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Y2S1 - Brain and Behaviour > Brain and Behaviour 1 > Flashcards

Brain and Behaviour 1 Flashcards

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1
Q

With regard to rats, define IC.

A

Isolated conditions

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2
Q

With regard to rats, define SC.

A

Social conditions

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3
Q

With regard to rats, define EC.

A

Enriched conditions

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4
Q

Define behave.

A

Act or function in a particular way

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5
Q

Define behaviour.

A

Response to a stimulus

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6
Q

Define behaviours.

A

What we see, we cannot see their motivation

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7
Q

Define motivate.

A

To give reason or inspiration for a course of action

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8
Q

Characterize an IC rat.

A

More aggressive, less motor activity, higher cortisol, higher body weight, smaller brains

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9
Q

Characterize an EC rat.

A

Friendly, more motor activity, cope with change better, thick cerebral cortex, increased synapse:neuron ratio

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10
Q

Describe an example of human IC/EC differences, and possible explanations.

A

US children in Vietnam, some returned to US, some remained. US children had higher DQ - could be cultural bias? Vietnam children has lower DQ - could be lower rate of maturation, possibly due to malnutrition?

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11
Q

What does cerebellum mean?

A

Little brain

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12
Q

What proportion of the brain is cerebellum?

A

11%

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13
Q

Proportionately, how many neurons are in the cerebellum compared to the brain?

A

More neurons than the rest of the brain put together

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14
Q

What inputs into the cerebellum (generally)?

A

Cerebral cortex, brain stem nuclei and sensory receptors

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15
Q

What does the cerebellum do?

A

Co-ordinates voluntary motor movement, balance, equilibrium and muscle tone

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16
Q

What does the cerebellum consist of?

A

Midline body and two lateral lobes separated by a deep cleft into which projects the falx cerebelli

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17
Q

Where is the cerebellum?

A

Occupies most of the posterior cranial fossa, resting on its floor, separated from the occipital lobe by transverse fissure and tentorium cerebelli

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18
Q

Describe the structure of the cerebellum.

A

3 layers - molecular, purkinje and granule (outer to inner)

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19
Q

Describe the inputs into the cerebellum.

A

Mossy fibred, via the middle peduncle, and climbing fibres, via the inferior peduncle

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20
Q

What is the main output of the cerebellum.

A

Purkinje cell axons from dentate to nucleus

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21
Q

What are the three peduncular connections from the cerebellum?

A

Superior link with nuclei in the midbrain, diecephalon and cerebrum; middle link with pons and midbrain; inferior link with nuclei in medulla as well as ascending and descending cerebellar tracts to/from the spinal cord

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22
Q

Where do climbing fibres to the cerebellum come from?

A

Olivocerebellar nuclei via the inferior cerebellar peduncle

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23
Q

What does the inferior cerebellar peduncle connect? What does this connection convey?

A

Medulla and cerebellum conveying muscle proprioception and vestibular inputs

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24
Q

Where do mossy fibres come from?

A

Pons and elsewhere via middle cerebellar peduncle

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25
Q

What does the middle peduncle connect? What information does this send?

A

Pons and cerebellum telling cerebellum of voluntary motor output

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26
Q

Where do most Purkinje cell axons go?

A

Dentate nucleus deep to cerebellar cortex (except from vermis)

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27
Q

Where do most Purkinje cell axons go after entering the cerebellum?

A

Superior cerebellar peduncle to decussate and pass to thalamus and red nucleus

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28
Q

What does the superior peduncle connect? Are connection mainly afferent or efferent?

A

Midbrain and cerebellum - efferent

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29
Q

What other cerebellar nuclei receive vermal Purkinje cell outputs?

A

Emboliform, globose, fastigial

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30
Q

What does cerebellar injury result in?

A

Movements that are slow and unco-ordinated

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31
Q

Damage to the cerebellum can lead to what?

A

Asynergia, dysmetria, adiadochokinesia, intention tremor, ataxic gait, hypotonia, ataxic dysarthria, nystagmus

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32
Q

Define asynergia.

A

Loss of co-ordination of motor movement

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33
Q

Define dysmetria.

A

Inability to judge distance and when to stop

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34
Q

Define adiadochokinesia.

A

Inability to perform rapid alternating movements

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35
Q

Define ataxic gait.

A

Staggering, wise based walking

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36
Q

Define hypotonia.

A

Weak muscles

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37
Q

Define ataxic dysarthria.

A

Slurred speech

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38
Q

Define nystagmus.

A

Abnormal eye movements

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39
Q

What are the effects of under nutrition on the adult body?

A

Significant reduction in body weight but less effect on the brain

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40
Q

What is the vulnerable period hypothesis?

A

Growing brains are much more vulnerable than adult brains to nutritional restriction

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41
Q

What does under nutrition during the period of rapid growth in the brain do?

A

Creates deficit, changing the relationships between features, and distortion

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42
Q

What does under nutrition do to cerebral growth? What effect does this have?

A

Reduces growth of axons and dendrites more than cell bodies, thus paradoxical increased in neuronal density

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43
Q

What are the two types of aggression?

A

Predatory - hunt for food; affective - posturing

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44
Q

What two things do all forms of aggression involve?

A

Motor system and ANS

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45
Q

Characterize a predatory aggression.

A

Relatively quiet; attacks to head and neck of prey; low levels of sympathetic activity

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46
Q

Characterize an affective aggression.

A

Noisy; unfocussed; high levels of sympathetic activity

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47
Q

What can simulate aggression?

A

Electrical stimulation of the amygdala

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48
Q

Where is the amygdala?

A

Sits in the medial part of the temporal lobe

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49
Q

What are the two main connections between the amygdala and hypothalamus?

A

Ventral amygdalofugal pathway and the stria terminalis

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50
Q

Describe the amygdala.

A

Almond shaped, consisting of 3 groups of nuclei - basolateral, corticomedial and central

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51
Q

What are the 3 groups of nuclei in the amygdala?

A

Basolateral, corticomedial and central

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52
Q

What can reduce aggression?

A

Bi-lateral lesions to the amygdala

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53
Q

What can reduce fear?

A

Bi-lateral lesions to the amygdala

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54
Q

What do bi-lateral lesions of the amygdala do?

A

Flattens emotion; reduces the ability to recognise facial expressions of emotion

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55
Q

What does the amygdala most respond to?

A

Faces showing fear more than any other emotion

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56
Q

When aspects of fear are learnt, what inputs into the amygdala?

A

Any stimulus is received by the inferior basolateral nuclei

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57
Q

When aspects of fear are learnt, what outputs from the amygdala?

A

Basolateral nuclei to the cerebral cortex carries emotion; central nucleus to PAG in the brainstem carries behaviour; central nucleus to hypothalamus carries any autonomic response

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58
Q

What other areas of the brain have been implicated in aggression?

A

Hypothalamus and PAG

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59
Q

What does PAG stand for?

A

Periaquaductal grey matter of the brainstem

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60
Q

What are the two connections from the hypothalamus to the mid-brain?

A

Medial forebrain bundle; lateral hypothalamus to ventral tegmentum

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61
Q

What kind of aggression is the hypothalamus associated with?

A

Predatory

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62
Q

What lesion to the hypothalamus can reduce aggression?

A

Dorsal longitudinal fasiculus from medial hypothalamus to PAG

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63
Q

What drug appears to have a role in the regulation of aggression?

A

Serotonin

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64
Q

What happens to aggression when serotonin synthesis is pharmaceutically blocked?

A

Increased levels of aggression

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65
Q

Why is the MRI safe?

A

Does not use ionising radiation like X-rays or CT scans

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66
Q

What does CT stand for?

A

Computed tomography

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67
Q

What particle does the MRI elicit a signal from?

A

Protons

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68
Q

Describe the MRI scanner.

A

Super cooled by liquid nitrogen, super-conducting coil; little resistance, little energy required

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69
Q

What does the scanner emit?

A

Powerful static magnetic field up to 9 tesla

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70
Q

In an MRI, which way do the protons naturally align?

A

Vertically

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71
Q

What is applied in an MRI to precess the protons?

A

Horizontal magnetic pulse applied at radio frequencies to make them wobble on their axes

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72
Q

What happens when a horizontal magnetic field is applied in an MRI?

A

All protons rotate horizontally in phase

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73
Q

What happens when a horizontal magentic field is disabled in an MRI?

A

Protons begin to de-phase from the horizontal position, leading to a loss of magnetisation

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74
Q

What is T2?

A

The time constant of the weaking field after a horizontal magnetic field has been disabled

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75
Q

What is the constant given to the time it takes for the weakening field in an MRI?

A

T2

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76
Q

What is T1?

A

The time it takes for the protons to re-align with the master field (vertically)

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77
Q

What is the constant given to the time it takes for protons to stand up in an MRI?

A

T1

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78
Q

What information is used to create the image in an MRI?

A

T1 and T2 graphs

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79
Q

What do T1 and T2 values depend on?

A

Surrounding matter - whether it causes de-phasing/realignment to happen quicker/slower; the different levels of brightness assigned

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80
Q

What is the theory behind fMRI?

A

Diameter of cerebellar arterioles slowly increases during cognitive applications, specific to task; deoxygenated blood is paramagnetic, oxygenated is not, thus deoxygentated blood can be detected

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81
Q

What possible reasons are there for increased blood flow to working areas of the brain?

A

Supply of nutrients/oxygen or to flush away metbolic by-products

82
Q

What is the BOLD signal?

A

Blood oxygenation level dependent signal

83
Q

What does the BOLD signal show?

A

Which part of the brain is active in almost anatomical detail

84
Q

What kind of blood is detectable in an MRI, and why?

A

Deoxygenated, because it is paramagnetic

85
Q

How is an fMRI image constructed?

A

Computer differentiates differences in magnetic field of blood, and displays image accordingly

86
Q

What programs are used to create fMRI images?

A

Statistical parametric mapping (Windows) or FSL (Apple)

87
Q

How does a computer map an fMRI image?

A

Calculates the probability that a voxel (small chunk) has a different BOLD signal than the next, using a t-test; each probability is assigned a colour, which is then overlaid on the anatomical MRI, mapping the activation

88
Q

What controversial about the nature of the BOLD signal?

A

Some think it has nothing to do with the nutrition to the brain; increased blood flow far exceeds requirements, so maybe it is a cooling system

89
Q

What is a voxel?

A

3D pixel of the brain

90
Q

What does SPM stand for?

A

Statistical parametric mapping

91
Q

What are the problems with fMRI?

A

Patterns of activation can vary in 10% of subjects performing the same task; applied to a standard template, the process can distort the image making it fuzzy

92
Q

What two things does controlling a muscle require?

A

Excitation and feedback

93
Q

What two anatomical features provide feedback from muscles?

A

Muscle spindle and Golgi tendon organ

94
Q

What three locations do muscle spindles give muscle length information?

A

Spinal cord - basic processing; cerebellum - 2nd level processing; ‘higher centres’ - such as the motor cortex

95
Q

What information does the muscle spindle feeback?

A

Length of muscle

96
Q

What information does the Golgi tendon organ feedback?

A

Tension and rate of change of tension of the muscle

97
Q

What shape are muscle spindles?

A

Fusiform

98
Q

Only under what circumstances are muscle spindle useful?

A

When they are under tension

99
Q

What are internal muscle spindle fibres called?

A

Intrafusal

100
Q

What are external muscle spindle fibres called?

A

Extrafusal

101
Q

What do extrafusal muscle spindle fibres do?

A

Relay the force of contraction to the brain

102
Q

What two types of intrafusal muscle spindle fibres exist?

A

Bag and nuclear chain

103
Q

Describe group Ia afferent muscle spindle axons.

A

Anulospiral, wrapped around the middle of both bag and nuclear chain intrafusal muscle fibres

104
Q

How do gorup Ia afferent muscle spindle axons relay information?

A

Pulling apart the coils initiates action potentials

105
Q

What is the appoximate conduction velocity of group Ia afferent muscle spindle axons?

A

240mph

106
Q

Describe group II afferent muscle spindle axons.

A

Flower spray terminal end, embedding in middle regions of bag fibres; have some anulospiral endings confined to nuclear chain fibres

107
Q

What kind of muscle spindle information do group Ia axons relay?

A

Dynamic phase of muscle stretch, i.e. as stretch is occuring

108
Q

What kind of muscle spindle information do group II axons relay?

A

Static phase of muscle stretch, i.e. its final length

109
Q

How does the muscle spindle maintain its tension?

A

When extrafusal fibres contract, gamma-motorneurones co-activate with alpha-motorneurones and spindle shortens in register with extrafusal fibres

110
Q

What are the two sub-types of bag muscle spindle fibres?

A

Dynamic and static

111
Q

What are the two sub-types of nuclear chain spindle fibres?

A

Long and short

112
Q

What class of motorneurones control spindle length?

A

Gamma motor neurones

113
Q

What is different about the muscle spindle contraction from the muscle contraction?

A

Muscle spindle contracts further to maintain its tension

114
Q

What increases gamma neuron activity?

A

Serotonin (5-HT)

115
Q

What decreases gamma neuron activity?

A

Noradrenaline

116
Q

What happens when gamma neurons receive 5-HT?

A

Stimulation - intrafusal fibres become more stiff and more information is conveyed

117
Q

What happens when gamma neurons receive noradrenaline?

A

Inhibtion - intrafusal fibres become more elastic and less information is conveyed

118
Q

What is unique about the tendon jerk reflex?

A

The only monosynpatic reflex in the body

119
Q

Describe the physiological steps in the tendon jerk reflex response.

A

Muscle stretched by hammer blow to its tendon; group Ia neurons fired to spine; synapses directly with alpha afferents of homonymous muscle; muscle contracts to counter stretch

120
Q

Describe the Jendrassik’s manoeuvre.

A

Patient pulls arms against each other or clenches their jaw together

121
Q

What does the Jendrassik’s manoeuvre cause?

A

Excitation in upper segments of the spinal cord - C5 - which spills over to the rest of the spinal cord

122
Q

What happens to alpha-motorneurons following the Jendrassik’s manoeuvre?

A

Brought slightly toward threshold and is more excitable

123
Q

What name is given by medics to the effect Jendrassik’s manoeuvre creates?

A

Facilitation

124
Q

Why is Jendrassik’s manoeuvre useful in a clinical setting?

A

Useful for people with lesser reflexes

125
Q

What famous scientist is often referred to as the Father of neuroscience?

A

Sherrington

126
Q

What new and novel model did Sherrington use to study the stretch reflex?

A

Decerebrate cat

127
Q

What was surgically done to a cat to make it decerebrate?

A

Surgical transection at level of midbrain, between the superior and inferior colliculi

128
Q

What three connections does a spindle Ia neuron make?

A

Excitatory to homonymous muscle; excitatory to synergistic muscle; inhibitory to antagonistic muscle

129
Q

What is a homonymous muscle?

A

The same muscle a neuron has left, i.e. Ia neurons often feedback to the same muscle they relay information

130
Q

What is another name for the somatosensory system?

A

Dorsal column medial lemniscal system

131
Q

How many synaptic relays are in the main somatosensory pathway?

A

Three

132
Q

Where are the three main synapses in the somatosensory pathway?

A

Gracile and cuneate nuclei in the lower medulla; ventral posterior lateral nucleus of the thalamus; primary somatosensory cortex

133
Q

Describe the main somatosensory pathway.

A

Entry into the spinal cord at the dorsal root ganglion, at the gracile and cuneate fascicle; ascension into lower medulla, with synaptic connection to the gracile and cuneate nuclei; decussation and ascension through medial lemniscus in upper medulla, pons and then midbrain; ascension into thalamus and synaptic connection with ventral posterior lateral nucleus; projection and synaptic connection to postcentral gyrus (somatic sensory cortex)

134
Q

How many somatosensory corteces are ther?

A

Two - primary and secondary

135
Q

Where are the somatosensory corteces?

A

Anterior parietal lobe and posterior parietal cortex

136
Q

Which sulcus is the secondary somatosensory cortex in?

A

Deep in the lateral sulcus

137
Q

What does lesioning of the primary somatosensory sulcus produce?

A

Proprioceptive deficits, inability to discriminate size, texture and shape of objects

138
Q

How many regions is the primary somatosensory cortex divided into?

A

Four

139
Q

What is the name given to the four somatosensory cortex divisions?

A

Cytoarchitectonic regions

140
Q

What is the incidence of schizophrenia?

A

1%

141
Q

What is the gender incidence of schizophrenia?

A

Men slighly more than women

142
Q

What are ‘prodromal signs’?

A

Preceding signs of schizophrenia

143
Q

List the positive signs of prodromal signs

A

Social isolation and withdrawal, impairment in normal fulfilment of expected roles, odd behaviours and ideas, neglect of personal hygeine, blunted affect

144
Q

What follows prodromal signs in schizophrenic patients?

A

Positive signs - presence of distinctively abnormal behaviours

145
Q

List the positive signs of schizophrenia

A

Loss of reality testing, memory disturbances, delusions, hallucinations, odd posture

146
Q

Schizophrenic episodes can be seperated by what?

A

Period where the patient isn’t overtly psychotic, but displays negative signs

147
Q

What are negative signs in schizophrenic patients?

A

Absence of normal social and interpersonal behaviours

148
Q

List negative signs of schizophrenia

A

Exccentric, socially isolated, low levels of emotional arousal, impoverished social drive, poverty of speech, poor attention span, lack of motivation

149
Q

What is the modern diagnostic criteria for schizophrenia?

A

Continuous illnes for 6 months with at least one psychotic episode that must include one or more of delusions/prominent/disorderered thoughts

150
Q

What three categories can schizophrenia be split into?

A

Paranoid, disorganised and catatonic

151
Q

Characterise paranoid schizophrenia.

A

Usually men, systematic delusions of persecution predominate

152
Q

Characterise disorganised schizophrenia.

A

Early onset, wide range of symptoms, profound deterioration of personality

153
Q

Characterise catatonic schizophrenia.

A

Rare form - mutism, abnormal posture predominates

154
Q

What is the monozygotic incidence of schizophrenia?

A

45%

155
Q

What is the dizygotic incidence of schizophrenia?

A

15%

156
Q

What is the incidence of schizophrenia amongst parents, children and siblings of sufferers?

A

15%

157
Q

What anatomical abnormalities characterise schizophrenia?

A

Reduced blood flow to globus pallidus, reduced increase in blood flow to working memory lobes, thinner medial temporal lobe, smaller anterior hippocampus, lateral and third ventricles enlarged

158
Q

Outline the two step model of schizophrenia.

A

Genetic predisposition with envirnomental activation

159
Q

What environmental factors are supposed to cause schizophrenic activation of genetic predisposition?

A

Developmental absnormality, viral infections, perinatal injury, lifestyle activities

160
Q

What developmental abnormality is implicated in schizophrenia?

A

Number of cells just below cortical layer VI in superficial white matter of prefrontal and temporal lobes has migrated 3mm or so deeper

161
Q

What is suggested as a trigger for schizophrenic developmental disturbances?

A

Exposure to influenze or premature switching off of genes involved in cell migration

162
Q

What is the name of drugs used to treat schizophrenia?

A

Antipsychotics

163
Q

What is the first choice of drug for schizophrenia?

A

Chlorpromazine

164
Q

What type of drug is chlorpromazine?

A

Antipsychotics

165
Q

What is chlorpromazine used to treat?

A

Schizophrenia

166
Q

What are the specific anti-psychotic actions of chlorpromazine?

A

Abolishes delusions/hallucinations and some types of disordered thinking

167
Q

What is the MOA of chlorpromazine?

A

Blockage of dopamine receptors

168
Q

What is the MOA of phenothiazines?

A

Blockage of D1/2

169
Q

What is the MOA of thioxanthenes?

A

Blockage of D1/2

170
Q

What is the MOA of butyrophenones?

A

Blockage of D1/2

171
Q

What is the MOA of clozapine?

A

Blockage of D2/3/4

172
Q

Where are D1 and D5 receptors mainly expressed?

A

Cortex and hippocampus

173
Q

Where are D2/3/4 receptors mainly expressed?

A

Caudate nucleus, putamen, nucleus and accumbens

174
Q

Where are D3/4 recetors mainly expressed?

A

Limbic system, cortex and weakly in basal ganglia

175
Q

What families of drugs are ‘typical’ antipsychotics?

A

Butyrophenones and thioxanthenes

176
Q

What type of antipsychotics are butyrophenones and thioxanthenes?

A

Typical antipsychotics

177
Q

Name three ‘atypical’ antipsychotics

A

Clozapine, risperidone, olanzipine

178
Q

What are the advantages of using ‘atypical’ antipsychotics?

A

Fewer side effects

179
Q

What are extrapyramidal effects also known as?

A

Side effects

180
Q

What are the three levels of motor control?

A

Highest level - primary motor cortex, middle level - brainstem, lowest level - spinal cord

181
Q

How does the primary motor cortex link into motor control?

A

Projects straight to spinal cord via corticospinal tract, regulates the motor tracts that originate in brainstem

182
Q

How does the brainstem link into motor control?

A

Lateral descending system controls distal limbs is important for goal orientated movements

183
Q

How does the spinal cord link into motor control?

A

Mediate reflexes, mostly polsynaptic synapses, some mono-synaptic

184
Q

How was Brodmann’s area 4 discovered?

A

Area of the brain where lowest intensity of stimulation elicited movement

185
Q

What is another name for the motor cortex?

A

Brodmann’s area 4

186
Q

Where is the primary motor cortex?

A

Located just before central sulcus, sometimes called the precentral gyrus to highlight its position

187
Q

What limbs have disproportionate representation in the primary motor cortex?

A

Fingers/hands/face have disproportionately large representation

188
Q

What is another name for the first motor cortex neurones?

A

Upper motor neurones

189
Q

What does UMN stand for?

A

Upper motor neurones

190
Q

What are UMN involved in?

A

Planning, initiating and directing movements

191
Q

What do UMN synapse with?

A

Lower motor neurones

192
Q

What does LMN stand for?

A

Lower motor neurones

193
Q

What are lower motor neurones otherwise known as?

A

Final common pathway

194
Q

What does the final common pathway innervate?

A

Muscles

195
Q

The primary motor cortex is hierarchical, but what happens if you artificially stimulate it?

A

Brain stem and spinal cord just twitch

196
Q

Why is direct stimulation not enough for hierarchical control of the motor system?

A

Other structures required to co-ordinate movement

197
Q

What other structures are required to co-ordinate movement?

A

Basal ganglia and cerebellum

198
Q

How do the ganglia and cerebellum help co-ordinate movement?

A

Receive information from many other cortical inputs through thalamus and they monitor the situation the person is in; if inappropriate signals are sent, they correct and submit to the PMC for approval before muscle override

199
Q

What does PMC stand for?

A

Primary motor cortex

200
Q

What does the basal ganglia comprise?

A

Caudate, putamen, substantia nigra, subthalamic nuclei

Y2S1 - Brain and Behaviour (4 decks)

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