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Neurobiology of Disease > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Addiction is a progressive behavorial syndrome characterized by _____ and ____ drug-seeking and consumption.

A

compulsive and out of control

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2
Q

Addiction is/isn’t curable and to determine effective treatment, we need to understand ________ and _________.

A

is not

physiology and pathology of motivated behaviors

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3
Q

Reward vs. Reinforcing (drugs do both)

A

Reward– a stimulus that is interpreted by the brain as intrinsically positive, or something that should be approached. (brain likes it)

Reinforcing– an increase in the probability of the occurence of a behavior that is paired (brain wants it)

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4
Q

________ is an experimental setup used to assess drug reward. How does it work?

A

conditioned place preference

Animals learn to associate one environment with passive drug adminsstration, and they will spend more time in the context in which they received the drug. (form of pavlovian conditioning

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5
Q

_________ is an experimental setup used to assess drug reinforncement. How does it work?

A

drug self-administration

Getting the drug is contingent on a specific behavior (lever-pressing)

The drug is interpreted as a reinforcer if it increases the occurrence of lever pressing.

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6
Q

The drug-induced _________ may be an important ______ for initial drug use in humans.

A

euphoria

reinforcing drive

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7
Q

Three central dopaminergic pathways

A

1) Nigrostriatal system:
SNc –> Striatum (putamen, caudate nucleus)

2) Mesolimbic system:
VTA –> NAc

3) Mesocortical:
VTA -> PFC

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8
Q

The nigrostriatal dopaminergic pathway is responsible for ______, but the _______ and ___ constitute the endogenous reward pathway

A

initiation of voluntary movement

mesolimbic and mesocortical

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9
Q

the mesocortical and mesolimbic systems are thought to be responsible for (2)

A

perception of reward

positive reinforcement

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10
Q

Dopamine produces overall inhibition of _____ in the _____ via activation of postsynaptic _____ receptors

A

GABAergic projection neurons

NAc

D2 (which is Gi coupled)

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11
Q

____________ allows for the identification of brain regions involved in reinforcement

A

intracranial self-stimulation

lever press leads to electrical stimulation of brain region

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12
Q

Stimulation of this region contains, which contains__________ elicits strongest reinforcement of self-stimulation behavior

A

medial forebrain bundle

mesocorticolimbic dopaminergic fibers

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13
Q

How do cocaine and amphetamine increase monoaminergic transmission

A

Cocaine inhibits monoamine transporter

Amphetamine induces reverse transport of monoamines

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14
Q

______________________ dramatically reduces the reinforcing effects of psychostimulants

A

Blockade of dopaminergic transmission in NAc (by administration of dopamine antagonists or dopaminergic neurotoxin)

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15
Q

The three types (name them) of opioid receptors are ____-coupled

A

mu, kappa, and delta

Gi

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16
Q

Action of opiates (2 mechanisms)

A

1) disinbition of VTA dopamine neurons via mu activation in GABAergic neurons, resulting in dopamine in NAc
2) dopamine-independent actions on mu and delta receptors, leading it inhibition of NAc projection neurons leading to reinforcement

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17
Q

___ and ___ receptors mediate the reinforcing effects of opiates, but ____ receptors cause _______, thus mediating aversion to opiates

A

mu and delta

kappa, reduction in dopamine release mediating aversive effects

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18
Q

Naltrexone, a ____________ reduces ethanol self-administration in animals

A

opioid receptor antagonist

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19
Q

Three actions of ethanol

A

1) directly activates VTA dopamine neurons, which
2) may inhibit GABA release onto dopamine neurons
3) induces relase of endogenous opioids in VTA or NAc

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20
Q

Two actions of nicotine

A

1) activates VTA dopamine neurons via nicotinic ACh

2) induce release of endogenous opioids

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21
Q

Three types of long-term changes in addiction course:

A

1) Compensatory adaptations in the brain regions that control somatic function (locus coeruleus)- days to two weeks
2) Adaptations in reward circuit (several weeks to lifetime)
3) Production of memories realated to drug use

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22
Q

LC compensatory adaptation is produced by _______ and ____ but not _____

A

opiates, alcohol

psychostimulants

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23
Q

Three adaptations in the brain reward circuit

A

1) tolerance— decrease in reinforcing effects of a drug which leads to a higher dosage
2) dependence– demad for drug to avoid emotional and physical withdrawal
3) sensitization– an increase in rewarding effexcts of a drg, which leads to more cravings and maybe psychostimulant psychosis

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24
Q

______ expose leads to ____, ____ while ____ exposure leads to ______

A

continuous– tolerance and dependence

intermittent– sensitization

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25
Q

Cue-induced relapse (examples)

A

1) relapse of withdrawal symptom if you visit the ste where you used drugs

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26
Q

The therapeutic actions of antidepressants and antipsychotics are dependent on ___________

A

time dependent adaptive changes in their respective brian regions

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27
Q

THe LC, the major ___________ nucleus, is responsible for three tings

A

noradrenergic

arousal, autonomic tone, and attention

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28
Q

LC activity is ______ by opiates via _________________

A

inhibited

activation of mu opioid receptors

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29
Q

How does continuous opioid use lead to tolerance? Dependence?

A

Tolerance– depressed firing in LC neurons gradually returns to normal after repeated opiate use

Dependence– administration of opioid antagonists causes a huge increase in LC fiting rates

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30
Q

_____________ is both necessary and sufficient to produce physical withdrawal symptoms

A

overactivation of LC neurons

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31
Q

Two mechanisms of how opiates inhibit LC neurons

A

1) activation of a certain type of K+ channel vira direct binding of Gi/o ro channel
2) inhibition of Na+ permeable channel via suppression of AC/cAMP cascade

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32
Q

Chronic opiate use leader to upregulation of __________ and ______ expression, leading to increased excitability o LC neurons via ______ activation

A

AC and PKA

Na+ channel

33
Q

upregulation of cAMP pathway in LC neurons causes (2)

A

1) return of LC firing rates to normal in continued opiate admins (tolerance)
2) increased firing above normal levels upon removal of opiates (dependence and withdrawal)

34
Q

Reinforcing effects of addictive drugs are also mediated by ____________, which keys into emotion and motivation in the context of dependence.

A

meoslimbic dopaminergic (upregulated = positive emotional state)

35
Q

cAMP hypothesis of withdrawal

A

chronic admin of pscyhostimulants, ethanol, opiates causes increased levels of PKA and AC and decreased levels of Gi/o in NAc, which leads to higher cAMP activation and negative emotional states

36
Q

Dopamine in the NAc does what path?

A

Inhibits NAc projection neurons and leads to increased reward/reinfrocement

37
Q

Evidence supporting cAMP hypothesis of withdrawal

A

1) Inactivating Gi or activating Gs in the NAc leads to lower drug reward
2) Administering a PKA activator or a D1-agonist in the NAc leads to lower drug reward
3) Admin a PKA inhibitor or a D2-agonist leads to higher drug reinforcement

38
Q

physical and emotional dependence go away relatively rapidly after stopping drugs, so ______________

A

they don’t account for high incidence of relapse (this is more in the sensitization)

39
Q

Drug sensitization can be measured in animal models by

A

an increase in locomotion induce by drug

40
Q

Locomotor sensitization can only be observed _______

A

when the drugis administered in the context that was previously paired with it

41
Q

Drug-induced hyperlocomotion is caused by

A

overstimulation of the nigrostriatal dopamine system

42
Q

The nigrostriatal system is also implicated in

A

habit formation

43
Q

Sensitization– Adaptations in the SNc and VTA

A

1) Downregulation of Gi (leads to less D atoreceptor mediated inhibition, an increased drug induced DA release in NAc)
2) Upregulation of AMPA (leads to increased glutamate excitation in DA neurons and increased cue-indced DA release)

44
Q

In relapse, the role of DA in the NAc is to strengthen and facilitate active ____ input from the ______ and tthe ______

A

Glu

amygdala and cerebral cortex

(acts as kind of a gatekeeper, chooses which signal is passed along)

45
Q

Two actions of DA:

A

1) promote long-term plasticicty: learning, reinfocement etc. in an input-specific manner

2) short-term: make decisions, motivation
(via LTP and LTD)

46
Q

Clonidine, an _____________, produces effects similar to ________ receptor activation in the LC, thus improving withdrawal symptoms

A

a2 adrenergic agonist

mu opioid

47
Q

Naltrexone, ______, can be used in the treatment of ______ because ____

A

mu opioid antagonist
alcoholism
ethanol induces release endogenous opioids

48
Q

Methadone

A

a long-acting mu opioid receptor agonist

49
Q

Potential treatments for addiction (4)

A

1) Slow onset long acting DAT blockers– which don’t have a reinforcing effect themselves
2) GABAb agonists to increase GABAb inhibition of VTA Da neurons
3) Vaccines?
4) Drugs that can help extinction during psychotherapy

50
Q

Learning v memory

A

learning = process by which behavioral response to stimulus is changed

memory = ability to maintain or retrieve pattern of response that have been previously learned

51
Q

HM patient underwent

A

billateral temporal lobe removal including HC for epilepsy (had anterograde amnesia_

52
Q

Anterograde v. retrograde amnesia (and brain regions)

A

anterograde– inability to learn new info after trauma (temporal and HC involvement)

retrograde– memory loss of events before trauma (frontal lobe)

53
Q

Neural conditions to associative memory

A

1) activation of A-B transmission coincides with excitation of B (by the US) repeatedly– associativity
2) potentiation occurs only in A-B transmission but not C-b transmission– input-specificity

54
Q

The HC and neocortex are important for

A

consolidation and storage of declarative memory

55
Q

LTP has two important properties that make it a good candidate for explaining storage of memories. This requires

A

associativity and input-sensitivity; coincident pre-synaptic and post-synaptic activity

56
Q

The ________ can act as a good coincident detector because it requires both _______ and _____ in order to pass current

A

NMDA receptor

glutamate (pre-synaptic activity) and delopmarization (post-synaptic activity.

57
Q

NMDA receptor passes ___, which activates _________ which result in LTP

A

Ca2+

Ca2+ dependent kinases

58
Q

Two ways Ca kinases result in LTP

A

1) insertion of more AMPA receptors into the plasma membrane
2) Changing the effectiveness of AMPA receptors already on the membrane

59
Q

What is dementia

A

a chronic impairment of learning, short term and long term memory, commonly caused by neuronal loss

60
Q

Wernicke Korsakoff syndrome is caused by _________

A

Thiamine B1 deficiency

61
Q

Pathological hallmarks of AD

A

1) Amyloid deposition– ab42 plaques in HC, cortex, and cholinergic nuclei (nucleus basalis of Mynert), neuronal loss around these plaques
2) Nuerofibrillary tangles– intracellular accumulation of helicl tau protein

62
Q

Evidence against ab plaques causing AD (2)

A

Even though all familial forms of AD share elevated plasma Ab levels,

1) Some aged people have lots of plagues but no cognitive deficits
2) Animal models of brian amylodiosis (overepxressed APP) don’t have all AD symptoms

63
Q

Early stage AD has fewer ______

A

fewer synapses in the cortex, maybe “something” is attacking the synapse?

64
Q

Evidence that ab plaque is not attacking the synapse but soluble ab is

A

Decrease in synapses occurs before plaques form but the level of soluble ab is correlated with degree of synaptic loss )attacks prior to the signs of memory loss)

65
Q

In initial stage AD, deficits in _______ occur but _____ is generally unaffected

A

short-term

long-term

66
Q

Evidence that solubl Ab causes synaptic defects (3) :

A

1) plasma levels of soluble AB corraltes with degree of synaptic loss
2) ICV injection of sol AB inhibits hippocampal LTP, with short-term memory loss
3) overexpression of human APP with AD-causing mutations sho deficits in synaptic transmission in HC before development of plaques

3)

67
Q

Injection of a ab antibody could

A

reverse impairment and reduce soluble ab in the brain BUT NOT CHANGE plaque levels

68
Q

Basal forebrain complex

A

Medial septal nuclei to HC

Basal nucleus of Meynert

69
Q

It is thought that activation of postsynaptic ACh receptors ___________

A

lowers the threshold for LTP induction in the HC

70
Q

______________ may play a role in learning and memory because administration of scopolamine, a ________ causes learning and memory defects

A

central muscarinic system

muscarinic antagonist

71
Q

Evidence of hypocholinergic hypothesis of learning memory (2)

A

1) Lesions of forebrain cholinergic nuclei produce memory defects which can be reversed by drugs that mimic Ach or muscarinic/nicotinic agonsits
2) Acetylcholinesterase inhibitors can bring back some of the cognitive deficits by enhancing LTP in hippocampus

72
Q

Therapeutic strategies for AD (5)

A

1) Anti-inflammatory agents – NSAIDS seem to reduce risk of AD
2) Antioxidants (vitamin E slows progression of AD)
3) NMDA receptor enhancer
4) beta-secratase inhibitor
5) Ab antibody

73
Q

Symptoms of Parkinsons (need 3/4)

A

Resting tremor

Walk but don’t swing arms, multiple steps while turning etc

Bradykinesia, akinesia

Rigidity and stiffness of limbs

74
Q

paroxysm

A

sudden recurrence of symptoms

75
Q

Three types of seizures

A

1) generalized– originating and rapidly engaging bilateral networks
2) focal– in one hemispheric network, involving one or multiple foci with conssitent ictal onset
3) unknown

76
Q

Not all seizures are electrographic– true of false

A

True (pseudo seizures are a thing_

77
Q

how to reduce reinforcing effects of psychostimulants

A

Block the dopamine release in the NAc by using a dopamine receptor antagonist or a dopaminergic neurotoxin

78
Q

Injection of —— in BLA block fear responses

A

Ampa antagonist

Neurobiology of Disease (2 decks)

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