive sites on the way (such as THC to fat), and while bound to these areas they are not available to act on targets or for metabolism. This process is reversible.
47
Q

What is special about the area postrema in regards to the BBB?

A
  • BBB not present in certain areas to allow for these areas to monitor changes in the blood, area postrema is one of these locations meant to detect toxins; when drugs detected it can elicit a vomiting reflex.
48
Q

What is Biotransformation? And what factors alter CYP enzyme functioning?

A
  • Process of converting drug into one or more metabolites; performed by enzymes found mostly in liver, but stomach and intestines as well.
  • Genetic variation (polymorphisms) can affect amount of CYP enzyme to be produced and the function of the CYP enzyme produced - result in people who are normal, slow, or fast metabolizers (reasoning behind personalized medicine)
  • Enzyme induction; when drugs and other substances increase the number of CYP molecules produced, resulting in excess metabolism of a drug.
  • Enzyme inhibition; a drug or substance inhibiting enzyme function, resulting in not enough metabolism
  • Drug competition; when more than one drug can compete for a single enzyme, reduces availability of enzyme for drug that is out-competed.
49
Q

What are Phase 1 and 2 biotransformation?

A
  • Phase 1: BT that produces metabolites that are more water soluble (for elimination). Occurs in liver, can on occasion also make an active metabolite (and in this case the metabolite would be the active form of the drug)
  • Phase 2: conjugation; addition of small molecules to drug; usually end result is larger, charged molecule less able to pass through membrane.
50
Q

How elimination works

A
  • Drugs mostly leave body via kidneys, but can also leave via lungs.
  • In order to be excreted drug needs to be less lipid soluble (this is how biotransformation and elimination are linked)
    Drugs eliminated at particular rate that follows one of two patterns:
    1. First order kinetics(most drugs): Drug is eliminated exponentially, constant fraction is removed at each time interval. Quantified by determining half-life.
    2. Zero-order kinetics (high dose alcohol): When there is so much drug present in the system that it out-populates enzymes, meaning elimination occurs at the rate in which enzymes can clear one molecule before moving on to the next.
51
Q

Targets for psychoactive drugs

A
  • NT receptors
  • NT transporters
  • Enzymes involves in synthesis or degradation.
52
Q

The actions of a drug at a receptor depend on:

A
  • How well the drug bins to the receptor (binding affinity)

- How the drug impacts the actions of the receptor.

53
Q

How is binding affinity quantified?

A
  • Kd value (dissociation constant); amount of drug required to bind 50% of receptors
  • Lower Kd value = higher binding affinity to receptor.
54
Q

What is binding affinity?

A

the degree of attraction between ligand and receptor

55
Q

Kd and binding affinity are related to the potency of a drug, and drugs with a lower Kd are likely to be more potent. How is potency measured?

A
  • Drug effects measured against drug dose (dose response curve) which determines the ED50 (the dose required to achieve 50% maximal effect)
56
Q

How is the therapeutic index calculated and what does it show?

A
  • Comparing dose required for thera. effect(ED50) with dose that results in toxicity(TD50) (TI=TD50/ED50)
  • The greater the TI the safer the drug.
57
Q

What are the two types of antagonist?

A
  • Competitive antagonist: when drug binds to the same site as NT, preventing NT from binding
  • Non-competitive antagonist: does not bind to same site as NT but does not allow NT to activate receptor.
58
Q

What are allosteric regulators and what are the types?

A
  • Can enhance or diminish aaction of a NT on its receptor.
  • Allosteric inhibition occurs when the drug acts as an inhibitor that binds to the allosteric site, causing a change in receptor shape resulting in an altered active site; activation is the opposite.
59
Q

What is tolerance and its characteristics?

A
  • Tolerance is a diminished response to a drug after repeated exposure or when higher and higher doses of a drug are required to maintain desired effects
  • Characteristics
  • reversible
  • depend on pattern of use and drug taking environ.
  • may occur rapidly, after chronic exposure, or never
  • not all drug effects show same degree of tolerance
  • diff. mechanisms can underlie
60
Q

What are the types of tolerance?

A
  • Pharmacokinetic: caused by increased ability to metabolize drug (enzyme induction) - also possible cause of cross tolerance
  • Pharmacodynamic: change in receptor number, chronic administration can result in less receptors present
  • Behavioural/Conditioned: when drug related cues trigger compensatory response.
61
Q

What is the mellanby effect?

A
  • A form of acute behavioral tolerance where behav. effects of alcohol more pronounced as blood alc level rising than when they are falling.
62
Q

What is withdrawal syndrome?

A

The collection of wothdrawl symptoms for a drug

63
Q

Physical vs. Psychological dependence/withdrawal

A
  • Physical: dependence causes withdrawal effects such as dizziness, nausea etc,
  • Psychological dependence causes withdrawal effects such as drug cravings and mood changes
64
Q

Discriminative stimulus

A

Created when response is reinforced in its presence, but not when it is absent.

65
Q

Conditioned stimulus

A

A previously neutral stimulus that, after becoming associated with the unconditioned stimulus, eventually comes to trigger a conditioned response

66
Q

Incentive salience

A

Attribution of salient motivational value to otherwise neutral stimuli.

67
Q

What is opponent-process theory?

A

When initial drug use focused on rewarding effects shifts to drug use to avoid negative effects of withdrawal, after chronic use opposing process outweighs drug effect.
Theorized to occur due to shift in allosteric baseline

68
Q

What is the incentive salience model?

A

Addiction involves a shift from liking the effects of a drug to wanting the drug.
Core to this model is that liking involves a separate neural circuit from wanting (just because you like it does not mean you have the motivational drive to attain it, where in wanting it doesn’t matter if you like it)
Emphasis is on increased salience of stimuli associated with drug in addicted state.
Salience part of model accounts for relapse; if opponent theory completely accurate then getting past withdrawal would be all that was needed to get past addiction

69
Q

What is Drive theory?

A

When people experience a powerful drive to seek out and achieve drugs positive reinforcig effects

70
Q

Disease model of addiction

A

Characteristic of drug addiction correspond to medical definition for a disease

71
Q

Gateway theory of drug use

A

The use of legal drugs tends to precede illegal drugs, and use of drug at one stage is a risk factor for use of drug at next stage.

72
Q

What are the three phases of the addiction cycle and the brain regions associated with them?

A
  • Binge/Intoxication: Two key parts of Basal Ganglia
  • Nucleus accumbens: reinforcement/reward; mesolimbic pathway (reward pathway) from VTA to NA is what most drugs of abuse activate
  • Dorsal striatum: involved in movements and habits, underlie compulsive behavioural patterns behind drug consumption.
  • Withdrawal/negative affect stage and extended amygdala
  • Amygdala: central control over stress response, during withdrawal it is thought that amygdala is hyperactive.
  • the Extended Amygdala however is thought to control the aversive experience of withdrawal.
  • Preoccupation/Anticipation stage:
  • Dorsolateral PFC seems to drive this, as the PFC is the stop and go system that works to balance impulses coming from basal ganglia, and in drug abuse the inhibitory function is disrupted meaining impulses from basal ganglia not being checked.
73
Q

What is the origin of Cathinones?

A

Catha edulis plant (khat), Cathinone extracted from this plant and used to synthesize other cathinones such as mephedrone.
Native to east africa and natives used to chew khat leaves or make tea.

74
Q

What is the origin of Ephedrines?

A

Derived from Ephedra sinica plant found in dry climates, used in china for medicine for thousands of years.
Ephedrine and pseudoephedrine isolated from this plant and are ingredients found in cold/sinus medicines
Used to synthesize methamphetamine

75
Q

What is the origin of Cocaine?

A

Alkaloid found in leaves of coca plant native to south america. Widely used in cola, smokes, etc. till regulations in 1900’s, then reappeared in popularity for illicit drug use after 1970’s
Can be snorted, injected (cocaine salt), or smoked (crack form).

76
Q

Origins of Amphetamine

A

Synthetic compounds developed to serve as equivalent to ephedrine
Used as therapeutic stimulant for various purposes (narcolepsy, weight loss, and ADHD)

77
Q

Origin of Methylphenidate

A

Synthetic compound discovered in 1944 used as a stimulant for ADHD

78
Q

Route of psychostimulant administration for therapeutic use vs. non-thera use, and how this effects abuse potential.

A
  • Therapeutic: oral or transdermal
  • Non-thera: Injection, inhalation, insufflation, oral
  • An immediate response is linked with higher abuse potential, therefore crack cocaine has higher abuse potential because it is immediately absorbed via lungs.
79
Q

How are psychostimulants metabolized and eliminated?

A
  • Many such as amphetamines and methamphetamines are metabolized by CYP enzymes in liver
  • Cocaine is metabolized by esterases, enzymes present throughout body.
  • Both pathways result in active metabolites.
  • Eliminated via the kidneys
80
Q

Half lives of psychostims from shortest to longest

A
  • Cocaine; 1/2 hr to hour and a half
  • Methylphenidate: 2 hours
  • Amphetamine: 10 hours
  • Methamphetamine: 11 hours
81
Q

Mechanism of action for Cocaine

A
  • Acts by inhibiting monoamine re-uptake transporters (VMATs) causing an accumulation in the synapse.
  • In high concentrations, it has numbing effect as it blocks volatge gated Na+ channels on nociceptors.
82
Q

Mechanism of action of Amphetamine, and to a lesser extent, methylphenidate and cathinone

A
  • Act by reversing DA and NE transporters and enhancing DA and NE available for release, increasing concentration in synapse and driving a continued response.
83
Q

Psychostim effects on behaviour (excluding ADHD)

A
  • Low doses increase purposeful behaviours

- High doses increase purposeless behaviours such as stereotyping and punding

84
Q

Psychostim effects for ADHD

A
  • Instead of increasing low baseline rates of behaviour it actually decreases initially high rates of baseline behaviours. Thought to result from increase D1 and alpha2A activation in PFC which increases activity in frontoparietal and frontostriatal circuits.
  • However, too much can result in opposing negative effects
85
Q

Approximately 10-20% of cocaine users develop cocaine use disorder. Why is this?

A
  1. Genetic differences in metabolism, or differences resulting in enhanced positive or negative subjective effects.
  2. Sex differences
  3. Psychosocial factors
86
Q

What are treatments for psychostim (cocaine) abuse?

A
  • Modafinil; because it is a weak psychostim and elevates DA a little in a long term manner it reduces the rewarding effects of taking cocaine (brings lowered baseline back up)
  • Cocaine vaccine: antibody response to cocaine where antibodies stick to cocaine and prevent it from crossing BBB (does not last very long however)
87
Q

Origins of nicotine

A

is an alkaloid found in the leaves of the tobacco plant.

little particles of nicotine containing tobacco called tar

88
Q

Nictotine Route of admin., absorption, and metabolism

A
  • Route of admin. via inhalation
  • Absorption via lungs (fastest route) and mucous membranes in mouth (slower)
  • Metabolized in liver via CPY2A6 into cotinine, which is excreted in liver.
  • Half life of 2 hours
89
Q

Nicotine and its effect on receptors, and action/effects

A
  • Nic works as nAChR agonist, and nAChR’s made up of 5 subunits from a variety of subunits, subunit configuration impacts receptor affinity for nictotine (muscle nAChR’s less affinity)
  • A short time after nAChR activation the receptor enters a desensitized state (even if receptor bound to agonist) for a short time; in this way nicotine also functions as a functional antagonist as when it activates these receptors it causes them to undergo a longer period of desensitization
90
Q

Nicotines effects on para and symp NS

A
  • stimulates NE and E release which increases heart rate
  • increases digestive secretions
  • increased contraction of gut muscles
91
Q

Distribution of nicotinic nAChR’s, effects on certain parts of brain

A
  • Hippocampus, VTA, Nuc Acc, amygdala, PFC, hypothalamus

- Nicotine admin into VTA and/or Nuc. Acc. leads to increased DA levels in Nuc Acc.

92
Q

Effects of nicotine on naive and chronic users

A
  • reduces appetite in both
  • may improve attention in both
  • in naive users nicotine produces negative subjective effects such as anxiety, dizziness and nausea
  • after chronic use it tends to produce positive subjective effects such as relaxation and a positive mood.
93
Q

What is acute tolerance to nicotine thought to be caused by?

A
  • Desensitization, where pleasure and arousal are present at first in the day and then as the day wears on use is associated with elimination of negative side effects from nicotine abstinence syndrome. (eg. anxiety, irritability, impatience, insomnia, nausea, hunger)
94
Q

Factors that contribute to nicotine dependence (genetic and otherwise)

A
  • reinforcing effects of nicotine
  • relief from withdrawal
  • associative learning
  • differences in nAChR subunit genes and levels of expression; example is “chippers” who are able to use tobacco long term but at a low levels, like a few a week but for years
  • Difference in CYP2A6 functioning; low metabolizers=less likely to develop dependence
95
Q

Pharma. treatments for tobacco use disorder

A
  • nicotine replacement therapy
  • bupropion: DA reuptake inhibitor and weak nAChR agonits
  • Varenicline: weak agonist for nAChR’s
96
Q

Pharmacokinetics of caffiene

A
  • orally administered and absorbed in small intestine
  • biotransformed by CYP1A2, eliminated in urine
  • Half life between 3-10 hours
97
Q

Pharmacodynamics of Caffeine

A
  • Caffeine is Adenosine receptor antagonist
  • Adenosine receptors widespread in brain
  • Adenosine is neuromodulator that plays a role in pain, anxiety, sleep, etc. and acts as CNS depressant; promotes sleep
  • ADR and DAR interact with each other but at cross-purposes as adenosine can antagonize DA signaling.
98
Q

Effects of caffeine administration

A
  • increased locomotor activity
  • reduced fatigue and enhanced energy
  • enhanced alertness and concentration
  • increased motivation
  • etc.
  • May enhance rewarding effects of cocaine in adolescents but not adults (rats)
  • Adverse effects (caffeine toxicity) includes increased anxiety, insomnia, hypertension
  • Physical dependence develops with chronic use and withdrawal symptoms include diminished energy, fatigue, headaches, reduced focus.

PsychoPharm (1 decks)

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