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Neuro 101 > Exam 4 > Flashcards

Exam 4 Flashcards

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1
Q

which brain structure monitors our internal drives/state?

A

hypothalamus

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2
Q

which brain structure monitors our external drives/environment?

A

amygdala

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3
Q

what motivates behavior?

A

physiological state, environment, and past history

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4
Q

classical conditioning/pavlovian conditioning

A

Involuntary/unconscious associations between stimulus and outcomes.

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5
Q

how is the amygdala important in emotional learning in classical conditioning experiments?

A

the centromedial portion of the basolateral amygdala sends projections to the ANS and to accomplish freezing behaviors

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6
Q

instrumental conditioning/operant conditioning

A

Voluntary/conscious associations formed between the behavior/action and the consequence. You know you’re being conditioned.

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7
Q

reinforcement learning

A

A specific example of instrumental conditioning. Describes how an organism learns, by trial and error, to act in a manner that maximizes reward and minimizes punishment. This is easy to learn but hard to forget.

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8
Q

mesolimbic DA pathway brain regions

A

ventral tegmental area (VTA), nucleus accumbens (NAc)/ventral striatum, amygdala, hippocampus, prefrontal cortex

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9
Q

role of the prefrontal cortex in the mesolimbic DA pathway?

A

executive function & cognitive control

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10
Q

role of the amygdala in the mesolimbic DA pathway?

A

stress/anxiety

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11
Q

role of the hippocampus in the mesolimbic DA pathway?

A

context/memory

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12
Q

role of the VTA and NAc in the mesolimbic DA pathway?

A

VTA neuron cell bodies release dopamine in the NAc

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13
Q

what 2 nuclei of the midbrain are DA cell bodies are found in?

A

VTA and substantia nigra

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14
Q

what happens if you block dopamine receptors?

A

it would reduce the
reinforcing effects of rewarding tasks

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15
Q

why do VTA neurons fire?

A

they fire and release dopamine as a signal for errors in reward prediction

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16
Q

reinforcement learning hypothesis

A

phasic bursts of dopamine in response to unpredicted rewards and cues modify future actions

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17
Q

VTA is in charge of ___, not liking

A

prediction

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18
Q

dopamine is involved in ____, not liking

A

wanting and predicting pleasure

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19
Q

how do drugs hijack the reward system?

A

The brain interprets the increased surge of dopamine from the VTA to the NAc as a reward even though it’s not helping

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20
Q

what does the mesolimbic dopamine signal represent?

A

a learning signal responsible for reinforcing constructive behavioral adaptation (ex. learning to press a lever for food)

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21
Q

abused substances generate a:

A

strong but inappropriate learning signal, thus hijacking the reward system and leading to the pathologic reinforcement

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22
Q

what do VTA interneurons produce?

A

GABAergic effect on VTA projection neurons

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23
Q

what do VTA projection neurons produce?

A

dopamine

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24
Q

D1 receptors

A

activated by DA to increase chances of goal-seeking behavior

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25
D2 receptors
suppress unwanted behaviors (lack of D2 receptors makes it more difficult to suppress non-goal-seeking behaviors)
26
what are the dopamine receptors on?
The GABAergic nucleus accumbens iMSNs (which happen to inhibit the ventral pallidum (VP) which goes to the PFC and amygdala)
27
how do alcohol and opioids indirectly release DA from the VTA onto the NAc and PFC?
they inhibit the GABAergic VTA interneurons, thus disinhibiting the control of DA, so more DA
28
how do cocaine and amphetamines directly release DA from the VTA onto the NAc and PFC?
They bind to the re-uptake pumps at the synaptic connection of VTA to NAc, therefore blocking the re-uptake of DA, so DA levels are very high. Sometimes they reverse the pump & DA is pumped out, so DA levels are very high
29
how does nicotine directly release DA from the VTA onto the NAc and PFC?
it activates and makes action potentials within VTA projection neurons (more DA to NAc)
30
drug abusers and people more likely to form addictions have a lack of which receptor?
D2 receptors
31
what brain structure is involved in the binge/intoxication stage?
the basal ganglia
32
what brain structure is involved in the negative affect/withdrawal state?
extended amygdala + hippocampus (you remember + learn how awful withdrawal is)
33
what brain structure is involved in the preoccupation/anticipation state?
prefrontal cortex (it becomes impaired to control behavioral impulses and is now obsessed with having drug)
34
factors associated with opioid addiction?
- impaired control (larger amounts or longer than intended) - social impairment (failing to fulfill major role obligations) - risky use (knowing that it is harming you) - pharmacological properties (increased tolerance + avoiding withdrawal)
35
extinction
when the drug is no longer available, there is an unlearning in animals and an extinction of the drug-seeking behavior
36
reinstatement
presentation of an environmental cue or experience of a stressor can lead to reinstatement of drug-seeking behaviors
37
How does the MOR inhibit the neuron?
the beta gamma subunits open K+ channels and block Ca++ channels, which hyperpolarizes the neuron and sends off less action potentials
38
opioid effect on NAc, amygdala, and VTA
activate reward circuit
39
opioid effect on medulla
nausea + depression of respiration
40
opioid effect on anterior cingulate cortex, periaqueductal gray, insula, and thalamus
analgesia
41
respiratory depression
depression of the brainstem respiratory center (medulla) prevents detection of higher levels of carbon dioxide in the blood (highest cause of death from opioids)
42
opioid antagonists
naloxone + naltrexone (bind to MOR and knock off the other opioid to cause instant opioid withdrawal)
43
full opioid agonist
methadone -- doesn't give you the massive high, but helps addicts go about their daily lives
44
partial opioid agonist
buprenorphine -- more likely to bind than morphine but half the biological effect
45
efficacy of a drug
ability of a drug to elicit a full biological response
46
potency of a drug
concentration of a drug needed to bind to same number of receptors (stickiness)
47
negative symptoms of schizophrenia
blunted affect, alogia, avolition, anhedonia, asociality
48
cognitive symptoms of schizophrenia
memory problems, poor attention span, difficulty making plans, reduced decision-making capacity, poor social cognition, abnormal movement patterns
49
what is a possible side effect of treating Parkinson's patients with L-dopa?
schizophrenic symptoms (due to more DA)
50
psychosis (loss of contact with reality) can result from:
schizophrenia, mood disorders, neurological damage, extreme stress, and drug use
51
changes to which receptors are a big factor in inheriting schizophrenia?
BDNF, D2R, NMDAR, DISC1
52
what gene has the strongest link to schizophrenia?
C4 "immune system"
53
in what cortices does the most severe thinning occur in prodromal schizophrenic brains?
frontal and temporal cortices
54
loss of matter in which cortex correlates with the severity of SCZ symptoms?
prefrontal cortex
55
why do individuals with SCZ have enlarged ventricles?
loss of gray matter + atrophy of hippocampus and amygdala
56
what causes cognitive symptoms in SCZ individuals?
loss of interneurons in cortical areas --> loss of inhibitory control of pyramidal neurons in cortex may lead to disordered cognitive function
57
where do SCZ individuals have disorganized pyramidal cells?
hippocampus
58
noradrenergic projection system
Locus coeruleus (in pons) projects axons to cortex, limbic system, hypothalamus, and cerebellum (produces feelings of alertness, focus, reward, learning, memory, pain analgesia)
59
hyperactivity of the mesolimbic pathway results in
SCZ positive symptoms
60
hypoactivity of the mesolimbic pathway results in
SCZ negative symptoms and cognitive impairment
61
first-gen antipsychotics
D2R antagonists. Their affinity for D2 receptors predicts their clinically effective dose. These only address positive symptoms.
62
chlorpromazine
low potency first-gen antipsychotic
63
haloperidol
high potency first-gen antipsychotic (less oral dose in exchange for increased side effects)
64
biggest downside of first-gen antipsychotics
extrapyramidal symptoms and movement disorders
65
Tardive Dyskinesia
Orofacial dyskinesia – involuntary repetitive facial movements (side effect of first-gen antipsychotics)
66
Neuroleptic Malignant Syndrome
Risk with any antipsychotic. Extreme rigidity, fever, unstable blood pressure, myoglobinemia. Can be fatal.
67
Akathisa
Subjective and objective restlessness (side effect of first-gen antipsychotics)
68
second-gen antipsychotics
affinity for D2R, but also have high affinity for other types of receptors. This makes them more helpful in relieving symptoms that are resistant to first-gen antipsychotics, such as negative symptoms.
69
clozapine
SGA that blocks the 5-HT receptor. Clozapine is more effective in treating SCZ in people who did not adequately respond to previous antipsychotics.
70
biggest side effect of clozapine
despite being clinically superior to FGA, it requires ongoing blood tests to monitor for potential agranulocytosis
71
upside of second-gen antipsychotics
less likely to produce neurological side effects (extrapyramidal symptoms and Tardive Dyskinesia)
72
risk of second-gen antipsychotics
associated with a greater risk of metabolic syndrome (abnormalities of blood pressure, lipids, glucose tolerance, BMI, increased risk for cardiovascular disease)
73
Black Box Warnings for second-gen antipsychotics
myocarditis, cerebrovascular events, QT prolongation
74
short term outcome of antipsychotics
helps individuals better fight off psychosis
75
long term outcomes of antipsychotics
individuals who learn to live with SCZ without medication are better at fighting off psychosis and keeping jobs
76
evidence supporting dopamine hypothesis for SCZ
- first-gen antipsychotics are D2 receptor antagonists - amphetamines promote the release of DA & NE (blocks DA reuptake) and can induce psychosis similar to SCZ
77
evidence that does not support dopamine hypothesis for SCZ
- drugs block D2R within hours, while SCZ symptoms take weeks to be reduced - 30% of patients don't respond to DA antagonists at all - second generation mechanism - glutamate hypothesis with PCP
78
glutamate hypothesis with SCZ
PCP acts as an antagonist at NMDA receptor, blocking glutamate. PCP abuse leads to a psychosis very similar to SCZ.
79
what does the glutamate hypothesis imply about negative and cognitive symptoms?
defective glutamate transmission can result in less activity in the frontal cortex which leads to negative and cognitive symptoms of SCZ
80
where is there increased blood flow activity in depressed patients?
prefrontal cortex and amygdala
81
where is there less activity in depressed patients?
posterior temporal cortex and anterior cingulate cortex
82
what brain regions have less volume in a depressed patient?
hippocampus, NAc, basal ganglia
83
all monoamine neurotransmitters modulate
mood, sleep-wake, arousal, motivation & reward, cognitive processing, pain perception, neuroendocrine function
84
what brain region neurons make serotonin
raphe nuclei neurons produce 5-HT and projects to thalamus, hypothalamus, basal ganglia, and cortex
85
presynaptic 5-HT auto-receptors
controls 5-HT synchronous firing across the brain
86
which antidepressants block SERT reuptake?
SSRIs, SNRIs, TCAs
87
which antidepressants block NET reuptake?
SNRIs and TCAs
88
SSRIs
Affect monoamine neurotransmitter systems. Increase neurogenesis and have adaptive effects on the hippocampus and other structures.
89
what kind of antidepressant is fluoxetine?
SSRI
90
what kind of antidepressant is venlafaxine?
SNRI
91
what kind of antidepressant is imipramine?
tricyclic/TCA -- first antidepressant and led to discovery of monoamine hypothesis of depression
92
TCAs adverse effects
Antagonist at adrenergic, histamine, and Ach receptors. Also cardiotoxic and can cause cardiac arrythmias. Must be given dose 1 week at a time
93
SSRI adverse effects
GI issues, 30-40% sexual dysfunction, increased rate of suicide
94
serotonin syndrome
spasms and fever caused by dangerously high serotonin levels due to drug interactions
95
drug that induces serotonin and can lead to serotonin syndrome when used with antidepressants
LSD
96
what can happen if you stop taking SSRIs?
serotonin discontinuation
97
neurogenic theory of depression
Depression appears to be a reversible, organic, neurodegeneration affecting neurons in the hippocampus and frontal cortex
98
what amino acid synthesizes NE & DA?
tyrosine

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