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PSYT 301 > Lecture 2: neurobiology > Flashcards

Lecture 2: neurobiology Flashcards

neurobiology

1
Q

what does the neurobiology of the brain attempt to understand?

A

the changes at the molecular, cellular, and neurocircuitry levels that mediate the transition from occasional, controlled substance use to loss of control in substance intake and addiction

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2
Q

why is it important to understand the neurobiology of addiction?

A

clinically relevant for treatment

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3
Q

what is the common pathway for all addictive drugs?

A

release dopamine in the nucleus accumbens

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4
Q

what is the path of neurons in the mesolimbic dopamine pathway?

A

starts in the ventral tegmental area (VTA), which is one of the principal dopamine producing regions of the brain, of the midbrain and projects to the nucleus accumbens (NAcc), which is strongly associated with the positive reinforcing effects of both natural rewards and addictive drugs

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5
Q

which addictive substances act direct on VTA DA and which act indirectly?

A

direct: alcohol nicotine, cocaine, amphetamine
indirect: cannabis, opioids, BDZs

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6
Q

what are the two general ways that addictive drugs stimulate dopamine release?

A
  • activate or disinhibiting VTA DA firing
  • increase amount of synoptically released DA
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7
Q

what neurotransmitter do opiates mimic?

A

endorphins

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8
Q

what receptors do opiates bind?

A

mu opioid receptors (agonists)

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9
Q

what neurotransmitter do psychostimulants mimic?

A

dopmaine

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10
Q

what do psychostimulants bind to?

A

dopamine transporter

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11
Q

what neurotransmitter does nicotine mimic?

A

acetylcholine

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12
Q

what receptor does nicotine bind to?

A

a2b4 nAChRs (agonists)

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13
Q

what neurotransmitter does alcohol mimic?

A

GABA and glutamate

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14
Q

what receptors does alcohol bind to?

A

GABAa (agonist) and NMDA (antagonist)

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15
Q

steps of synaptic DA transmission

A
  1. DA Synthesis
  2. DA is encapsulated into vesicles
  3. Action potential opens calcium channel –> calcium influx
  4. Vesicle migrates to membrane for exocytosis
  5. DA is released and binds to postsynaptic receptors
  6. Reuptake of DA into presynaptic neuron
  7. DA is recycled back into vesicles or metabolized
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16
Q

effect of amphetamine on synaptic DA transmission

A

AMP enters the presynaptic neuron via DAT
- AMP forces DA out of storage vesicles
- DAT starts working in reverse
–> DA expelled
- MAO inhibition (high doses)

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17
Q

effect of cocaine on synaptic DA transmission

A

DAT blockade (no DA reuptake)

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18
Q

effect of opioids on synaptic DA transmission

A

binds GABAa receptors, which causes inhibition of GABA release, which decreases the inhibition on dopaminergic neurons, increasing dopamine release

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19
Q

what are benzodiazepines used for?

A

anxiety disorders and short-term insomnia

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20
Q

which BDZs are used to treat anxiety and which are used for insomnia?

A

Anxiety Medications: alprazolam (Xanax), lorazepam (Ativan), diazepam (Valium)

Insomnia Medications: lorazepam (Ativan), zopiclone (Imovane)

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21
Q

why are BDZs so addictive?

A

they affect the dopamine production within the brain just like other highly addictive substances

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22
Q

mechanism of action of BDZs

A
  • Benzodiazepines bind to and activate GABA-A receptors (high affinity for α1 subunits) on GABA interneuron cells in the VTA
  • Interneurons ordinarily inhibit the activity of dopaminergic neurons in the VTA
  • Activation of the GABA-A receptors reduces the amount of inhibition (i.e., disinhibition) which increases the activity of the VTA’s dopaminergic neurons
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23
Q

what is tolerance?

A

Decreased brain response following repeated drug use

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24
Q

what is sensitization?

A

Enhanced brain response following repeated drug use

25
Q

what happens to the brain after acute and long-term drug use?

A
  • acutely modified brain chemistry in a local and short-term way – causes tolerance
  • but repeated drug use causes pervasive changes in the brain that persist long after the individual stops taking the drug (at the cellular, molecular, structural, and functional level) – causes sensitization if the person stops drug use for a certain amount of time
26
Q

what is cross-sensitization?

A

repeated administration of one drug (e.g., amphetamine) will later sensitize animals to the effects of a different drug (e.g., heroin)

27
Q

what is the self-administration model?

A
  • behavioral procedure used to assess voluntary drug-intake in rodents (exposure controlled by the animal)
  • Operant learning in which drug-naïve rodents are trained to perform a specific behavior (e.g., lever pressing or nose-poking) that is contingent on the availability of the drug, thus making the drug a reinforcer of that behavior
28
Q

what are self-administration models useful for?

A

for studying processes such as drug motivation, extinction, and reinstatement (relapse) following an abstinence period

29
Q

what is conditioned place preference (CPP) model?

A

a form of appetitive Pavlovian conditioning used to determine the association strength between drugs of abuse and a specific context

30
Q

how does the Conditioned Place Preference (CPP) Model work?

A

there are two learning stages and one test:
1. First, the drug of interest (e.g., cocaine or heroin) is administered in a particular environment (e.g., a chamber with white walls)
2. In the second stage, a different environment (e.g., a chamber with black walls) is paired with the absence of the drug (e.g., vehicle administration)
3. Test: the time spent in each of the environments in the absence of the drug is recorded

Rodents that exhibit heightened place preference spend significantly more time in the drug-paired compartment and are therefore responding to the rewarding effects of the drug

31
Q

what are the three interdependent processes linked with behaviors towards rewards?

A

liking, wanting, and learning

32
Q

explain the process of liking

A

the pleasurable experience evoked by rewards

33
Q

explain the process of wanting

A

the motivation (willingness/effort) to pursue reward (aka incentive motivation)

34
Q

explain the process of learning

A

Cues and events closely associated with rewards acquire predictive and incentive motivational properties. Central representations (encoding) of such learned associations are essential in modifying behavior as a function of conditions under which rewards are sought and secured

35
Q

The way in which cues associated with drug rewards acquire _______and _______ motivational properties is central to understanding compulsive drug-seeking behaviors

A

predictive and incentive

36
Q

do the “liking” and “wanting” behaviors come from the same brain mechanisms?

A

no, they are dissociable from each other, which explains how many addicts want the drug but don’t like it

37
Q

compare “liking” and “wanting”

A

Liking or the actual pleasurable impact of reward consumption, is mediated by small neural systems, and is independent of dopamine

‘Wanting’, or incentive salience, is a form of motivation, that is generated by much larger and robust neural systems that include mesolimbic dopamine

38
Q

what is incentive salience?

A

psychological process that makes stimuli become excessively attractive, attention-grabbing, and salient (more important)

39
Q

how does incentive salience work?

A
  • Attribution of incentive salience gives rise to drug “wanting”
  • Causes excessive cue-triggered ‘wanting’ to take drugs
  • Results in an enhanced motivation to “seek the drug”
    (Drugs and drug cues acquire pathological motivational value)
40
Q

what part of the brain mediates incentive salience?

A

mediated by the mesocorticolimbic dopamine system (Repeated drug use makes the dopamine system hyper-responsive to drug cues)

41
Q

how can you assess incentive salience in animals and what makes it difficult?

A

Predictive and incentive motivational properties of reward cues are usually acquired together, so dissociating them from each other is difficult.

But, using a Pavlovian
Conditioned Approach (PCA) paradigm, where a cue (lever-CS) that predicts an impending reward is separated in space from the location of reward (US) delivery

42
Q

what can you see when testing for incentive salience in animals?

A

they naturally diverge in the way they attribute salience to a conditioned stimulus:
- goal tracking: directs its attention and behavior toward the reward itself
- sign tracking: directs its behavior towards the CS itself often treating it as if it has inherent reward value (Ascribe incentive salience to cue)

43
Q

compare and contrast the behavior seen in a “goal tracker” and a “sign tracker” mouse when using the Pavlovian Conditioned approach.

A

Goal tracker: it only briefly engages with the lever-CS, instead all their focus goes to the location where the food reward will come out – although there is some predictive value, they do not find the lever attractive

Sign tracker: persistently engage with the lever-CS and moving to get the food reward only after the lever is retracted – they treat the lever as highly desirable so will work to earn the CS

in both, they have developed a conditioned response, but only in the STs have they gained incentive salience

44
Q

how does Pavlovian Conditioned approach affect the DA release and what does this tell us?

A
  • for both the ST and GT, NAcc DA release is initially seen in response to the food but not the CS
  • after 5 sessions:
    for the ST, we see DA release in response the to the CS but gradually decreases for the food-US
    for the GT, we see some DA release in response to the CS, but no change for the food

NAcc DA is necessary for the attribution of incentive salience to reward cues, and not for encoding the predictive value

45
Q

how is stress related to drug se/addiction?

A
  • exposure to stressors is a significant risk factor for drug addiction
  • Heightens the addictive liability of most drugs, increasing the likelihood of engaging in drug-taking
  • Contributes to the escalation from recreational use to problematic drug-seeking
  • Increases the likelihood of relapse
46
Q

what is the effect of stress on the brain?

A

it potently activates dopamine transmission in the prefrontal cortex and also activates DA transmission in the NAcc

47
Q

PFC is heavily implicated in ______________________

A

regulating behavioural and neuroendocrine responses to stressors

48
Q

DA transmission in NAcc is activated by _______and ________

A

rewards and stressors

49
Q

preclinical models of addiction in relation to stress have shown what?

A

that exposure to stress can enhance the rewarding effect of drugs and the acquisition of drug-seeking behaviors (Stress facilitates the formation of associations between contextual information and drugs)

50
Q

what is stress?

A

defined as the perception, evaluation, and response to harmful, threatening, or challenging events, and stressors can be either emotionally or physiologically based

51
Q

Experiencing an environmental stressor, as perceived by the brain, results in the activation of __________

A

the HPA axis

52
Q

explain the HPA-axis.

A
  1. higher order of brain areas (e.g. PFC) can activate (e.g. by stress) or inhibit this axis
  2. Hypothalamus releases corticotropin-releasing hormone (CRH)
  3. anterior pituitary releases adrenocorticotropic hormone (ACTH)
    4/ causes activation of adrenal cortex that releases cortisol
53
Q

what is the effect of experiencing frequent or intense stress?

A

dysfunction of the HPA axis negative feedback

54
Q

what are the worse stressors?

A

the unpredictable/uncontrollable ones

55
Q

what are some morphological changes seen in the brain in response to chronic exposure to stress?

A

decreases the number and length of dendrites, and the number of spines in the PFC (along with a decrease of the birth of new neurons)

56
Q

how does the break point change between control and maternally separated animals?

A

the break point is much higher in maternally separated animals

57
Q

how can we model relaspe in animals?

A

reinstatement paradigm:
- animals trained to press lever to earn IV drug
- once stable rates of self-administration is achieved, you take away the reward, which stops the behavior (which can take 4-6 weeks)
- then, you see what will cause it to relapse

58
Q

what events will precipitate relapse in drug-taking?

A

the drug itself, conditioned stimuli (cue), stress

59
Q

what parts of the brain is implicated in stress-induced relapse?

A
  • HPA axis
  • VTA DA projection to NAcc and PFC
  • extended amygdala

PSYT 301 (8 decks)

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