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neuroscience > brain function and malfunction > Flashcards

brain function and malfunction Flashcards

1
Q

hippocampal sub regions

A

cornu ammonis (CA1-CA3)
dentate gyrus
subiculum

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2
Q

the two different hypotheses for hippocampus and memory

A

1 - Immediate storage of incoming information,
Temporary memory buffer ‘consolidating’ information before sent to cortex

2 - Long-term memory storage in hippocampal formation

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3
Q

two different forms of long term memory

A

declarative or implicit (non declarative)

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4
Q

declarative memory includes

A

episodic (events) or semantic (facts)

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5
Q

implicit (non declarative) memory includes

A

priming, habits, skills, implicit emotions

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6
Q

episodic memory relies on

A

the hippocampus and associated structures

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7
Q

does semantic memory rely on the hippocampus?

A

no

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8
Q

common factors behind neurodegeneration

A 
genes and  environment 
Age
Protein misfolding & aggregation
Oxidative stress & calcium dis-homeostasis
Inflammation	
Loss of trophic factors
 Neuronal death
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9
Q

risk of dementia >85 years

A

50% per year

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10
Q

AD effects what percentage of the pop.

A

10%

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11
Q

end stage AD pathology

A

β-Amyloid (βA) plaques

Tau tangles

Enlarged ventricles

Inflammation

Tissue loss (atrophy), particularly cortical

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12
Q

tau based staging method for AD

A

Tau-based Braak Staging

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13
Q

Tau-based Braak Staging 5-6

A

Severe AD

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14
Q

Mild cognitive impairment Braak staging

A

2-3

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15
Q

other than braak post mortem staging for AD?

A

The ABC score

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16
Q

The ABC score consists of

A

Composite of the Thal stage (Amyloid deposition),
Braak stage of neurofibrillary tangles (NFTs / Tau),
and the CERAD neuritic plaque score (C).

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17
Q

AD dominant inheritance percentage of cases

A

1%

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18
Q

AD complex inheritance percentage of cases

A

4%

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19
Q

amyloid genetic links are

A

Mutations in APP (chr. 21), Presenilin 1 + 2 (chr. 14 and 1)

Trisomie 21 [Down‘s syndrome]

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20
Q

risk genes for AD are associated with

A

Amyloid production, transport & clearance

Inflammation

Metabolic function

Cytoskeletal function

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21
Q

which APOE allele increases risk of AD

A

allele ε4 of ApoE (chr. 19

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22
Q

homozygous E4 increases risk of AD by

A

14.9x

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23
Q

cholinergic hypothesis of Ad is

A

Reduced levels of ChAT (synthesis of ACh)

Loss of cholinergic neurones, especially in nucleus basalis of Meynert

Affected target areas of projections: hippocampus and cortex

Currently the only symptomatic treatment target

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24
Q

overall AD pathogenesis is

A

is a diverse and multi-factorial disease with multiple potential initial inducers

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25
Q

AD diagnosis

A

General Physical Examination
Cognitive testing

Brain Imaging
EEG
Genetics
Blood & CSF biomarkers

Post-mortem confirmation

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26
Q

stage 1 AD

A

Occurs in first 3 years. Short term memory, mild amnesia, forgetting conversations

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27
Q

stage 2 AD

A

10 years. Difficulty with speech, forgetting basic tasks (eating, sleeping etc). Emotionally unstable

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28
Q

stage 3 AD

A

8 – 12 years. All intellectual functions decline. Personality loss. Eventually almost vegetative state.

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29
Q

benefits of using EEG in Ad diagnosis

A 
EEG can measure brain activity and function in ‘real time’
Non-invasive
Inexpensive
Versatile
Fast & simple
Applicable to humans and rodents
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30
Q

limitations of using Fast Fourier Transformation (FFT) for EEG analysis

A

Result is heavily contaminated by “noise” and artefacts.

Destroys information about time.

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31
Q

benefits of using newer Auto-regressive Spectral Estimation for EEG analysis

(AR-spec)

A

Data based modelling approach.
Reconstructs a power spectrum free from chaotic activity (noise).
Preserves information about time.

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32
Q

resting EEG in AD demonstrates

A

reduced higher freq. power

increased low freq. power./

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33
Q

reduced higher freq. power in AD infers

A

Beta-Gamma) changes occur early in the disease.

Beta + Gamma are features of engaged brain networks

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34
Q

increased low freq. power. in AD infers

A

(delta) waves are an indication of the brain at rest,

ie not engaging with cognitive processes

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35
Q

cerebral cortex for movement neurotransmitters

A

glutamate/aspartate

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36
Q

SNc/VTA to striatum neurotransmitters for movement

A

dopamine

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37
Q

striatum to GPi/SNr neurotransmitters for movement

A

GABA

substance P

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38
Q

striatum to GPe neurotransmitters for movement

A

GABA

enkephalin

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39
Q

GPe to STN neurotransmitters for movement

A

GABA

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40
Q

STN to GPi/SNr neurotransmitters for movement

A

glutamate

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41
Q

GPi/SNr neurotransmitter for movement to thalamus

A

GABA

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42
Q

thalamus to cortex neurotransmitter for movement

A

glutamate

aspartate

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43
Q

Direct pathway steps

A

cortex->striatum (SNc/VTA influences striatum too) -> GPi/SNr->thalamus

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44
Q

indirect pathway steps

A

cortex->striatum->Gpe->STN-GPi/SNr->thalamus

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45
Q

how are the various motor system organised?

A

into loops

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46
Q

some examples of the loop organisations in the cortex?

A

motor, oculomotor, prefrontal and limbic

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47
Q

common stages in the cortex loops

A

input->striatum->output->thalamus

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48
Q

common link with the thalamus for each loop

A

always feeds back to the input

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49
Q

striatal anatomy: limbic and association centres feed into

A

striosomes

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50
Q

associations centres, somatosensory and motor layers feed into

A

matrix

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51
Q

striatal direct pathways ultimately causes

A

action selection

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52
Q

striatal indirect pathway ultimately causes

A

action suppression

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53
Q

striatal anatomy: medium spiny neurones are often found in the

A

striosomes

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54
Q

striatal interneurons consist of

A

cholinergic interneurons

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55
Q

the thalamus relationship with the cortex is

A

excitatory (glutamate)

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56
Q

Gpi +SNr relationship with the thalamus is

A

inhibitory (GABA)

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57
Q

motor cortex relationship with putamen is

A

excitatory (glutamate)

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58
Q

putamen relationship with Gpi Snr is

A

inhibitory (GABA)

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59
Q

sub nuclei direct pathway consists of

A
  1. thalamus (+)
  2. motor cortex (+)
  3. putamen (-)
  4. Gpi/Snr (x)
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60
Q

putamen relationship with GPe

A

inhibitory (GABA)

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61
Q

GPe relationship with subthalamic nucleus

A

inhibitory (GABA)

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62
Q

subthalamic nucleus relationship with Gpi-SNr

A

excitatory (glutamate)

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63
Q

sub nuclei indirect pathway consists of

A
  1. thalamus (+)
  2. motor cortex (+)
  3. putamen (-)
  4. GPe (x)
  5. subthalamic nucleus (+)
  6. Gpi/Snr (-)
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64
Q

normally the subthalamic nucleus would be

A

inhibited preventing it from stimulating Gpi/SNr

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65
Q

the reward pathway for the subnuclei is

A

pre-frontal cortex->SNc->putamen via D2/D1

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66
Q

Snc communicates with putamen via

A

dopamine D1/D2

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67
Q

D2 receptor in the putamen stimulates

A

indirect pathway

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68
Q

D1 receptor in the putamen stimulates

A

direct pathway

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69
Q

symptoms of parkinsons

A 
Characterised by hypokinesia
Cardinal features  include: 
Tremor
Rigidity
Bradykinesia (slow movement)
Akinesia (slow initiation)
Postural Instability
loss of facial expression and hypophonia (soft speech)
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70
Q

how long does parkinsons take to progress

A

15-20 years

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71
Q

other symptoms of parkinsons include

A

depression, dementia , attention impairments and autonomic dysfunction

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72
Q

diagnosis of parkinsons requires

A

bradykinesia + 1 one the following:

muscular rigidity
4-6hz tremor
postural instability not caused by other organic means

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73
Q

pathological hallmark of parkinsons is

A

loss of the dopaminergic neurones in the substantia nigra pars compacta (SNc)

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74
Q

what level of depletion of he dopaminergic neurones in the substantia nigra pars compacta (SNc) is necessary?

A

80%

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75
Q

pathological criteria for diagnosis of Parkinson

A

α-synuclein protein aggregates: Lewy Bodies

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76
Q

parkin mutation impairs specifically

A

“Ubiquitin-proteasome system”

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77
Q

gene mutations for parkinsons accounts for

A

5%

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78
Q

risk factors for PD include

A 
pesticides 
well water, farming, rural
manganese, copper, 
encephalitis lethargica 
flu
head injury
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79
Q

symptomatic treatment for parkinsons

A 
Levodopa
 Dopamine agonists, e.g. bromocriptine
 MAO-B inhibitors, e.g. selegiline
 COMT inhibitors, e.g. entacapone
 Anticholinergics, e.g. benztropine
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80
Q

symptoms of Huntington’s

A

Hyperkinesia – abnormal and exaggerated movement, rapid and uncontrollable

Progresses to rigidity and bradykinesia

Difficulty with speech and swallowing, leading to weight loss

Slowed eye movement

Depression, anxiety, psychosis, progressive dementia, altered personality

Death after 10-15 years of onset

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81
Q

cause of Huntington’s

A

Autosomal dominant disorder, gene defect on chromosome 4, codes for glutamine in huntingtin protein

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82
Q

specific Huntington’s mutation

A

over repetition
of CAG trinucleotide coding
sequence

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83
Q

adult Parkinson’s cases usually involve how many repeats?

A

36-50

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84
Q

Parkinson’s pathophysiology

A

Brain volume decreases as disease progresses
Caudate nuclei and putamen decrease
Ventricular space increases

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85
Q

supportive tx for Huntington’s includes

A 
Anticonvulsants (Valproic acid)
Dopamine antagonists (Chlorpromazine)
GABA agonists (Baclofen)
Antipsychotics (Risperidone)
Antidepressants (Tricyclic, SSRI’s)
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86
Q

role of the cerebellum in motor control is

A

sensory coordination of ongoing movements and modulation

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87
Q

does the cerebellum initiate movement?

A

no - bar nystagmus

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88
Q

cerebellum inputs includes

A 
position and state of muscle, joints and muscle tone (proprioception)  		
				- spinocerebellar tract-
equilibrium state of the body 
					-vestibulocerebellar tract-
‘orders’ sent from cerebral cortex 
					-corticopontocerebellar tract-
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89
Q

cerebellar cortex is divided based on

A

source of input

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90
Q

cerebrocerebellum receives input from

A

cortex

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91
Q

cerebrocerebellum role

A

highly skilled spatial and temporal movement sequences

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92
Q

spinocerebellum inputs

A

spinal cord

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93
Q

how is the spinocerebellum mapped?

A

somatopically

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94
Q

vestibulocerebellum input?

A

vestibular nuclei

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95
Q

vestibulocerebellum role

A

regulation of movements underlying posture + reflexes

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96
Q

mossy fibres connect to

A

parallel fibres

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97
Q

parallel fibres connect to

A

purkinje cells (glutamate) and basket/stellate cells)

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98
Q

one climbing fibre connects to one

A

purkinje cell (glutmate)

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99
Q

purkinje cells in the cerebellum connect to

A

deep nuclei nuclear cells (glutumate)

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100
Q

basket/stellate cells role

A

inhibit (GABA) purkinje fibres

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101
Q

sensory cortex feedback to the cerebellum arrives via

A

sensory cortex->inferior olive->cerebellum

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102
Q

motor action information is arrives to the cerebellum via

A

motor cortex->pontine nucleus->cerebellum

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103
Q

theories of functions of the cerebellum

A

Comparator of signal
Damping of movement
Movement initiation (nystagmus)
Control of duration

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104
Q

cerebellar dysfunction entails

A

Asynergia (lack of co-ordination of movements)
Dysmetria (loss of movement accuracy)
Ataxia (unsteadiness of movement, disturbance in gait)
Nystagmus (oscillatory eye movements)

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105
Q

non-motor cerebellar functions

A

Motor learning (nictitating membrane reflex; rotarod test)

Cognition and language (dyslexia)

Cerebellar stimulation is beneficial for intractable epilepsy

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106
Q

Pascinian corpuscles

A

rapidly-adapting mechanoreceptors

respond to vibration or tickle

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107
Q

Pascinian corpuscles connect to

A

large myelinated axons

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108
Q

Pascinian corpuscles located in

A

subcutaneous tissue in palms of hands and soles of feet, joints, genitals and GIT

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109
Q

tonic receptors mean

A

slow adapting receptors that respond during stimulus duration

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110
Q

phasic receptors mean

A

rapidly adapt, fire when stimulus turns on and off

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111
Q

Meissner’s corpuscles

A

rapidly-adapting mechanoreceptors

  • respond to tapping
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112
Q

Meissner’s corpuscles located

A

subepidermal location in hands, feet, forearm, lips and tip of tongue

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113
Q

Merkel cells

A

slow-adapting mechanoreceptors

respond to skin indentation

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114
Q

Merkel cells associated with

A

whiskers

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115
Q

Merkel cells located in

A

basal layer of skin

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116
Q

Ruffini’s corpuscle

A

slowly-adapting, with tonic resting firing rate

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117
Q

Hair root nerve endings

A
  • rapidly adapting Aδ fibres

fire on hair displacement, not on hair release

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118
Q

Thermoreceptors located

A

throughout epidermis

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119
Q

Thermoreceptors- cold receptors fibres are

A

myelinated

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120
Q

thermoreceptors hot receptors fibres are

A

unmyelinated fibres

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121
Q

Thermoreceptors

tonic or phasic?

A
  • fire constantly and indefinitely

firing rate dependent on temperature

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122
Q

mechanoreceptor nociceptors fibres are

A

myelinated (Aδ) or unmyelinated (C) fibres

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123
Q

nociceptors located

A

all layers

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124
Q

mechanothermal nociceptors fibres are

A

unmyelinated (C) fibres

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125
Q

proprioceptors include

A

golgi tendon organs
Neuromuscular spindles
joint capsules
flexor reflex afferents

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126
Q

nociceptors enable

A

withdrawal reflex

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127
Q

golgi tendon organs enable

A

stretch reflex

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128
Q

Neuromuscular spindles enable

A

crossed extension reflex

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129
Q

Neuromuscular spindles

are

A

nerve endings encircle intrafusal muscle fibres

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130
Q

sweet stimuli receptor

A

T1R

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131
Q

bitter stimuli receptor

A

T2R

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132
Q

umami receptor

A

t-mGluR4

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133
Q

t-mGluR4 detects

A

glutamate

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134
Q

sodium salt and acid sensation receptor example

A

MDEG/ENaC

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135
Q

t-mGluR4, T2R, T1R are all

A

7-pass transmembrane receptors

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136
Q

types of taste bud

A

circumvallate, foliate, fungiform

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137
Q

variations in taste are due to

A

heterodimer variation between receptors binding or the amino acid sequence of the receptors or distribution of papillae and receptors

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138
Q

taste transduction involves

A

essentially depolarisation of the cell with intracellular calcium release and then neurotransmitter release.

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139
Q

why is taste linked to sensation and mood?

A

dynamic sensory processing in the brain

Cranial nerve innervate the pontine parabrachial nucleus and the nucleus of the solitary tract in the brainstem.

projections between gustatory cortex and orbitofrontal cortex via the thalamus.

There is also input to gustatory processing from somatosensory and visceral systems

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140
Q

Mechanism of odorant signal transduction

A

odorant receptors activation leads to G protein-mediated activation of adenylate cyclase, which catalyses cAMP production.

cAMP activates calcium channels leading to calcium and sodium influx and depolarisation.

The depolarisation is potentiated by calcium then activating chloride channels, which lets chloride ions out of the cell.

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141
Q

how is the odour code “sharpened”

A

convergence and lateral inhibition not only within the bulb but the cortex.

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142
Q

does competition exist between olfactory cells?

A

yes -After 60 days, the inactive channel-deficient neurons were eliminated unless all channels were inactive

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143
Q

osciles in order from external to internal

A

stapes->malleus->incus

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144
Q

sound transduction

A

cochlear fluid vibrations are transmitted to the basilar membrane.

Movement of the basilar membrane causes displacement of the organ of corti.

Movement of the hair cells due to the vibration of the basilar membrane causes the hair cell cilia to move relative to the tectorial membrane.

Displacement of the hair cells leads to increased or decreased firing of the auditory nerve endings, depending on the direction of movement of the cilia.

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145
Q

high pitch sounds vibrate the basilar membrane distally or proximally

A

proximally

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146
Q

low pitch sounds vibrate the basilar membrane distally or proximally

A

distally

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147
Q

do hair cells depolarise in the ear?

A

no, Instead, the influx of calcium leads to neurotransmitter release from vesicles at the presynaptic membrane. Once in the synapse the neurotransmitter is detected by postsynaptic receptors and a signal is transduced causing ion channels in the postsynaptic neuron to open and depolarise the cell, leading to the propagation of an action potential. The neurotransmitter vesicles in the hair cell are attached to an electron dense body called the synaptic ribbon, or synaptic body

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148
Q

vestibular anterior superior horn detects

A

movement of the head up and down, as done when nodding an affirmative response

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149
Q

vestibular lateral (or horizontal) horn detects

A

sideways shake of the head

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150
Q

vestibular posterior canal detects detects

A

tilting motion from side to side

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151
Q

cristae in the ampullae detect

A

rotation

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152
Q

maculaeare in the maculae detect

A

linear acceleration and head position

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153
Q

cristae in the ampullae detect rotation because

A

endolymph around the gelatinous cupula in a crista causes movement detected by the hair cells

Cells on one side of the head increase firing, while those on the other side decrease firing

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154
Q

maculaeare in the maculae detect linear acceleration and head position by

A

otolith crystals layered on top of the cupula move under gravity, thus triggering hair cells

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155
Q

for near vision the lens

A

round ups up due to the ciliary muscles contracting and pulling the suspensory ligaments

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156
Q

for distant vision the lens

A

ciliary muscles relax

and suspensory ligaments pull the lens into a flatter shape.

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157
Q

long-sightedness (hyperopia) requires

A

convex lens

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158
Q

short-sightedness (myopia) requires

A

concave lens

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159
Q

when light arrives a the retina…

A

it is detected by rods and cones, the photoreceptor cells at the rear of the retina. These are lined by a pigmented epithelium, which absorbs excess light. Activation of photoreceptors leads to release of pigment and depolarization of bipolar cells. These in turn activate retinal ganglion cells (RGCs), whose axons converge on the optic nerve head and exit the eye into the optic nerve.

160
Q

three types of cones are?

A

RGB

161
Q

retinal pigment activation elicits

A

a cGMP-mediated change in release of neurotransmitter and postsynaptic activation of bipolar cells. Convergence of the signal occurs due to many receptors synapsing onto bipolar cells, as well as lateral inhibition mediated by horizontal cells.

162
Q

outer segment of cones and rods contain

A

disks filled with rhodopsin

163
Q

in darkness rhodopsin is

A

inactive
cGMP high
ion channels open
tonic release of neurotransmitters to bipolar neurones

164
Q

in light rhodospin is

A

opsin decreases CGMP
closes sodium channels
hyperpolarises cell
neurotransmitter release decreased in proportion to light

165
Q

identification of shapes and edges are viable because

A

off centre and on centre visual fields that either excite or inhibit ganglion cells bases on whether light is shined on centre or surrounding

166
Q

precise positional cues for individual axons between RGCs for the retina and tectum is feasible because

A

Temporal axons, having more receptor, are inhibited from projecting deep into the tectum

Nasal axons, having progressively less receptor, project progressively further into the tectum

Complementary expression of ligands and receptors in the D-V axis provides a 3-D map

167
Q

retinal-tectum 3D map is dependent on

A

ephrin-A being increased in nasal retina and posterior tectum

EphA being increased in temporal retina and anterior tectum

168
Q

Scotomas mean

A

defects of central fields

169
Q

early onset schizophrenia tend to

A

have more disorganized features and worse prognosis for recovery and function preservation

170
Q

positive schizophrenic symptoms

A

delusion , hallucinations, catatonic behaviours

171
Q

Negative symptoms schizophrenic symptoms

A

Affective blunting, alogia, anhedonia, avolition, asociality

172
Q

other symptoms of schizophrenia

A

Cognitive symptoms
- Attention, episodic & working memory, processing speed

Disorganized symptoms – disorganized speech & behaviours

Affective symptoms – Depression, anxiety, anger, hostility, aggression

173
Q

delusion means

A

fixed, false beliefs that conflict with reality. Despite contrary evidence,
a person in a delusional state can’t let go of these convictions

174
Q

types of delusions

A

erotomanic, grandiose, persecutory, jealous

175
Q

types of hallucinations

A

auditory, visual, tactile, olfactory, gustatory

176
Q

Alogia means

A

decrease in verbal communication, poverty of content and speech, thought blocking

177
Q

Dx of schizophrenia

A

Two of following symptoms for most of 1 month :
-delusions, hallucinations, disorganizes speech, grossly disorganized or
catatonic behaviours,negative symptoms

organic symptoms ruled out

178
Q

dopamine hypothesis of schizophrenia

A

PET studies show increased levels D2 of receptors

Drugs which block dopamine reduce psychotic symptoms

179
Q

four dopamine pathways

A

Mesolimbic pathway
Mesocortical pathway
Nigrostriatal pathway
Tuberoinfundibular pathway

180
Q

Mesocortical pathway

is between

A

VTA to prefrontal cortex

Cognition and executive function

181
Q

Mesolimbic pathway

is between

A

VTA to the nucleus accumbens, amygdala and hippocampus

Regulation of emotional behaviour

182
Q

Mesocortical pathway is associated with what schizophrenic symptoms

A

Negative symptoms (hypodopaminergic):
Alogia
Affective flattening
Avolition

183
Q

mesolimbic pathway is associated with what schizophrenic symptoms

A 
Positive symptoms 
(hyperdopaminergic):
Delusions
Hallucinations 
Disorganised thought, speech, behaviour
184
Q

problems with treating a schizophrenic patient with D2 antagonist antipsychotics

A

also reduces signalling in the mesocortical pathway

185
Q

an example of a dopamine partial agonist

A

aripiprazole

186
Q

glutamate hypothesis of schizophrenia entails

A
  1. Hypofunction of NMDA receptors on GABAergic interneurons
  2. Diminished inhibitory influences on neuronal function
  3. Disinhibition of downstream glutamatergic activity
  4. Hyperstimulation of cortical neurons through non-NMDA receptor
  5. disinhibition of glutamatergic projections onto midrbain dopamine neurones
  6. increased glutamate release
  7. increased dopaminergic neuronal activation.
187
Q

when does schizophrenia usually arise

A

nearly always emerges in late adolescence or early adulthood, with a peak between the ages of 18 and 25, when the prefrontal cortex is still developing

188
Q

does schizophrenia have neurodevelopmental origins?

A

could include reduced elaboration of inhibitory pathways, and excessive pruning of excitatory pathways, leading to altered excitatory–inhibitory balance in the prefrontal cortex

189
Q

synaptic pruning is important for

A

is critical for maturation of the frontal cortex, which is involved in so-called executive functions such as planning and decision-making. It makes adolescence and early adulthood a highly sensitive period, during which people are more susceptible to various kinds of mental illness.

190
Q

post mortem schizophrenic brain tissue has implicated what cell?

A

activated Microglia: primary innate immune cells in the brain
in charge of synaptic pruning

191
Q

microbiome differences in schizophrenia

A

Patients with schizophrenia had greater abundance of lactic acid bacteria
There were differences in the metabolic pathways controlling glutamate and B12 transport (increased in schizophrenia) and carbohydrate and lipid metabolism (decreased in schizophrenia)

192
Q

does early onset schizophrenia have a stronger genetic component?

A

yes

193
Q

Dx of major depressive disorder

A

Sad mood or Loss of interest of pleasure (anhedonia)
Symptoms are present nearly every day, most of the day, for at least 2 weeks
Symptoms are distinct and more severe than a normative response to significant loss

+ 4 other symptoms

194
Q

other symptoms of major depressive disorder

A

Sleeping too much or too little
Psychomotor retardation or agitation
Poor appetite and weight loss, or increased appetite and weight gain
Loss of energy
Feelings of worthlessness or excessive guilt
Difficulty concentrating, thinking, or making decisions
Recurrent thoughts of death or suicide

195
Q

Tx of MDD

A

Selective serotonin reuptake inhibitors(SSRIs)

Serotonin-norepinephrine reuptake inhibitors(SNRIs):

Serotonin modulators

Tricyclic antidepressants(TCAs)

Monoamine oxidase inhibitors (MAOIs

atypicals

196
Q

SSRIs mechanism

A

Block the reuptake of serotonin, increasing serotonin concentrations in the synaptic cleft and postsynaptic neuronal activity

197
Q

SNRIs mechanism

A

inhibit the reuptake of both serotonin and norepinephrine

198
Q

TCAs mechanism

A

block the absorption of serotonin and norepinephrine into nerve cells, as well as another neurotransmitter known as acetylcholine

199
Q

MAOIs mechanism

A

One of the first classes of antidepressants developed ,

inhibits the action of an enzyme called monoamine oxidase, whose role it is to break down monoamines

200
Q

aetiology of major depressive disorder hypothesis

A

abnormality in neural circuit (Excitation inhibition imbalance) disturbs neurotransmitter system

Stress causes major changes in the GABAergic system in the prefrontal cortex
reduces levels of GABA, GABA receptors

homeostatic down regulation of glutamate receptors

thus consideration for ketamine treatment

201
Q

psychological Tx of major depressive disorder

A 
interpersonal psychotherapy
cognitive therapy
mindfulness 
behavioural activation 
couples therapy

ECT

202
Q

an example of a rare genetic variant for severe schizophrenia and depression

A

chromosomal translocation between chromosome 1 and chromosome 11 And they found a gene at the breakpoint on the chromosome 1 , and called disrupted in schizophrenia 1, DISC1

203
Q

dentate gyrus in the hippocampus can produce how many neurones a day?

A

1400

204
Q

DISC1 can impact

A

axonal targeting, cell positioning, GABA action switch, synaptic development and cell morphology

205
Q

the progression of cells involved in cortical development for mice

A 
Neuroepithelial cells
Radial Glial cells (RGCs)
Intermediate progenitor cells (IPCs)
Neurons
Astrocytes
Oligodendrocyte progenitor cells
206
Q

difference in morphology between human and mice brain aside from size

A

human brains are gyrencephalic whereas mouse brains are lissencephalic

207
Q

Neuroepithelial cells can selfrenew to generate more

neuroepithelial cells through what form of division

A

vertical

208
Q

Radial glial cells generate

neurons through

A

vertical
divisions and Notch signalling is involved in
the cell division.

209
Q

outer radial glial cells are made through

A

Radial glial cells generate outer
radial glial cells by undergoing a
horizontal division.

210
Q

outer radial glial cells propagate through

A

horizontal division

211
Q

layers of a developing cortex

A 
Marginal zone
Cortical Plate
Intermediate zone
Outer subventricular zone
Inner subventricular zone
Ventricular zone
212
Q

how does the cortex develop in terms of the cellular progression (outside in or inside out?)

A

inside out, new cells pass through layers to reach the external surface before settling

213
Q

difference between mouse brain and human brain in cellular content?

A

human brains contain (?more) outer radial glial cells compared to mice

214
Q

development of the dentate gyrus involves

A

Neural stem
cells at the dentate
neuroepithelium start to migrate
away during early development

The migrate in the dentate
migratory stream

They populate the subgranular
zone of the dentate gyrus and
remain there throughout life
while retaining the capacity to
generate neurons.
215
Q

in the developing dentate gyrus what is the main form of cellular division

A

the NSCs switch from vertical to horizontal

216
Q

the dentate gyrus is part of the

A

hippocampus

217
Q

the neural stem cells in the dentate gyrus are

A

radial glial like cells (RGLs) and are multipotent NSCs and usually quiescent

218
Q

the dentate gyrus forms part of what pathway

A

hippocampal tri-synaptic pathway

219
Q

dentate gyrus receives input from

A

Entorhinal cortex

220
Q

the new-born neurones of the dentate gyrus project to

A

send axons to CA3

of the hippocampus

221
Q

the new neurones of the dentate gyrus is essential for

A

are important for

learning and memory.

222
Q

what cells are the most important for human cortical development and upper layer expansion

A

Outer radial glial cells

223
Q

progression of cortical human development

A

Neuroepithelial cells
Radial Glial cells (RGCs)
Intermediate progenitor cells (IPCs) form:

Neurons
Astrocytes
Oligodendrocyte progenitor cells

224
Q

what factors are used to reprogram fibroblasts

A

the Yamanaka factors

225
Q

Outer and ventricular Radial Glial Cells marker

A

SOX2+

226
Q

Seckel syndrome inheritance

A

autosomal recessive

227
Q

Seckel syndrome causes

A

intellectual disability

Microcephaly

228
Q

Seckel syndrome mutation

A

CPAP

229
Q

neural stem cell marker

A

nestin

230
Q

Seckel syndrome study into cortex found

A

thinner ventricular zone

231
Q

seckel organoids also revealed what change in cell division

A

increased horizontal division

232
Q

CPAP mutation thus causes

A

long cilia, retarded cilia
disassembly
Thinner VZ
Disrupted division plane

233
Q

seckel syndrome primarily effects what cells then

A

radial glial cells

234
Q

zika virus spread

A 
Primarily spread by female
mosquitos.
• Can be passed on by sex and
blood transfusion and through
pregnancy.
235
Q

zika virus usually causes

A

Usually causes mild fever,

sometimes asymptomatic.

236
Q

rare risk with zika virus and pregnancy

A 
5%-14% give birth to children
with signs of congenital Zika
syndrome
• 4%-6% subset have children with
microcephaly.
237
Q

what cortical cells does zika virus infect

A

neural stem cells and not neurones which induces death and reduces proliferation

238
Q

zika ultimately causes what to happen to the cortical layers then?

A

reduced thickness of
the ventricular zone and neuronal
layer.

239
Q

zika virus then usually affects what cortical developmental cells then?

A

radial glial cells and outer radial glial cells

240
Q

SARS-CoV-2 infects what cerebral cells

A

Choroid plexus epithelial cells

241
Q

what mutation can be used to replicate macrocephaly in organoids

A

RAB39b–PI3K–mTOR

242
Q

what happens to the cortical layers in macrocephaly

A

Over proliferation of NPCs
• Thicker VZ
• leading to an increased overall size

243
Q

macrocephaly ultimately effects what cells

A

radial glial cells

244
Q

Miller Macrocephaly-Dieker -Syndrome causes

A

Lissencephaly

245
Q

Miller Macrocephaly-Dieker -Syndrome induces what change in the ventricular zone

A

increased apoptosis

246
Q

Miller-Dieker Syndrome then ultimately affects what cells

A

Neuroepithelial cells
Radial Glial cells (RGCs)
Outer Radial Glial cells (RGCs)

247
Q

what occurs in the dentate gyrus in AD

A

Patients suffering from
Alzheimer’s disease have
fewer newborn neurons

248
Q

seizures during development alter the dentate gyrus by

A

casing aberrant neurogenesis leading to the question of does inhibiting neurogenesis stop the seizure rusk

249
Q

classic pathology and natural history of spinal muscular atrophy

A

degeneration of lower, alpha motor neurones in the ventral horn with progressive denervation and atrophy ogf skeletal muscle proximally with eventual paralysis

250
Q

SMN in in relation to spinal muscular atrophy (SMA) refers to

A

survival motor neurone protein

251
Q

genetics of SMA are

A

autosomal recessive

252
Q

why does missing SMN not be fatal in humans

A

we have two copies (SM1/SM2)

253
Q

what is the issue with SMN2

A

single point mutations in exon 7 results in unstable protein production

254
Q

what are the classifications of SMA?

A

type 1 (severe) - type 4 (mild)

255
Q

severity of SMA is dependent on

A

milder SMA means more copies of SMN2 gene

256
Q

the classification of SMA focuses on

A

inability to gain function

257
Q

type 1 SMA maximum function

A

unable to sit

258
Q

most variable staging of SMA is

A

type 2

259
Q

type 2 SMA maximum function

A

sit, never walk

260
Q

type 4 SMA maximum function

A

walking during adulthood

261
Q

Do other species have multiple copies of SMA

A

no

262
Q

roles of SMN

A

role in RNA processing and splicing but this couldn’t be linked to disease severity

interacts with ribosomes altering their location and function

263
Q

what has recent data about SMA and ribosomes revealed

A

these are concentration dependent, vary in different tissues and at different stages of development, and act on specific disease-relevant pathways in neurons

264
Q

SMA axonal pathology at birth

A

Motor systems are normal at birth, pathology arises post-natally

265
Q

mechanisms and details of SMA axonal pathology

A

impaired axon-genesis and synaptic maintenance may be responsible

266
Q

is restoration of SMN to muscle alone sufficient to ameliorate disease?

A

no despite defects independent of denervation also present in the skeletal muscle

267
Q

non-muscular pathology of SMA

A

Cardiac arrhythmias and heart defects in patients

Digital and peripheral necrosis in artificially ventilated patients and drug treated mice

Independent vascular defects in skeletal muscle, spinal cord and retina

Now, bone, pancreas, liver, spleen and kidney are reported to be defective in SMA mouse models

268
Q

what therapies exist for SMA

A

gene therapy

HDAC inhibitors

269
Q

SMA gene therapy entails

A

self-complimentary adeno-associated viruses

270
Q

SMA gene therapy name

A

Zolgensma

271
Q

SMA gene therapy efficacy

A

mice lifespan from 13-250 days (controversial because of cost)

272
Q

Histone deacetylase inhibitors are

A

non-specific regulators of transcription

273
Q

Histone deacetylase inhibitors role in SMA is to

A

increases SMN2 promoter activity

274
Q

Histone deacetylase inhibitors efficacy in SMA

A

12-38 days is the best recorded outcome in treated severe mouse models

275
Q

ASO treatment in SMA refers too

A

antisense oligonucleotides

276
Q

antisense oligonucleotides role in SMA

A

bind to intronic splice silencers to promote inclusion of exon 7 in SMN2 transcripts, therefore generating increased amounts of full length functional SMN protein

277
Q

ASO efficacy in SMA

A

increase lifespan 10-248 days

278
Q

ASO most efficacious for SMA when delivered

A

pre-symptomatic, systemic administration

279
Q

Zolgensma is approved for

A

Approved for Type 1 and patients with ≤3 copies of SMN2 as a single dose therapy

280
Q

Risdiplam is a

A

Daily, liquid, orally-delivered SMN2 splice modifier

281
Q

an example of non SMN pathways in SMA

A

Ubiquitin-dependent pathways regulate neuromuscular pathologies in SMA

282
Q

is there any therapy for non SMN pathways in SMA

A

Therapy with quercetin can ameliorate neuromuscular symptoms

But: these more healthy mice do not live longer

283
Q

in hippocampus (learning and memory) each astrocyte defines a

A

unique 3-D spatial domain, with minimal peripheral overlap

284
Q

all synapses in a confined volume may be controlled / modulated by

A

one astrocyte

285
Q

how do astrocytes communicate with one another?

A

using waves of Ca2+

286
Q

can astrocytes signal in response to neurones AP

A

yes

287
Q

Astrocytes regulate synaptic transmission via

A

tripartite” synapses

288
Q

do astrocytes have neurotransmitter receptors?

A

yes

289
Q

astrocyte Ca2+ waves can release

A

neuromodulators: gliotransmitters such as glutamate, D-serine, ATP

290
Q

astrocytes can therefore locally regulate

A

neurotransmission and local blood flow

291
Q

Dendritic spines, synapses and astrocyte sheaths :

..…may ALL change shape

A

over minutes – coordinately

292
Q

astrocytes are coupled across the brain via

A

gap junctions

293
Q

CA2+ astrocytes signalling wave works through

A

Ca2+ dependent release of ATP and of glutamate

ATP spreads to neighbours - activates P2Y receptors and increases Ca2+ - spreads to more neighbours like ripples on a pond.

294
Q

in the hippocampus astrocyte Ca+ waves increase

A

glutamate release –

this helps sychronize firing of clusters of pyramidal neurons

295
Q

whisker stimulation, visual stimuli and running : all increase and is mediated by what in regards to astrocytes

A

Ca2+ in sensory cortex astrocytes - mediated by mGluR

296
Q

photoactivation of specific astrocyte in visual cortex causes Ca2+ waves AND

A

changes neuron-specific responsiveness to orientation preferences

changes the basal firing rate of specific neurons and somehow modifies neuronal orientation responsiveness
So - astrocytes alter integration of sensory information processing

297
Q

how could astrocytes produce higher order organization of information

A

astrocyte modulation of synapses + coupling of large domains of synapses, introduces a code above and beyond a binary, synapse specific coding

Astrocytes produce slower signals and carry large
amounts of information over long distances

298
Q

Astrocytes key roles in development

A

radial glial cells assist in laying down guidelines for neurone migration and become astrocytes

299
Q

how can astrocytes control synapse number?

A

Thrombospondin 1 and 2 are released by astrocytes and cause a three fold increase in synapse numbers

Antibodies to thrombospondins inhibit this

300
Q

what time frame does astrocytes best regulate synapse numbers

A

Time window of astrocyte release : high in brain postnatal week 1,
as synapses are forming and drops off by postnatal week 3

301
Q

Time window of astrocyte synapse regulation infers

A

astrocytes down regulate their own ability

to increase synapse numbers developmentally

302
Q

dendrites in contact with astrocytes have

A

a longer lifetime and are morphologically more mature

303
Q

how is dendritic maturation regulated by astrocytes

A

there is local activation of Ephrin A receptors on dendritic spines by astrocytic ephrin-A3 ligand

304
Q

astrocyte regulation of neurogenesis is by

A

infusion of ephrin B2 into the lateral ventricles causes an increase in stem cell proliferation in the SVZ

ephrin B2 on hippocampal astrocytes promotes differentiation of sub granular zone neural stem cells in adult mouse

305
Q

So activation of astrocyte CB1R by cannabinoids induces

A

LTD in hippocampus and impairs spatial working memory

306
Q

what happens when human astrocytes are grafted into mice

A

they stay bigger and cortex and hippocampus is colonized in 4 – 12 months.
Gap junction coupled, grafted human astrocyte Ca2+ waves are 3 x faster than mouse

mice with human astrocytes are much faster to learn maze and fear conditioning

307
Q

how may Fragile x pathology relate to astrocytes

A

mutation in gene FMR1

FMR protein lost

FMRP is an RNA binding protein that associates with polyribosomes

hippocampal neurons grown on FMR1 deficient astrocytes – have stunted dendritic arborisation, but are OK on WT astrocytes - so astrocytic involvement.

308
Q

how may Rett syndrome pathology relate to astrocytes

A

loss of transcriptional repressor methyl CpG binding protein 2 (MeCP2)

MeCP2 is present in neurons and astrocytes

hippocampal neurons cultured with conditioned medium or on astrocytes from MeCP2 deficient mice have stunted dendrites

309
Q

can Astrocyte calcium waves signal injury?

A

yes

310
Q

how does a propagating astrocyte calcium wave signal long range injury

A

Calcium waves in gap junction coupled astrocytes increase NSC division and migration
through notch signalling

311
Q

transcranial stimulation induced what in astrocytes?

A

induced large amplitude synchronous Ca2+ surges in astrocytes

thus Astrocytes may be involved in synaptic plasticity induced by tDCS

312
Q

Activation of target designer receptors

in hippocampal astrocytes caused:

A
  1. increased Ca2+ signals/waves
  2. increased transmitter release from CA1 neurones
  3. potentiated synaptic transmission at CA3 to CA1 synapses and LTP
313
Q

thus astrocyte activation in the hippocampus is associated with

A

improved memory

314
Q

neural tube arises from

A

dorsal ectoderm

315
Q

spinal cord embryologically formation

A

neural plate->neural fold->neural tube->spinal cord

316
Q

secondary neurulation involves

A

Tail bud cells condense and epithelialize then hollow out to form a secondary neural tube caudally- region of the coccyx and cauda equina

317
Q

primary neurulation occurs around

A

Primary neurulation

Days 22-26

318
Q

secondary neurulation occurs around

A

Secondary neurulation

Days 26-42

319
Q

dorsal root ganglia is formed by

A

After fusion, neural crest cells migrate away from the dorsal side of the neural tube to form the sensory neurons of the dorsal root ganglia (DRG).

320
Q

the three layers of the neural tube are

A

ventricular layer
mantle layer
marginal layer

321
Q

ventricular layer of the neural tube consists of

A

undifferentiated, proliferating cells, forms the lining of the central canal

322
Q

mantle layer of the neural tube consists of

A

differentiating neurons that will form the grey matter of the spinal cord

323
Q

marginal layer of the neural tube consists of

A

nerve fibres and will be the white matter

324
Q

dorsal portion of the neural tube is termed the

A

alar plate and forms the sensory area

325
Q

the ventral portion of the neural tube is termed the

A

basal plate and forms the motor area of the spinal cord.

326
Q

dura mater

A

tough outer membrane

327
Q

epidural space

A

protective pad of loose connective and adipose tissue

328
Q

arachnoid mater

A

middle layer of meninges

329
Q

subarachnoid space

A

between arachnoid and pia mater

330
Q

pia mater

A

attached to surfaces of brain and spinal cord

331
Q

order of the meninges

A 
dura mater 
 epidural space 
 arachnoid mater
subarachnoid space - 
pia mater
332
Q

impulse conduction via the cord occurs through

A

white matter

333
Q

reflex integration occurs via the

A

grey mater

334
Q

two spinal enlargements are

A

cervical C3-T2

lumbar T9-T12

335
Q

spinal nerve pairs

A

31

336
Q

4 nerve plexuses

A

cervical
brachial
lumbar
sacral

337
Q

central pattern generators can

A

can produce rhythmic network activity in the absence of external timing cues- without rhythmic sensory feedback or rhythmic activation by descending neurons

338
Q

central pattern generator (CPG) examples

A

stepping, scratching, swimming, flying, respiration

339
Q

Central pattern generators are coordinated by

A

coordinated via propriospinal neuron pathways (PNs)

340
Q

what could trigged a CPG?

A

spontaneous or triggered by stimulation (tactile, electrical, pharmacological)

341
Q

how can a CPG be refined?

A

dynamic interaction of supraspinal signals (motor cortex) and sensory feedback to the spinal network

342
Q

do we know the physical location of all CPG’s yet?

A

no

343
Q

neural tube defects

A

craniorachischisis. anencephaly, encephalocele, iniencephaly, spin bifida occulta, closed spinal dysraphism, meningocele, myelomeningocele

344
Q

craniorachischisis -

A

completely open spinal cord and brain

345
Q

anencephaly -

A

open brain and lack of skull vault

346
Q

iniencephaly -

A

occipital skull and spine defects with extreme retroflexion of the head

347
Q

encephalocele -

A

herniation of the meninges

348
Q

closed spinal dysraphism -

A

deficiency of at least two vertebral arches

349
Q

spina bifida prevention is with

A

Supplement maternal diet with folic acid, a naturally occurring, water soluble B vitamin (B9)

350
Q

what alternative preventative treatment for spina bifida for highly predisposed women exists>

A

Inositol

351
Q

traumatic causes of spinal injury

A

Hyperflexion: bending the spine forwards
Hyperextension: stretching the spine backwards
Rotation: twisting the spine sideways
Vertical/axial compression : squashing the spine.

352
Q

non-traumatic causes of spinal injury

A

cord compression
infection
cyst or tumour
lack of blood flow

353
Q

initial injury to the spine in trauma usually is

A

compression

354
Q

initial injury site of the spine is

A

central

355
Q

why is spinal trauma injury site usually central?

A

Greatest deformation of a gel inside a compressed tube is at centre

Forces at the centre produce a haemorrhage

Gray matter is more vascularized than white matter, so more vulnerable

A “rind” of white matter is spared at the periphery

356
Q

secondary spinal injury mechanics

A

cell death in grey matter
Wallerian degeneration in white matter
localised breakdown of nerve followed by “die back” of the distal portion- influx of calcium

357
Q

chronic cellular consequences of spinal injury

A

fibroglial” scar formation- invasion by
collagen-producing fibroblasts
Astrocytes- activated microglia
macrophages- cavities

358
Q

spinal microlesion description (cellular)

A

BBB minimally disrupted

astrocytes produces CSGS and KSPGs along injury

Axons cannot regenerate

macrophages invade

359
Q

contusive injury spinal description

A 
BBB disrupted but meninges intact
cavitation as epicentre 
altered astrocyte alignment 
Gradient astrocytic production of ASPGS and KSPGs 
penumbra 
macrophage invasion 
dystrophic axons
360
Q

large spinal stab injury description

A 
BBB disruption 
cavitation 
astrocyte alignment altered
CSPG and KSPG gradient 
fibroblasts invade and express SEMA3
macrophages invade and release inflammatory cytokines 
dysrohic neuones repelled by lesion
361
Q

C4 injury

A

quadriplegia

362
Q

C6 injury

A

partial paralysis of hand and arms as well as paralysis of lower body

363
Q

T6 injury

A

paraplegia below chest

364
Q

L1 injury

A

paralyses below waist

365
Q

ASIA A grade

A

complete

366
Q

Asia B

A

no motor function S-S5 and below

367
Q

ASIA C

A

motor function below injury have grade <3

368
Q

ASIA D

A

motor function above injury >3

369
Q

Asia E

A

normal

370
Q

complications of spinal cord injury

A

pressure sore
infection
spasticity
autonomic dysreflexia

371
Q

autonomic dysreflexia can cause

A

over activity of the autonomic nervous system causes a life threatening increase in blood pressure
mainly when injury is T5 or higher
caused by irritating stimulus below the level of SCI

372
Q

barriers to spinal cord injury recovery

A

Scar is non-permissive for regeneration

Spared cells in white matter are demyelinated

Retained remnants of degrading myelin prevent axonal growth

373
Q

why is a spinal scar Scar is non-permissive for regeneration

A

Fibroblasts and their matrix deflect growth
E.g. semaphorin-3A
Astrocytes provide chemical inhibitory signals
chondroitin sulphate proteoglycans (CSPGs), tenascin

374
Q

what Retained remnants of degrading myelin prevent axonal growth

A

Nogo-A, myelin-associated glycoprotein (MAG) etc can be retained for at least a year

375
Q

what limits non-neuronal lesion core/peripheral spinal neuronal regeneration

A

inadequate facilitators:
intrinsic growth potential
matrix support
chemoattractant

376
Q

spinal lesion compartments consist of

A

Lesion compartments
Non-neuronal core- residual inflammatory cells that remain after debris clearance
Astrocyte scar at periphery restricts inflammation
Spared but reactive neural tissue undergoing circuit reorganisation

377
Q

targets for SCI repair

A

1) Damaged nerves/support cells must survive or be replaced- prevent secondary injury
adult nerves don’t usually divide, so unlikely to get significant recovery without intervention
2) Surviving neurons must regrow axons, despite scar tissue and inhibitory molecules
3) Axons must migrate toward appropriate targets
4) Axons must form effective synapses
5) Target cells must be able to respond to neurotransmitters (no major muscle fibre loss)
6) Neural circuitry must compensate for changes in spinal cord circuitry following injury

378
Q

incomplete SCI treatment requires

A

Stimulate reorganisation of spared circuitry

379
Q

anatomically complete SCI requires

A

neuron grafts or stimulate regrowth across lesion

380
Q

does sciatic nerve bridges work?

A

peripheral nerves graft enable axonal growth but issue when entering a hostile CNS

381
Q

other acute injury treatments for SCI

A

Cooling injury site
Acute intermittent hypoxia
Methylprednisolone

382
Q

acute SCI cooling site injury risks

A

reduces swelling and necrosis due to hypoxia

but cause additional damage to cord- dangerous surgery for collar

383
Q

Acute intermittent hypoxia for SCI entails

A

1.5 min AIH, @ 1 min intervals, 15 x daily, 5 consecutive days
Improves walking inpatients with chronic SCI

384
Q

SCI Methylprednisolone must be administered within

A

8 hours

385
Q

for SCI is Methylprednisolone administered anymore?

A

no

386
Q

transplants and implants for SCI include

A

Foetal spinal cord transplants, alone or in combination with:
growth factors
anti-apoptotic agents
molecules that counteract inhibition by myelin-associated proteins (Nogo-A and MAG, CSPG’s)

polymer scaffolds (± stem cell seeding)

387
Q

other strategies for treating SCI include

A

modulate cAMP levels
stem cells
extracellular DC voltage gradients

388
Q

modulate cAMP levels for SCI involve

A

increased cAMP overcomes MAG inhibition of axon growth

improve regeneration in adults using drugs that elevate cAMP?

389
Q

what stem cell research was being conducted for SCI

A

oligodendrocyte precursors injected into lesion site- aimed to remyelinate axons

390
Q

extracellular DC voltage gradients for SCI involve

A 
electric fields (EFs) in developing and regenerating systems
neurons grow directionally in electric field in vitro
391
Q

EF with cathode distal to SCI lesion prevents

A

die back

392
Q

EF with cathode proximal to lesion enhances

A

die back

393
Q

Chronic electrical stimulation of motor cortex enhances

A

sprouting of spared corticospinal tracts

394
Q

some ideas as to why electrical stimulation encourages nerve growth

A

Induces action potentials in neurons
Calcium transients
via voltage gated channels
via mechanosensitive channels

Increases transcription of regeneration associated genes (RAGS)

395
Q

most improvement for a SCI occurs when?

A

6 months after trauma

396
Q

Electrotherapy plus physical therapy can

A

improve symptoms with return to bipedal locomotion with support but only during electrical stimulation

397
Q

why does Electrotherapy plus physical therapy work?

A

likely by stimulating central pattern generators

neuroscience (2 decks)

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