Block 4 Neuro part 1 Flashcards

1
Q

Modes:

A

the physical forms of stimuli carrying information

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2
Q

unimodal:

A

one mode of information. For example, light. unimodal association could be integration of direction and intensity of light

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3
Q

unimodal cortex-

A

area adjacent to primary cortex that recieves input from only that primary cortex

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4
Q

multimodal cortex-

A

area where we integrate multiple senses

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5
Q

Primary visual cortex is broca’s area 17 and it’s unimodal broca’s areas are

A

18 and 19

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6
Q

primary somatosensory cortex is broca’s areas 3, 1, 2 and it’s unimodal broca’s areas are

A

5 and 7

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7
Q

primary auditory cortex unimodal association areas are brocas areas:

A

41, 42

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8
Q

primary motor cortex brocas area:

unimodal association cortex brocas areas:

A

4

6, 8

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9
Q

limbic lobe is composed of what parts?

A

cingulate gyrus, hippocampus, parahippocampal gyrus, hypothalamus, mamillary bodies, and fornix (connects hippocampus with mamillary bodies)

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10
Q

the neocortex is organized in 2 ways:

A

laminar and regional

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11
Q

what is unique about motor cortex lamina?

A

heterotypical agranular with large layer V containing Betz cells

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12
Q

what is unique about sensory cortex lamina?

A

heterotypical granular cortex with large layer IV containing granule cells

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13
Q

granule cells recieve afferent input from the

A

thalamus

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14
Q

what is unique about association cortex lamina?

A

homotypical (all layers about the same size)

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15
Q

recite the broadmann’s areas associated with this region:

parietal-occipital

A

5-7, 18-19

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16
Q

recite the broadmann’s areas associated with this region:

occipital-temporal

A

37, 20-21

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17
Q

recite the broadmann’s areas associated with this region:

speech areas

A

22, 39-40, 42, 44-45

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18
Q

recite the broadmann’s areas associated with this region:

prefrontal areas

A

9-11, 46-47

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19
Q

parieto-temporal association cortex function
parietal:
temporal:

A
  • mediates spatial relationships and attention

- object and face recognition

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20
Q

the ____ part of the parieto-temporal association cortex is in the non dominant hemisphere, while the _____ is bilateral

A
  • parietal

- temporal

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21
Q

the parieto-temporal-frontal association cortex is in the dominant/non dominant hemisphere?

A

dominant

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22
Q

the parieto-temporal-frontal association cortex is involved in:

A

mediating language comprehension (wernicke; parietal/temporal), language expression (broca; frontal), and reading and writing

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23
Q

the prefrontal association cortex mediates-

A

planning, judgement, and intellect, leading to goal directed behaviors

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24
Q

the prefrontal association cortex has significant connections with ______ areas, which integrate _________

A
  • limbic

- cognition with emotions

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25
Q

limbic cortex mediates:

A

emotions and memory

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26
Q

where do inputs to an association cortex come from?

A

thalamus (Dorsomedial, lateral posterior, and pulvinar), primary and secondary sensory cortical regions (of ipsilateral hemisphere), association cortex of contralateral hemisphere, brainstem, and motor and premotor cortex

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27
Q

where do outputs from an association cortex go?

A

thalamnic nuclei, premotor–>motor, caudate/putamen–> VA/VL–> motor/premotor, cerebellum, and other primary and secondary sensory cortical regions

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28
Q

where do outputs from an association cortex go?

A

thalamnic nuclei, premotor–>motor, caudate/putamen–> VA/VL–> motor/premotor, cerebellum, and other primary and secondary sensory cortical regions

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29
Q

ventral intraparietal cortex is highly associative for aspects of ________ and _______

A

somatosensory and visual information

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30
Q

multimodal responses-

A

one cell can respond to multiple stimuli

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31
Q

cells of the VIP respond to both somatosensory and visual info, but they also respond according to the stimulus’s ____, _____, and _____

A

size, location, and direction of movement

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32
Q

cells of the VIP respond to both somatosensory and visual info, but they also respond according to the stimulus’s ____, _____, and _____

A

size, location, and direction of movement

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33
Q

the VIP’s function is to integrate multimodal information for constructing a:

A

spatial representation of the external world

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34
Q

the VIP compares the visual response of what something looks like to the:

A

sensory response of how it feels

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35
Q

a lesion to the VIP would manifest as

A

optical ataxia. bad hand eye coordination. there would be a mismatch between what you see and how you go about grasping for the object you see. It is not ataxia (it is not a loss of control). It is really a misforming of the correct pattern

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36
Q

inferotemporal cortex is the ______ pathway

A

what

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37
Q

faces and objects are recognized by the _______ cortex

A

inferotemporal

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38
Q

Prosopagnosia-

A

an inability to recognize faces of specific people while maintaining generic face recognition

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39
Q

prosopagnosia is produced by:

A

bilateral damage to the fusiform gyrus area

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40
Q

the “where” pathway is the _____ cortex

A

posterior parietal

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41
Q

inferotemporal cortex is the P system visual pathway, while the posterior parietal cortex is the __ system visual pathway

A

M

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42
Q

spatial integration and location pathway is the _____ cortex

A

posterior parietal

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43
Q

apperceptive agnosia-

A

impaired ability to match or copy complex visual shapes or objects

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44
Q

apperceptive agnosia is caused by damage to

A

posterior inferior temporal cortex

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45
Q

associative agnosia-

A

impaired ability to match or copy an object, but their ability to identify objects is impaired

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46
Q

associative agnosia is caused by damage to

A

anterior inferior temporal cortex

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47
Q

when looking at a face, brain activity increases in the _____________ area

A

fusiform face area (FFA)

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48
Q

when looking at an object, brain activity increases in the __________ area

A

parahippocampal place area (PPA)

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49
Q

we organize facial features in the same way that we organize ____________

A

orientation within the visual cortex

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50
Q

which cortex carries out executive planning?

A

prefrontal

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51
Q

Executive planning-

A

the use of results from previous experience to weigh alternatives and consequences of a behavior that is designed to achieve a goal or objective. Based on prior knowledge of the means to achieve an end. Requires predictive skills

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52
Q

Executive planning is divided into 3 characteristics:

A

restraint, initiative, and order

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53
Q

most important characteristic of restraint:

A

inhibiting socially inappropriate responses

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54
Q

most important characteristic of initiative:

A

shifting cognitive set

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55
Q

is perseverance under restraint or initiative?

A

restraint

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56
Q

most important characteristic of order:

A

sequencing of behaviors

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57
Q

patients with damage confined to the prefrontal cortex will present as normal in _______(3) but have a disorganized and inappropriate ________(2)

A
  • perception, motor skills, and intelligence

- emotional state and behavior

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58
Q

most efferent projections from prefrontal cortex are arranged in a _______ fashion

A

rostral to caudal

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59
Q

7 restraint functions of the frontal lobe:

A

judgement, foresight, perseverance, delaying gratification, inhibiting socially inappropriate responses, self-governance, and concentration

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60
Q

8 initiative functions of the frontal lobe-

A

curiosity, spontaneity, motivation, drive, creativity, shifting cognitive set, mental flexibility, and personality

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61
Q

8 order functions of frontal lobe-

A

abstract reasoning, working memory, perspective taking, planning, insight, organization, sequencing, temporal order

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62
Q

8 order functions of frontal lobe-

A

abstract reasoning, working memory, perspective taking, planning, insight, organization, sequencing, temporal order

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63
Q

what defines the prefrontal cortex anatomically?

A

the part of the frontal cortex lying anterior to the motor, premotor, and limbic areas

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64
Q

Dorsolateral prefrontal cortex BA

A

46

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65
Q

ventrolateral PFC BA

A

47,45,44

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66
Q

medial cortex BA

A

9

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67
Q

orbitofrontal BA

A

11-13

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68
Q

ventromedial PFC BA

A

32

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69
Q

the largest proportion of input to the prefrontal cortex is from

A

the thalamic dorsomedial nucleus

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70
Q

In order for executive function to work in the prefrontal cortex, we need extensive connections with _________ systems. We need to recognize the relationships between those systems e.g. ________ signals from BG. Also requires _________ of goals and flexibility in _______

A
  • sensory and motor
  • reward signals
  • memory; choice
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71
Q

For executive function to incorparate reward signals and see multivariate relationships, the PFC must have reciprocal connections with the

A

BG (nu. accumbens)

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72
Q

in order for executive function to incorporate memory of goals and flexibility of choice. e.g. memory of choices to consider future choices, there must be reciprocal connections with the ____ lobe

A

temporal lobe

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73
Q

DLPFC recieves multi-sensory input via

A

parietal association cortex

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74
Q

DLPFC outputs are to:

A

supplementary motor areas and basal ganglia

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75
Q

DLPFC encodes behavior related to: (3)

A

spatial relationships, working memory, and shifting cognitive sets

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76
Q

VLPFC recieves visual association input from

A

temporal lobe

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77
Q

VLPFC encodes behavior specific to: (3)

A

object recognition tasks, relational reasoning, and forming analogies

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78
Q

orbitofrontal cortex and medial cortex are connected to the _______ areas and are related to _________

A
  • medial temporal limbic areas

- affect and motivation

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79
Q

Behaviors related to the orbitofrontal and medial cortex require ____________

A

restraint and delay in gratification

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80
Q

what tasks are affected by lesions of the DLPFC? 4

A

verbal fluency, delayed response, wisconsin card sort

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81
Q

what tasks are affected by lesions of the DLPFC? 4

A

verbal fluency, delayed response, wisconsin card sort

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82
Q

Lesions of DLPFC generally lead to 2 issues:

A

cannot follow rules of a task and cannot perform a task that requires a delayed response

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83
Q

Anterior cingulate cortex monitors _____________

A

behavioral conflict

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84
Q

Anterior cingulate cortex (ACC) influences the praparation or organization of the _______

A

behavior in the DLPFC

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85
Q

ACC activity supports the avoidance of

A

mistakes

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86
Q

damage to the orbitofrontal and VMPFC results in

A

insensitivity to reward; no emotional response to poor return

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87
Q

when you predict a reward, _____ neurons of the ______ cortex fire.

A

pre-reward

orbitofrontal PFC

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88
Q

_____ modulates ______ which modulates reward in PFC (especially orbitofrontal)

A
  • VTA

- N. accumbens

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89
Q

Neurons in VTA correspondingly increase spike rate with

A

increased reward

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90
Q

without a cue for reward, dopaminergic neurons will spike when reward is recieved. After conditioning….

A

the VTA will spike with anticipation for reward.

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91
Q

If reward is anticipated but then not recieved, what happens with VTA

A

there is a depression of activity in the VTA, and a corresponding depression of the reward pathway

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92
Q

BG support ______ control

A

cognitive

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93
Q

BG doesn’t only gate motor output. It also gates cognitive output. Describe the prefrontal loop:

A

DLPFC–>anterior caudate–> GPI, substantia nigra reticulata–> mediodorsal (including pulvinar) and ventral anterior nuclei–>cortical targets

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94
Q

Prefrontal loop modulates

A

executive control of behaviors

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95
Q

affective loop modulates

A

emotional behavior

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96
Q

route of affective loop

A

amygdala, hippocampus, orbitofrontal, anterior cingulate, temporal cortex–> ventral striatum–> ventral pallidum–> mediodorsal nucleus–> cortical targets

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97
Q

the orbitofrontal cortex and basal ganglia are hyperconnected in

A

OCD

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98
Q

there is a region of DLPFC that fires more intensely as certainty of _______ increased

A

discrimination

99
Q

if you lesion the area of DLPFC that fires in correlation with decision certainty, what will be the result?

A

they will be very indecisive.

100
Q

deductive reasoning-

A

true or false depends on the logical relation of the premises

101
Q

deductive reasoning activity is seen in the ______________ cortex

A

inferior prefrontal

102
Q

inductive reasoning-

A

true or false depends on the probabilities of premises

103
Q

inductive reasoning activity is seen in the _________ cortex

A

dorsolateral prefrontal

104
Q

5 functions dominated by the left hemisphere

A

speech, writing, lexical and syntactic language, analysis of right visual field, mathematical skills

105
Q

5 functions dominated by the right hemisphere

A

rudimentary speech, prosodic aspects of language, analysis of left and right visual fields, musical skills, and spatial abilities

106
Q

because many higher order functions are lateralized to a hemisphere, how do we send information to them from sensory areas?

A

use the corpus callosum

107
Q

neurons that fire when watching someone else perform a task to give you an idea of what it feels like to be in their position

A

mirror neurons

108
Q

theory of mind leads to

A

empathy

109
Q

mentalizing-

A

ability to imagine what other people might be thinking or feeling

110
Q

conspecific recognition-

A

ability to recognize us vs them

111
Q

cognitive empathy-

A

collaborative goals

112
Q

emotional empathy-

A

sympathy for others

113
Q

where is theory of mind located?

A

DMPFC, VMPFC, temporal parietal junction, posterior superior temporal sulcus, extrastriate body area

114
Q

What part of theory of mind does this area supply?

DMPFC

A

cognitive empathy collaboration

115
Q

What part of theory of mind does this area supply?

VMPFC

A

attribution of emotional empathy

116
Q

What part of theory of mind does this area supply?

TPJ (temporal parietal junction)

A

recognizing the mental state of a person

117
Q

What part of theory of mind does this area supply?

PSTS (posterior superior temporal sulcus)

A

understanding intention or goal of a person

118
Q

What part of theory of mind does this area supply?

EBA (extrastriate body area)`

A

detecting presence of a person

119
Q

What part of theory of mind does this area supply?

EBA (extrastriate body area)`

A

detecting presence of a person

120
Q

emotion-

A

spontaneous moods that include blah blah blah

121
Q

Schachter-Singer theory-

A

emotion integrates role of physiological arousal and cognitive factors. Emotion exert a steering function over general physiological arousal

122
Q

emotional state has 2 components-

A

a conscious feeling and a physical sensation

123
Q

Magda Arnold’s “appraisal” theory

A

unconscious, implicit evaluation of a stimulus is followed by action tendencies, then peripheral responses, and finally conscious experience

124
Q

Broca’s Le Grande Lobe Limbique-

A

the “rim” around the diencephalon

125
Q

What plays a central role in emotion?

A

amygdala

126
Q

ventral amygdalofugal pathway

A

connects amygdala to nucleus accumbens

127
Q

ventral amygdalofugal pathway is responsible for

A

emotional memory and instrumental action

128
Q

stria terminalis pathway-

A

begins in amygdala and passes over the thalamus to innervate septal nuclei

129
Q

stria terminalis is responsible for

A

visceral or autonomic emotion

130
Q

aversion system consists of and mediates-

A
  • septum, amygdala, posterior hypothalamus

- fear, anxiety, rage

131
Q

gratification system consists of and mediates

A
  • nu. accumbens, anterior hypothalamus, brainstem nuclei

- pleasure and reward

132
Q

emotional memory system consists of and mediates-

A
  • hippocampus, dorsal medial nucleus of thalamus, amygdala

- short term memory associated with emotion

133
Q

Kluver-Bucy Syndrome =

A

bilateral lesions of the anterior temporal lobe (including amygdala)

134
Q

symptoms of Kluver-Bucy Syndrome-

A

visual agnosia, hypermatamorphosis, oral tendencies, hyper-appetitive, hypersexuality, loss of emotional valence, tame behavior

135
Q

symptoms of Kluver-Bucy Syndrome-

A

visual agnosia, hypermatamorphosis, oral tendencies, hyper-appetitive, hypersexuality, loss of emotional valence, tame behavior

136
Q

visual agnosia-

A

loss of object recognition

137
Q

hypermatamorphosis-

A

object obsession

138
Q

3 nuclei of the amygdala

A

lateral, basal, and central

139
Q

afferent input to amygdala is directed towards the ______ nucleus

A

lateral

140
Q

lateral nucleus and basal nucleus make up the

A

basolateral complex

141
Q

output from basal nucleus of amygdala pathway =

A

basal nucleus–> ventral amygdalafugal pathway–> ventral striatum (nucleus accumbens)

142
Q

output from central nucleus of amygdala pathway =

A

central nu.–> stria terminalis–> hypothalamus, brainstem, and modulatory systems

143
Q

output from central nucleus of amygdala carries ______ information

A

emotional: visceral, autonomic response, and arousal

144
Q

output from basal nucleus of amygdala carries ______ information

A

instrumental action (motor response, memory, reward)

145
Q

learned fear-

A

conditioned eversion in which we pair a benign stimulus with an aversion stimulus

146
Q

3 ways amygdala mediates fear response:

A
  • emotional response: amygdala to cortex–> cortical arousal, attention, action
  • visceral behavioral reaction: amygdala to periaqueductal grey–> flight or freezing response
  • autonomic response: amygdala to hypothalamus–> sympathetic (HR, blood pressure, sweating) response
147
Q

What was Ralph Adolphs’ patient missing?

A

her amygdalas

148
Q

DA neurons in the VTA release DA onto __________ neurons in the NA. If that release is coincident with input to NA from the _______ and/or _______, NA neurons are more likely to fire and disinhibit activity of the ______ system.
What results is that a particular emotional state is attached to an event. If it’s a good event, it is given reward and more likely to be sought or craved in order to obtain the benefits of the rewarding event.

A

DA neurons in the VTA release DA onto medium spiny neurons in the NA. If that release is coincident with input to NA from the amygdala and/or orbital – medial PFC, NA neurons are more likely to fire and disinhibit activity of the limbic system.
What results is that a particular emotional state is attached to an event. If it’s a good event, it is given reward and more likely to be sought or craved in order to obtain the benefits of the rewarding event.

149
Q

DA neurons in the VTA release DA onto __________ neurons in the NA. If that release is coincident with input to NA from the _______ and/or _______, NA neurons are more likely to fire and disinhibit activity of the ______ system.
What results is that a particular emotional state is attached to an event. If it’s a good event, it is given reward and more likely to be sought or craved in order to obtain the benefits of the rewarding event.

A

DA neurons in the VTA release DA onto medium spiny neurons in the NA. If that release is coincident with input to NA from the amygdala and/or orbital – medial PFC, NA neurons are more likely to fire and disinhibit activity of the limbic system.
What results is that a particular emotional state is attached to an event. If it’s a good event, it is given reward and more likely to be sought or craved in order to obtain the benefits of the rewarding event.

150
Q

electrical stimulation of the nucleus accumbens mimics _____ use

A

cocaine

151
Q

VTA stimulates the nucleus accumbens through the ___ during reward prediction and anticipation.

A

MFB

152
Q

Reward system has regulatory feedback inhibition via dampening of the ____ by _____ neurons

A

VTA

GABAergic neurons

153
Q

withdrawal is not caused by the suppressed reward system as much as it is caused by the upregulated _______ system

A

anti-reward

154
Q

negative reinforcement system is quiet in the ______ state

A

non-dependent

155
Q

anti reward system increases release of NE from ________, which increases release of CRF from _______

A
  • locus ceruleus

- paraventricular nucleus

156
Q

CRF from the paraventricular nucleus activates the ______ to create aversive feelings of ______

A
  • amygdala

- dysphoria (withdrawal symptoms)

157
Q

cravins are modulated by the _______ based on _______

A
  • DLPFC

- drug cues/context

158
Q

Stimulating the DLPFC does what to craving?

A

reduces

159
Q

when there is a drug cue for an addict, they will crave it. The DLPFC can modulate that craving up or down. It cannot however do what?

A

cannot “win”

cannot bring you back to normal. the craving is always there, it can just be suppressed a certain amount

160
Q

cravings are processed by:

A

orbitofrontal cortex, anterior cingulate, and nucleus accumbens

161
Q

context (which will potentiate or reduce a craving) of craving is processed by

A

hippocampus, insula, central nucleus of amygdala, and bed nucleus of the stria terminalis

162
Q

cravings are modulated by the

A

DLPFC

163
Q

descartes theory on mental illness-

A

arises from separation of mind and body; treat spiritually

164
Q

freud theory on mental illness-

A

conflict between Id and Ego/superego; treat with psychoanalysis

165
Q

skinner theory on mental illness-

A

arises from maladaptive learned responses; treat by reinforcing positive behaviors and punishing negative behaviors

166
Q

major mental disorders include disorders of _____ and _____

A

mood and thought

167
Q

2 disorders of mood-

A

bipolar and depression

168
Q

2 disorders of thought-

A

schizophrenia and delusional paranoia

169
Q

6 personality disorders-

A

narcissism, paranoia, antisocial, psychopathic, borderline personality

170
Q

symptoms of anxiety disorders-

A

objective behaviors, subjective moods, biological symptoms, cognitive probs

171
Q

objective behaviors of anxiety-

A

nervousness; rapid breathing; motor restlessness; racing heart

172
Q

subjective moods of anxiety disorders-

A

terror, panic, fear of death, sense of depersonalization

173
Q

biological symptoms of anxiety disorders-

A

dizziness, trembling, sweating, dry mouth, hyperventilation due to sympathetic activation

174
Q

cognitive symptoms of anxiety disorders-

A

poor memory and concentration

175
Q

treatments for anxiety disorders-

A

benzodiazepines, SSRIs, CRH receptor antagonists

176
Q

therapeutic goal in treating anxiety is to inhibit

A

the amygdala

177
Q

amygdala receptor targeted by benzodiazepines to treat depression-

A

GABAa ionotropic receptor

178
Q

specific binding site targeted by anxiolytics on a GABAa receptor

A

alpha 2

179
Q

if drugs bind alpha 1 binding site on GABAa receptor, result is

A

sedation

180
Q

if drugs bind alpha 2 binding site on GABAa receptor, result is

A

reduce anxiety; anxiolytic

181
Q

if drugs bind alpha 2 binding site on GABAa receptor, result is

A

reduce anxiety; anxiolytic

182
Q

3 anxyolytic medications

A

diazepam, alprazolam, and lorazepam

183
Q

besides GABA receptor modulation, how can we treat anxiety?

A

SSRI’s. (low serotonin levels are associated with anxiety)

184
Q

besides GABA receptor modulation, how can we treat anxiety?

A

SSRI’s. (low serotonin levels are associated with anxiety)

185
Q

low levels of serotonin lead to enhanced glutamatergic activity in the _____ nucleus of the amygdala, leading to _______

A
  • lateral

- anxiety

186
Q

amygdala upregulates ______ nucleus, stimulating _____ release. The cascade that follows causes a ramped up production of _________. The excess cortisol has a negative feedback effect on the ________ and a positive feedback effect on the ________. However, the _______ inhibits the HPA, which means that the positive feedback is actually causing enhanced negative feedback on the HPA. This system should work just fine, but the problem is stress hormones (cortisol) kill _______ cells and ruin the negative feedback. Obviously destruction of the hippocampus will lead to memory problems. It will also lead to a loss of regulation of the stress response which is essentially a chronic stress/anxiety problem.

A

amygdala upregulates paraventricular nucleus, stimulating CRF release. The cascade that follows causes a ramped up production of glucocorticoids. The excess cortisol has a negative feedback effect on the HPA and a positive feedback effect on the hippocampus. However, the hippocampus inhibits the HPA, which means that the positive feedback is actually causing enhanced negative feedback on the HPA. This system should work just fine, but the problem is stress hormones (cortisol) kill hippocampus cells and ruin the negative feedback. Obviously destruction of the hippocampus will lead to memory problems. It will also lead to a loss of regulation of the stress response which is essentially a chronic stress/anxiety problem.

187
Q

amygdala upregulates ______ nucleus, stimulating _____ release. The cascade that follows causes a ramped up production of _________. The excess cortisol has a negative feedback effect on the ________ and a positive feedback effect on the ________. However, the _______ inhibits the HPA, which means that the positive feedback is actually causing enhanced negative feedback on the HPA. This system should work just fine, but the problem is stress hormones (cortisol) kill _______ cells and ruin the negative feedback. Obviously destruction of the hippocampus will lead to memory problems. It will also lead to a loss of regulation of the stress response which is essentially a chronic stress/anxiety problem.

A

amygdala upregulates paraventricular nucleus, stimulating CRF release. The cascade that follows causes a ramped up production of glucocorticoids. The excess cortisol has a negative feedback effect on the HPA and a positive feedback effect on the hippocampus. However, the hippocampus inhibits the HPA, which means that the positive feedback is actually causing enhanced negative feedback on the HPA. This system should work just fine, but the problem is stress hormones (cortisol) kill hippocampus cells and ruin the negative feedback. Obviously destruction of the hippocampus will lead to memory problems. It will also lead to a loss of regulation of the stress response which is essentially a chronic stress/anxiety problem.

188
Q

objective behaviors of depressive disorder

A

poverty of speech, tearfulness, paucity of movement, agitation, no eye contact

189
Q

subjective moods of depressive disorder-

A

hoplessness, low self esteem, guilt, suicidal thought, anxiety

190
Q

biological symptoms of depressive disorder-

A

fatigue, insomnia, loss of appetite, reduced libido, early morning rumination

191
Q

biological symptoms of depressive disorder-

A

fatigue, insomnia, loss of appetite, reduced libido, early morning rumination

192
Q

Most common primary care complaint after hypertension-

A

major depressive disorder

193
Q

4th highest cause of disability

A

major depressive disorder

194
Q

HPA axis is ______ in depression

A

elevated

195
Q

diffuse brainstem transmitter systems are involved in depression, including which 2 NT’s?

A

5-HT and NE

196
Q

anatomically, what brain portion is reduced in size in depression?

A

hippocampus

197
Q

in major depressive disorder, increases or decreases in cerebral blood flow are observed in what areas?

A

orbitofrontal cortex, anterior cingulate cortex, amygdala, medial thalamus, ventral striatum

198
Q

SSRI’s block _____

A

SERT

199
Q

What is the immediate effect of SSRI’s?

A

little change, it takes time to go into effect.

200
Q

NE projections form the _______ innervate the limbic system, which is implicated in the regulation of emotions

A

locus coeruleus

201
Q

NE projections form the _______ innervate the limbic system, which is implicated in the regulation of emotions

A

locus coeruleus

202
Q

the long term effects of SSRIs are down regulation of _______ and reduction of ______ receptors

A
  • 5HT autoreceptors

- 5HT2A postsynaptic receptors

203
Q

the binding of 5HT to autoreceptors causes

A

decrease in release of 5HT

204
Q

Even though the accumulation of 5HT in the synapse due to SSRI’s causes a decrease in 5HT receptors, why is net 5HT action still enhanced?

A

possibly an upregulation of release of 5HT

205
Q

How does ketamine treat depression?

A

it blocks NMDA receptors which leads to a glutamate accumulation that stimulates a ramp up on AMPA receptor production and use. This strengthens the synapse and enhances glutamate release

206
Q

anti depressants increase expression of ______ which causes synaptogenesis

A

brain derived neurotropic factor (BDNF)

207
Q

Depression is really not treated with immediate effects, it really comes down to _______

A

synaptic enhancement (which takes time)

208
Q

Stem cells are generated in the _______ zone within the _____ gyrus of the hippocampus

A
  • sub granular

- dentate gyrus

209
Q

the development of a mature granule cell neuron from a type 1 radial glia progenitor

A

radial glia progenitor (Type 1)–> transit amplifying progenitors (Type 2)–> neuroblasts (Type 3)–> newborn neuron–> immature neuron–> mature granule cell neuron

210
Q

antidepressants are thought to upregulate the maturation of stem cells in the ________. _________(3) are thought to down regulate this pathway.

A
  • granular cell layer of the dentate gyrus

- drugs, stress, and x-radiation

211
Q

a stressed hippocampus treated with fluoxetine demonstrated _________

A

increased neurogenesis or synaptogenesis from stem cells from the SGZ in the dentate gyrus in the hippocampus.

212
Q

stress enhances CRF, which reduces _______, leading to the reduction of hippocampal dendrites and neurogenesis

A

BDNF

213
Q

although a stressed hippocampus gets damaged, it also becomes primed to have a stronger response to _____

A

BDNF

214
Q

BDNF enhances survival by increasing sythesis of survival factors such as _____

A

bcl-2

215
Q

BDNF enhances survival by increasing sythesis of survival factors such as _____

A

bcl-2

216
Q

Post partum depression is due to a chain of events that is the exact opposite of _____

A

SSRI effects

217
Q

how does increased estrogen (like in pregnancy) cause increased 5HT?

A

it competes with tryptophan for binding sites on albumin, making more tryptophan available for conversion into 5HT

218
Q

Estrogen competitively inhibits _____ leading to higher levels of serotonin and catecholamines in the brain

A

MAO

219
Q

the effect of ketamine is essentially the same as _____

A

Long term potentiation

220
Q

Ketamine causes a glutamate burst, which leads to an increase in the insertion of ____ receptors on synapses and an increase in the release of ______

A
  • AMPA

- BDNF

221
Q

stress causes the internalization of ______ receptors

A

glutamate

222
Q

sadness is concentrated in:

A

anterior cingulate cortex subgenual area

223
Q

what area of the subgenual area sees an increase in activity during depression and is responsible for positive symptoms (loss of appetite, sleep problems, reduced libido)

A

Cg 25

224
Q

what area of the subgenual area sees a decrease in activity during depression and is responsible for negative symptoms (apathy, loss of attn.)

A

dFr 9 and 46

225
Q

what area is targeted by DBS?

A

sACCg25, which is the subgenual anterior cingulate gyrus area 25

226
Q

after DBS of sACCg25, what resulted?

A

increase in activity of dFr 9 and 46 with decreased activity in sACCg25. Correlates with improvement in depressed ppl. even though activity in dFr 9/46 increased

227
Q

objective behaviors of schizophrenia-

A

odd mannerisms, purposeless movements, talking to self as third person, auditory hallucinations

228
Q

subjective moods of schizphrenia

A

lack of emotional responsiveness, violent expressions, delusions, paranoia

229
Q

biological symptoms of schizophrenia-

A

auditory and verbal hallucinations, motor disturbances

230
Q

cognitive symptoms of schizophrenia-

A

disorganized language, abnormal train of thought, not goal directed

231
Q

Etiology of schizophenia:
onset-
gender preference-
% of pop.-

A
  • adolescent
  • male
  • .5-1%
232
Q

______ gene for COMT is implicated in schizophrenia

A

22q11

233
Q

damage to circuitry of 5 areas have been linked to schizophrenia-

A

dorsolateral prefrontal cortex, hippocampus, amygdala, nucleus accumbens, and mediodorsal nucleus of thalamus

234
Q

schizophrenia may be due to ______ regulation deficit

A

dopamine

235
Q

short term schizo. leads to a decrease in the volume of:

A

parietal and frontal lobes

236
Q

long term schizo leads to a decrease in the volume of:

A

superior temporal gyrus and DLPFC

237
Q

not only cortical volume but also _____ is lost in schizophrenia

A

neuron number

238
Q

not only cortical volume but also _____ is lost in schizophrenia

A

neuron number

239
Q

anti-psychotic drugs block ____ and _____

A

dopamine receptors and dopamine release

240
Q

schizophrenics have increased density of which dopamine receptors?

A

D1-4, particularly D2

241
Q

what does COMT do?

A

metabolizes dopamine via methylation

242
Q

mesolimbic dopaminergic system route and what it is associated with in schizo

A
  • VTA–>various portions of the cortex and ventral striatum including nucleus accumbens
  • associated with the positive symptoms of schizophrenia (hallucinations and delusions)
243
Q

mesocortical dopaminergic system route and what it is associated with in schizo

A
  • VTA–>wide areas of prefrontal cortex, particularly medial aspects of hemispherer
  • associated with negative symptoms (thought disorders and decreased emotional response)