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PSHL231 Neurophysiology > Systems Neurophysiology > Flashcards

Systems Neurophysiology Flashcards

1
Q

What is the somatosensory system and what does it do?

A

The Somatosensory system is about bodily sensations.

It provides the brain with information about the state of the body, and about some aspects of the external environment.

This information is used to help guide behaviour and to maintain homeostatic function.

The brain also receives important sensory information from the special senses.

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2
Q

What are the three kinds of sensory receptors distributed throughout the body?

A

Exteroceptive receptors (respond to environmental sensations such as skin contact and temperature).

Proprioceptive receptors (give the brain information about body position).

Enteroceptive receptors (recognises internal organ status).

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3
Q

What are the four main features of a stimulus that somatosensory receptors can encode?

A

Modality
Intensity
Location
Duration

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4
Q

How does modality work?

A

Modality is about receptor specificity. Different stimulus are reported by different receptors and signalled separately to the brain.

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5
Q

How is intensity coded for in sensory information?

A

The frequency of action potentials firing and the number of activated axons in a sensory axon is dependant on the intensity/strength of a stimulus.

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6
Q

How is the location of a stimulus encoded?

A

Located on the post-central gyrus of the brain is the primary somatosensory cortex organisation. The somatotopic mapping of receptors in specific areas allows the location of the stimulus to be known.

(With the exception of referred pain).

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7
Q

How is the duration of stimulus encoded?

A

The beginning/end and pattern of action potentials firing can encode the start and end of a stimulus.

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8
Q

How does the brain know the difference between weak and strong stimulus?

A

Through a change in the frequency of action potentials.

The AP stay the same size no matter what the strength of the stimulus (as long as depolarisation it is over threshold) but the frequency changes dependant on the strength of stimulus.

Therefore with a big stimulus there is a high frequency of AP meaning more neurotransmitters being released.

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9
Q

What are the three somatosensory receptors in the skin and what are they receptive to?

A

Mechanoreceptors (touch and pressure)

Thermoreceptors (temperature)

Nociceptors (noxious stimuli such as pain)

(All types of exteroceptive sensory receptors).

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10
Q

What is glabrous skin?

A

Skin that has no hair.

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11
Q

What causes skin mechanoreceptors channels to open and close?

A

Mechanical deformation (all have mechanosenstive ion channels).

When skin is moved by applied pressure it opens channels. When pressure is removed the channels close again.

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12
Q

What are the five skin mechanoreceptors?

A

Meissner’s corpuscles
Pacinian corpuscles
Merkel’s discs
Ruffini endings
Hair units

(my precious mother really happy)

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13
Q

What are the features of meissner’s corpuscles?

A

Found mostly on glabrous skin.
Responsive to pressure.
Dyamic and rapidly adapting.
low threshold of activation,

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14
Q

What does it mean if a receptor is rapidly adapting?

A

Means they are responsive to change.

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15
Q

What does it mean if a receptor has static pressure?

A

Not responsive to change - opposite of rapidly adapting receptors.

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16
Q

What are the features of pacinian corpuscles?

A

Subcutaneous (all skin).
Responsive to deep pressure and vibration.
Dynamic and rapidly adapting.
Low threshold.
Interosseous (situation between bones)

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17
Q

What are the features of Merkel discs?

A

All skin
Static pressure
Convery information about shape and texture of objects
Slow adapting
Low threshold

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18
Q

What are the features of Ruffini endings?

A

All skin
Deep pressure and stretch
Slow adapting
Low threshold

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19
Q

What are the features of hair units?

A

Found on hairy skin
Responsive to hair displacement
Low threshold
Rapidly adapting

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20
Q

How are skin thermoreceptors and nociceptors typically classified?

A

By their type of axon: either myelinated or unmyleinated axons.

Thermoreceptors = myelinated

Nociceptors = unmyelination or very thinly myelinated axons

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21
Q

What are proprioceptors?

A

Mechanoreceptors in muscles and tendons.

They provide information relating to the position of the limbs in order to plan movements.

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22
Q

What receptors are crucial for stretch reflex?

A

Proprioceptors

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23
Q

What are enteroceptors?

A

Sensory receptors and afferent nerves associated with internal organs.

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24
Q

What are enteroceptors important for?

A

Homeostatic reflexes

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25
Q

What are chemoreceptors?

A

Sensory cells with receptors that respond to presence of a specific chemical

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26
Q

Where are central chemoreceptors and what do they respond to?

A

Located on surface of medulla.

Detect pH of cerebrospinal fluid.

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27
Q

What receptors are crucial in control of breathing?

A

Peripheral chemoreceptors

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28
Q

What do peripheral chemoreceptors detect?

A

Aortic and carotid bodies detect pCO2, H+ and O2 in blood

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29
Q

Where is the cell body of a sensory primary afferent neuron located?

A

Dorsal root ganglia or cranial nerve ganglia

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30
Q

What are the characteristics of sensory neuron receptive fields?

A

Determined by location of the neurons sensory apparatus.

Size of field relates to two-point-discrimination.

Size of receptive field may vary eg skin on shoulder vs fingertip.

Fingertips have smaller receptive fields which means they have greater discrimination of sensations - better are performing fine movements.

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31
Q

Why is the sensory map distorted?

A

because regions with high receptor density and small receptive field sizes occupy a disproportionately large area.

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32
Q

What does dorsal mean?

A

On the back

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33
Q

What does ventral mean?

A

Relating to the front part of the body

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34
Q

What do the ascending somatosensory pathways do?

A

Carrying sensory information from receptors around the body TO the somatosensory cortex in the brain.

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35
Q

What are the three ascending somatosensory pathways?

A

1) Dorsal Columns
2) Spinothalamic Tract
3) Spinocerebellar Tract

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36
Q

What is the ascending somatosensory pathway in the dorsal columns?

A

The pathway of information arriving in the brain from fine touch and vibration.

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37
Q

Where do neurons synapses and where does information cross the midline in the dorsal column ascending somatosensory pathway?

A

Axons enter dorsal roots and ascend in the spinal cord dorsal columns to synaptic contract on neuron’s in the medulla.

First synapse is in the gracile nucleus in the medulla.

It is in the medulla that neuron’s project across the midline.

After crossing the midline the neurons synapse in the thalamus with thalamic neurons. Thalamic neuron’s project to the somatosensory cortex.

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38
Q

What is the medial lemniscus?

A

The second neuron in the dorsal column pathway.

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39
Q

What is the effect of midline crossing of neurons?

A

It means that sensations are represented in the brain on the opposite side to the sensation.

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40
Q

Where do thalamic neurons project to?

A

Somatosensory cortex

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41
Q

What is the ascending somatosensory pathway in the spinothalamic tract?

A

The pathway of information arriving in the brain from pain, temperature and crude (non-discriminative) touch.

Spinothalamic refers to from the spinal cord to the thalamus.

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42
Q

Where are the synapses and midline crossing in the spinothalamic tract somatosensory pathway?

A

Axons from pain and temp fibres enter via dorsal root and synapse on neurons in the dorsal spinal cord.

Neurons project across the midline in the spinal cord and ascend to neurons in the thalamus.

Thalamic neurons project to somatosensory cortex and their nuclei involved in pain response.

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43
Q

What somatosensory pathway is in the dorsal horns?

A

Spinothalamic

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44
Q

What is the ascending somatosensory pathway in the spinocerebellar tract?

A

The pathway of information arriving in the cortex and cerebellum of the brain from proprioception e.g., information about limb position and movement.

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45
Q

What are the synapses of the spinocerebellar tract pathway and how many times do neurons cross the midline?

A

Axons from sensory neurons in legs and lower body synapse in spinal cord.

Axons from arms and upper body synapse on neurons in the medulla.

Secondary neurons send axons to cerebellum via three tracts: dorsal spinocerebellar tract, ventral spinocerebellar pathway and cuneocerebellar tract.

Neuron’s cross the midline twice so synapse on cortex same side as the sensation.

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46
Q

What is pain?

A

An unpleasant sensory and emotional experience associate with or resembling actual or potential tissue damage.

Pain is a sensation. It is the product of the brain processing a variety of neural signals.

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47
Q

What are the three main types of pain?

A

Acute, chronic, and intermittent

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48
Q

What is acute pain?

A

Pain that arises suddenly and has a specific cause - but is resolved quickly.

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49
Q

What is chronic pain?

A

Pain that is long term that persists long after the original stimulus has subsided.

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50
Q

What is intermittent pain?

A

Pain that comes and goes.

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51
Q

What are nociceptors and what activates them?

A

Pain receptors.

Activated by noxious stimuli.

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52
Q

What three purpose does pain serve?

A

Alerts us to injuries, diseases and infection

Helps prevent severe tissue damage

Promotes behaviours to minimise severity/duration of triggering event

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53
Q

What is CIPA?

A

A genetic defect that causes a loss of pain sensation due to not making nociceptors.

Therefore the brain has no mechanism to receive information from pains stimuli.

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54
Q

What causes CIPA?

A

Mutation in a gene that codes for a nerve growth factor receptor, resulting in developmental failure of a subset of sensory and autonomic nerves.

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55
Q

Where are nociceptors absent?

A

Brain

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56
Q

What are the three main classes of nociceptors and what are they activated by?

A

Thermal - high and low temperatures.

Mechanical - intense pressure.

Polymodal chemical stimuli - high intensity mechanical, thermal or chemical stimuli both internal and external.

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57
Q

Are thermo and mechnorecetpors myelinated?

A

They are thinly myelinated axons - this means they can signal acute onset.

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58
Q

Are polymodal receptors myelinated?

A

They are C fibres with unmyleinated axons - they signal ongoing slow full pain.

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59
Q

What somatosensory pathway is used for pain?

A

Spinothalamic

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60
Q

What is hyperalgesia?

A

Persistent or enhanced pain sensation.

Often due to inflammation and release of chemicals from damaged cites (where if you touched normally there would not be pain).

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61
Q

What is allodynia?

A

A type of hyperalgesia.

Pain in response to innocuous (harmless) sensory stimuli.

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62
Q

What is analgesia?

A

Selective suppression of pain without effects on consciousness e.g., the effect of pain relief.

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63
Q

What is the gate control model?

A

Theory that pain signalling can be gated by stimulation of non-pain sensory fibres from the same area.

The activation of non pain sensory fibres stimulates the inhibitory interneuron therefore making it harder for projection neurons to reach threshold and continue the transmission of pain to the brain.

In action when hurt thumb and you automatically go to hold it.

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64
Q

Where are inhibitory interneurons located?

A

Dorsal horn

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65
Q

What are endogenous opiates?

A

Analgesics made by our own bodies.

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66
Q

What are examples of endogenous opiates?

A

Endorphins
Enkephalins
Dynorphins

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67
Q

What cells is histamine released from?

A

Mast Cells

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68
Q

What are the two places that increased sensitisation (hyperalgesia) can be?

A

Peripheral site of injury or in the CNS

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69
Q

What does histamine do?

A

Activates nociceptors

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69
Q

What causes mast cells to release histamine?

A

Substance P

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70
Q

What are examples of voluntary movements?

A

Walking, eating, talking and mating.

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71
Q

What system is used for voluntary movements?

A

Somatic

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72
Q

What are the four basic neural systems involved in the control of movement?

A

Local spinal cord and brainstem circuits
Descending systems
Cerebellum
basal Nuclei

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73
Q

Where do motoneurons have their cell bodies?

A

Ventral horn of spinal cord

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74
Q

What does it mean if something is a ‘local circuit’?

A

Means that it doesn’t involved higher levels - everything is done within the spinal cord and brainstem.

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75
Q

What provides input to lower motor neurons?

A

sensory and local neurons

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76
Q

All somatic motor functions occur via what?

A

Action of motor neurons

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77
Q

What are Central Pattern Generators (CPGs)?

A

Biological neural circuits that produce rhythmic outputs in the absence of rhythmic input from higher centers.

They are the source of the tightly-coupled patterns of neural activity that drive rhythmic/repetitive and stereotyped motor behaviours like walking, swimming, breathing, or chewing.

They do not use higher levels but can be initiated and modulated by higher centres.

Occurs from a bursting activity of neurons and reciprocal inhibition.

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78
Q

What is reciprocal inhibition?

A

Reciprocal inhibition describes the relaxation of muscles on one side of a joint to accommodate contraction on the other side.

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79
Q

What is sensorimotor transformations?

A

The term ‘sensorimotor transformation’ refers to the process by which sensory stimuli are converted into motor commands.

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80
Q

Draw out the motor control hierarchy:

A

Highest level: Command neurons, including the sensorimotor cortex areas involved with memory, emotions and motivations.

Middle level: Sensorimotor complex, Basal nuclei, cerebellum, Brainsteam, thalamus.

Local level: brainstem and spinal cord interneurons, receptors, muscle fibers.

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81
Q

What does the basal nucleus do?

A

Modifies voluntary and reflexive motor patterns at the subconscious level.

Planning, initiating and monitoring of movments

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82
Q

What does the cerebral cortex do?

A

Plan and initiates voluntary motor activity

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83
Q

What does the hypothalamus do?

A

Controls reflex motor patterns related to eating, drinking and sexual activity: modifies respiratory reflexes.

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84
Q

What does the thalamus and midbrain do?

A

Control reflexes in response to visual and auditory stimuli

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85
Q

What does the cerebellum do?

A

Helps plan, execute and learn motor programs.

Integrates sensory info with planned events.

Organises timing of muscle contraction.

Compares planned movement with actual result, modifies ongoing activity to make movements smooth and accurate.

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86
Q

What does the brainstem and spinal cord do?

A

Control simple cranial and spinal reflexes

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87
Q

What does the pons and medulla oblongata do?

A

Control balance reflexes and more complex respiratory reflexes

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88
Q

What is the most complex area of the brain?

A

Cerebal cortex

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89
Q

What is the pathway of planning a movement within the brain?

A

Decision made in the frontal lobe, sent to premotor cortex, then to basal nuclei and cerebellum - basal nuclei adjusts patterns of movement and cerebellum monitors valance and equilibrium and adjusts upper motor neuron’s activity.

Basal nuclei sends information to primary motor cortex.

Then from Primary Motor Cortex the final pathway of sending information to lower motor neurons down the corticospinal pathway.

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90
Q

What is the two ways the basal nuclei can adjust patterns of movement?

A

(1) They alter the sensitivity of the pyramidal cells to adjust the output along the corticospinal tract.

(2) They change the excitatory or inhibitory output of the medial and lateral pathways.

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91
Q

Where is the primary motor cortex located?

A

On the pre-central gyrus.

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92
Q

What is the area devoted to muscle on the somatotpic organisation of the primary motor cortex related to?

A

The level of fine control and movement complexity.

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93
Q

What does the lateral corticospinal tract control?

A

Outputs from motor cortex controls the fine movements.

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94
Q

What is an interneuron compared to a motoneuron?

A

Motor neurons carry information from the CNS to PNS. Interneurons carry information between sensory and motor neurons in the CNS only.

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95
Q

Where are motoneurons for most limb muscles located?

A

Laterally in Spinal Cord Grey Matter

(grey matter is a group of cell bodies).

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96
Q

What does the ventral corticospinal tract control?

A

Output from motor cortex for coarse movements e.g., trunk neck and shoulders

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97
Q

Where do axons cross in the lateral corticospinal tract?

A

Axons reach the medulla ipsilaterally (on same side of body as muscle), then cross midline and descend as lateral CST.

98
Q

Where do axons cross in the ventral corticospinal tract?

A

They do not cross - they stay ipsilateral and descend in VCST.

99
Q

Where are motoneurons of the brainstem descending pathways located?

A

Medially in spinal cord grey matter

100
Q

What does the midbrain locomotor region interact with?

A

CPGs in Spinal Cord

101
Q

What does the midbrain locomotor region initiate?

A

Walking behaviour

102
Q

What does loss of cerebellar function result in and some specific examples?

A

Ataxia = Movements that are slow and uncoordinated.

Drucken gait, dysmetria, tremors, muscular weakness, slurred speech, abnormal eye movements.

103
Q

What is the medical name for muscle weakness?

A

Hypotonia

104
Q

What is the medical name for slurred speech?

A

Ataxic dysarthria

105
Q

What is the medical name for abnormal eye movements?

A

Nystagmus

106
Q

If your cerebellum is damaged on the right side where will the motor impairment be?

A

On the same side (right side) because the cerebellar pathways cross the midline twice.

107
Q

What are the 3 deep cerebral nuclei that form the basal nuclei?

A

Caudate nucleus
Putamen
Globus pallidus

108
Q

What is the mid-brain nuclei called?

A

Substantia Nigra (SN)

109
Q

Where in the basal ganglia do inputs first go to?

A

Caudate and putamen nuclei

110
Q

What neurotransmitter regulates both the basal nuclei pathways?

A

Dopamine

111
Q

What is the excitatory neurotransmitter in the basal ganglia pathways?

A

Glutamate

112
Q

What is the inhibitory neurotransmitter in the basal ganglia pathways?

A

GABA

113
Q

What disease results from a disruption to dopaminergic input to the caudate/putamen from substantial nigra (SN)?

A

Parkinson’s disease

114
Q

What is the effect of a death of substantial nigra (SN) neurons?

A

Reduction in dopamine output from striatium (cluster if nuclei in basal agnglia) which results in an inability to initiate movements, slowed movements, stiffness and tremor = Parkinson’s disease.

115
Q

What are the treatments for Parkinson’s disease?

A

Drugs that either mimic or replace dopamine. Including dopamine precursor levodopa.

Deep brain stimulation = surgical implantation of stimulating electrodes into nuclei in thalamus, globes pallidus, sub thalamic nuclei (not painful as no pain fibres in the brain).

116
Q

What is the prefrontal cortex important for?

A

Organises thoughts and actions.

Cognitive function - acquiring knowledge through thought and experience.

Social behaviour

Language, decision making, risk assessment, personality, emotion etc.

Recall past events to help plan future events.

117
Q

What is the last area to mature?

A

Prefrontal cortex

118
Q

What is lobotomy?

A

Old surgical procedure used to get rid of “mental illness”. Mental illness was thought to be due to networks of neuron’s becoming caught in fixed distributive circuits leading to obsessive ideas and delirium.

You would go through the eye lope and cause damage to the prefrontal cortex.

119
Q

What are the two key spoken language areas of the brain?

A

Wernicke’s and Broca’s areas

120
Q

What is the result of a damaged wernicke’s area?

A

Fluent Aphasia

Meaning that you can speak perfectly articulated sentences but they are nonsense.

121
Q

What aspect of language is the wernickes area involved in?

A

Ability to understand spoken and written language

Talking flaunted and with clear meaning

Awareness of conversation

122
Q

What is aphasia?

A

Clinical name for speaking defects

123
Q

What is the result of a damaged Broca’s area?

A

Expressive (non-fluent) aphasia.

Meaning that you understand the conversation and know what you want to say but have great difficulty saying it - problems with the oral and breathing movements necessary to make recognisable sounds.

124
Q

What is learning?

A

The acquisition and storage of information as a result of experience

125
Q

What is memory?

A

The storage mechanism for what is learned?

126
Q

What are the two kinds of memory?

A

Declarative memory = retention and recall of conscious experiences that can be put into words.

Procedural memory = memory of how to do things independent of conscious understanding.

127
Q

What areas of the brain are crucial in making declarative memories?

A

Hippocampus
amygdala
limbic system

128
Q

What ares of the brain are crucial in making procedural memories?

A

sensorimotor cortex
cerebellum
basal nuclei

129
Q

Explain short and long term memory

A

Short term memory records and retains information for seconds-minutes.

Long term memory may be stored for years.

130
Q

How can you convert short term memories into long term memories?

A

Through consolidation: emotional impact, survival value, repetition and links to exisiting memories.

131
Q

What is the typical limit of items for recalling short term memories?

A

5-9

132
Q

What areas of the brain are involved in short term memories?

A

Hippocampus and prefrontal cortex

133
Q

Long term memories require…

A

Permanent changes in brain function and or storage and long term potentiation (long term changes in strength of specific synapses).

134
Q

What is loss of memory called?

A

Amnesia

135
Q

What is retrograde amnesia?

A

Loss of memories held from a period before the incident that caused the memory loss.

Typically loss of STM whilst LTM are retained

136
Q

What is anterograde amnesia?

A

Inability to consolidate short term memories into long term memories.

137
Q

What is anterograde amnesia typically due to?

A

Damage to limbic system and hippocampus

138
Q

What is long term potentiation?

A

The mechanism for making memories. It is a change in synaptic strength as a consequence of recent activity e.g., increase in the effectiveness of synapse.

The cellular mechanism for LTP has two phases - early and late phase. Process lasts for seconds to minutes.

139
Q

What is the key difference between the early and late LTP phases?

A

The early phase is not dependant on protein synthesis and the late phase is.

140
Q

What neurotransmitter is involved in early phase of long term potentiation?

A

Glutamate

141
Q

What does glutamate act on in early phase of long term potentiation?

A

NMDA glutamate receptors

142
Q

What does the NMDA glutamate receptor do and what does it activate?

A

Essentially acts as a calcium channel - results in an influx of Calcium at post synaptic cite.

Result of this is activation of CaMKII which then phosphorylates AMPA receptors that are inserted into membrane.

More AMPA receptors means more glutamate sensitive cells on the post synaptic membrane (dendrite spine) –> larger post synaptic response in subsequent activation.

143
Q

What happens in the late phase of LTP?

A

Early phase LTP activates variety of kinases which increase protein synthesis. Increased protein synthesis can result in increased number of AMPA receptors and/or increased volume of dendrite spine (more surface area for receptors).

144
Q

What are the three branches of the autonomic nervous system (ANS)?

A

Sympathetic
Parasympathetic
Enteric

145
Q

What does the ANS do?

A

Homeostasis regulation = perform sub-conscious functions to help maintain constant internal environment

Modulates function of various organs in response to external stimuli.

Responds to sensory input.

146
Q

Where is the Enteric division of the ANS located?

A

Within the wall of the GI tract - Neurons and axons in the wall of GI tract.

147
Q

Where does the ANS receive input from?

A

Somatic, visceral, special sense and endocrine system

148
Q

Where does the ANS deliver output to?

A

Motor and endocrine system

149
Q

What are the relative lengths of the pre and post ganglionic axons in the sympathetic and parasympathetic divisions of the autonomic nervous system?

A

Sympathetic: Pre axon short and post axon long

Parasympathetic: Pre axon long and post axon short

150
Q

Where is the adrenal medullar?

A

On top of the kidneys

151
Q

What neurotransmitters are released from the adrenal medullar?

A

Adrenaline and Noradrenaline (neurotransmitters released from the post ganglionic neuron’s in sympathetic nervous system).

152
Q

Where are preganglionic neurons in SNS?

A

Thoracic and upper lumbar spinal cord

153
Q

Where are postganglionic neurons in SNS?

A

paravetebral or prevertabral ganglia

154
Q

What is unique about the adrenal medullar in relation to sympathetic nervous system?

A

It has no axons and release their neurotransmitter (adrenaline and noradrenaline) directly into the bloodstream.

This differs to the PSNS released of neurotransmitters through axons and therefore act locally only.

155
Q

What is the sympathetic nervous system preparing you for?

A

Preparing the body for action - fight or flight.

Does this by increase blood pressure, heart rate, blood flow to lungs and muscles. And decreasing GI activity.

156
Q

Where are the preganglionic neurons in the PSNS?

A

Brainstem and sacral spinal cord

157
Q

Where are the postgnaglionic neurons in the PSNS?

A

cranial ganglia and in ganglia in or near visceral organs.

158
Q

Does SNS or PSNS act locally?

A

PSNS (hence by postganglionic axons are short).

Distributed less widely than SNS - means many axons carried in vagus nerve.

159
Q

What is the PSNS preparing the body for?

A

Rest and digest - decreases heart rate, increase activity of digestive tract and salivation.

160
Q

What does ACh released from PSNS post ganglionic neurons act on?

A

Muscarinic AChR.

161
Q

What do the neurotransmitters (adrenaline or noradrenaline) released from SNS post ganglionic neuron’s act on?

A

Adrenergic receptors

162
Q

What is the name of the cells in adrenal medullar that release neurotransmitters into bloodstream?

A

Chromaffin cells

Release mainly adrenaline but also noradrenaline and dopamine.

163
Q

What type of receptors are muscarinic receptors and what does it mean?

A

GPCR - means that they do not act as an ion channel causing direct action - instead binding of x2 ACh causes a downstream cascade of actions.

164
Q

What are the two types of adrenergic receptors?

A

Alpha (1 and 2) and Beta

All GPCR

165
Q

Do muscarinic receptors activate secondary messaging pathways ?

A

yes

166
Q

What is the effect of activating beta adrenergic receptors?

A

Activation of adenylate cyclase, increase cAMP and PKA activation.

***note different beta receptors can cause different responses in different tissues.

167
Q

What are the two types of alpha adrenergic receptors, there general function and the coupled G-protein ?

A

Alpha 1 generally excitatory -coupled to Gq.

Alpha 2 generally inhibitory - coupled to Gi.

168
Q

What is the main CNS centre involved with autonomic control?

A

Hypothalamus

169
Q

What is special about the Enteric nervous system?

A

It can operate independently of the SNS and PNS (but typically modulated by them)

170
Q

What is in the submucosal plexus of the GI Tract?

A

Sensory and motor neurons

Supplies the mucosal epithelium and muscle with nerves.

171
Q

What is in the myenteric plexus of the GI tract?

A

Sensory chemoreceptors and mechanoreceptors that drives GI smooth muscle

172
Q

What does the ENS do?

A

generates GI activity pattens - peristalsis segmentation that propels and mixes food through the GIT

Regulates secretion of GI hormones

173
Q

What transmitters and receptors are involved in the ENS?

A

ACh
VIP
5-HT
Substance P

174
Q

What reflexes of the ENS don’t go to (bypass) the CNS?

A

Short reflexes - used in simple localised reflex actions

175
Q

What does it mean to be conscious?

A

Alert, Aware, and Responsive (Able to response immediately to environmental cues).

176
Q

What is Sleep?

A

Sleep is defined by suspension of normal consciousness and onset of a specific pattern of brain activity.

It is a complex pattern of brain states.

Able to be roused but typically not aware of surroundings.

177
Q

What are two examples of unconscious states?

A

Coma
Vegetative state.

178
Q

What does unconsciousness mean in relation to being in a coma?

A

Prolonged absence of wakefulness or awareness, no response to external stimuli, unable to be roused and lack of normal sleep-wake cycle.

179
Q

What causes you to be in an unconscious state of coma?

A

Dysfunction of cortex and/or reticular activating system

180
Q

What does unconsciousness mean in relation to being in a vegetative state?

A

May show signs of wakefulness, but no signs of awareness. May have sleep-wake cycles, some degree of autonomic function intact but no cognitive function.

181
Q

How long does a vegetative state have to last to be considered persistent?

A

More than 4 weeks

182
Q

Are you unconscious when you are asleep?

A

No, just altered consciousness

183
Q

What are the three key disorders of consciousness?

A

Schizophrenia
Hallucinations
Epilepsy/Seizures

184
Q

What is Schizophrenia?

A

Disorder of thinking, awareness and behaviour.

185
Q

What is psychosis?

A

Difficulty distinguishing real from not real resulting in an abnormal perception of the world.

186
Q

What do psychotic hallucination typically cause someone to do?

A

Act on the hallucinations e.g., if you are hallucinating voices in your head telling you to stab people then you would go and stab people.

187
Q

What is schizophrenia thought to be due to?

A

Hyperactivity in brain dopamine systems.

Stimulants such as amphetamines and cocaine act via dopaminergic system and can trigger schizophrenia-like psychotic episodes.

BUT there is no definitive cause (could be genetics, developmental or environmental factors).

188
Q

What is an effective drug therapies for schizophrenia?

A

Specific D2 (dopamine) receptor blockade

189
Q

What are hallucinations?

A

Apparent ‘real’ wakeful perceptions in the absence of an external stimulus.

Normal sensory perceptions typically arise as a result of sensory input giving rise to co-ordinated neural activity in specific parts of the brain If those parts of the brain become active without a normal stimulus, a perception arises but is hallucinatory.

Hallucinations are common in schizophrenia.

190
Q

What is non-psychotic hallucinations?

A

Hallucinations that don’t urge interaction with the hallucination e.g., if voice in your head telling you to stab someone you wouldn’t actually stab someone.

191
Q

How are hallucinations different to dreams?

A

Dreams don’t involve “wakefulness”.

192
Q

What is Epilepsy?

A

Excessive abnormal synchronised activity of cortical neuron’s, may result in loss of consciousness and may be associated with aberrant sensory perceptions.

193
Q

What is a period of epileptic brain activity known as?

A

A seizure

194
Q

Seizures may be convulsive or non-convulsive. What is the difference?

A

Convulsive means causing uncontrolled muscle contraction due to involvement of motor areas in the brain.

Non-convulsive (or absence seizures) is where the patient is absent for a brief period of time due to reduced consciousness/awareness.

195
Q

What is an aura?

A

Where a patient has visual, auditory, or olfactory sensation (depending on which part/s of the brain are involved) that tells them they are about to have a seizure.

196
Q

What does treatment for seizures typically involve and give a specific example?

A

Drugs that interact with ion channels to modulate neuronal excitability.

e.g., Phenytoin - V dependent block of V-gated Na channels.

197
Q

What is a widely used technique for measuring brain activity?

A

EEG - electroencephalogram.

Used to monitor behavioural state and diagnose epilepsy and sleep disorders.

198
Q

What do EEG indicate?

A

Strength and synchrony of synaptic activity in dentrites of cortical neurons.

199
Q

What is wakefulness?

A

Wakefulness is a brain state in which we are conscious and able to respond coherently to external stimuli.

200
Q

What does sleep deprivation lead to?

A

Reduced immune function
Poor memory consolidation
Short attention span
Emotional instability
Increased blood pressure (and tiredness)
Ultimately death (thought that can probably go about 10-12 days without sleep before you would die).

201
Q

What are the two drivers for sleep?

A

Homeostatic and Circadian systems

202
Q

How does homeostatic systems drive sleep?

A

Long periods of wakefulness build up “homeostatic pressure” by:

The increased production of adenosine as a by product of using energy.

Adenosine interacts with adenosine receptors that are on groups of neuron’s in the brain that suppress CNS activity.

203
Q

How does caffeine work to make you feel less tired?

A

Caffeine has a stimulatory effect as it blocks adenosine receptors - therefore reduces suppression of CNS activity.

204
Q

What is circadian controlled by?

A

SCN - Suprachiasmatic nucleus

205
Q

What sort of cycle of activity does SCN have?

A

Daily cycle relayed to body via neural and endocrine circuits

Regulated by exposure to day/night cycle

206
Q

What is the natural circadian cycle and what makes it 24 hours instead?

A

Natural cycle is about 25-26 hours but is entrained by exposure to sunlight (making it 24 hours)

207
Q

Where is melatonin released from and what modulates its release?

A

Activity of SCN neurons modulates release of melatonin from pineal gland.

208
Q

What increases melatonin release and when does release peak?

A

Melatonin release increases as light levels fall - promoting sleep.

Peak is around 3am and then falls so we become more wakeful in the morning.

209
Q

Where is the circadian clock?

A

Suprachiasmatic nucleus

210
Q

What nucleus does the eye send light stimuli signals to?

A

Lateral geniculate nucleus

211
Q

When we become drowsy what frequency of alpha waves appear in a EEG?

A

Synchronised waves around 10Hz.

212
Q

What are the stages of slow wave sleep?

A

Stage 1 = theta waves (around 5Hz)
Stage 2 = theta waves interrupted by 12 Hz bursts and large slow spikes
Stage 3 = delta waves with spindles (around 1Hz)
Stage 4 = delta waves

213
Q

What is REM sleep?

A

Rapid Eye Movement sleep.

Brain activity during REM sleep is similar to that of wakefulness, with rapid and random eye movements, increased heart rate, and irregular breathing.

214
Q

When does SWS occur?

A

About every 90 minutes, after about 10 minutes of REM, the brain cycles back through SWS, but cycle typically omits stage 4 of SWS after 2 rounds.

215
Q

What is lost during REM sleep?

A

Muscle tone (but phasic contraction of eye muscles becomes pronounced)

216
Q

When does most dreaming occur?

A

During REM

217
Q

What are the two stages of sleep that make up the sleep cycle?

A

REM - rapid eye movement sleep (lighter sleep).
SWS - slow wave sleep (deep sleep)

218
Q

What is the transition between wakefulness and sleep states regulated by?

A

A group of neuron’s in the brainstem = the reticular activating system (RAS). And their interactions with nuclei in the thalamus, hypothalamus and cortex.

219
Q

What releases orexin and what does it do?

A

Orexin is a neuropeptide that promotes wakefulness.

It is released by a small group of neurons in the hypothalamus.

220
Q

What inhibits orexin neurons?

A

Melatonin

221
Q

What do people with defective orexin neurons suffer from?

A

Narcolepsy (abnormal sleep-wake cycle) and excessive daytime sleepiness.

222
Q

Why do some types of antihistamines cause drowsiness?

A

Because some inhibit the excitatory influence of histamine from the RAS.

Histamine is a chemical released by your body when you have an allergic reaction. Antihistamines are medicines that block the effects of histamine, helping to relieve allergy symptoms like sneezing and itching.

Some antihistamines can make you feel sleepy. This happens because they not only block histamine but also affect a part of your brain called the reticular activating system (RAS). The RAS helps control your sleep-wake cycle. When antihistamines block histamine in the brain, they can also interfere with the RAS, making you feel drowsy.

223
Q

For movement to be executed what motor area needs to be active?

A

Cortical motor area / primary motor cortex.

It plays a crucial role in the initiation and coordination of voluntary movements throughout the body

224
Q

What neurotransmitter needs to be released to activate the primary motor cortex?

A

Glutamate (released from neuron’s who cell bodies are in the thalamic nuclei).

225
Q

What are thalamic nuclei (needed for release of glutamate) inhibited by?

A

The GPi (Globus Pallidus)

226
Q

What is the effect of an active GPi?

A

Inhibition on thalamic nuclei - thalamic nuclei need to be active to release glutamate and glutamate required for activating primary motor cortex. Therefore an active GPi is inhibiting movement.

227
Q

Does the direct or indirect basal ganglia pathway inhibit GPi?

A

Direct pathway

228
Q

How does the indirect basal ganglia pathway reduce cortical activation and make movement harder?

A

Because it stimulates the GPi which inhibits thalamic nuclei which prevents glutamate release.

229
Q

What makes the indirect basal ganglia pathway “indirect”?

A

Input goes from the caudate/putamate to GPi via the GPI and sub thalamic nucleus.

Whereas direct pathway goes straight from caudate /putamate to GPi.

230
Q

What do opiates do?

A

Block pain transmission pathways

231
Q

How do NSAID’s reduce pain?

A

They act by inhibiting production of postroglandins which minimises activation of nociceptors.

232
Q

What are some examples of NSAID’s?

A

Aspirn, Ibuprofen, paracetamol

233
Q

What are the lobes of the brain and what are their key function?

A

Frontal Lobe = language and Personality

Pariental Lobe = Somatosensory

Occipital Lobe = Vision

Temporal = Memory and Hearing

234
Q

What are major targets of painkillers?

A

Cyclooxygenase

235
Q

What is the unit of EEG recordings?

A

Microvolts (uV)

236
Q

What is ‘aura’?

A

Unusual sensation or feeling that alert someone that a seizure is coming

237
Q

Nociceptors typically feature members of what family of receptors?

A

TRP - Transient Receptor Potential

238
Q

What is the main area of the brain involved in autonomic control?

A

Hypothalamus

239
Q

What type of fibres do thermal and mechano nociceptors have and what do they signal?

A

Aa-fibres thinly myelination
Signal acute onset of pain.

240
Q

What type of fibres do polymodal nociceptors have and what do they signal?

A

C-fibres unmyelinated
Signal ongoing slow dull pain.

241
Q

Famous patient HM had amygdala and hippocampus removed as treatment for what?

A

Epilepsy

242
Q

When the amygdala and hippocampus was removed from patient HM what abilities did Hm loose?

A

Ability to make new long term memories (could recall events from years ago but nothing beyond a minute or two post-surgery)

PSHL231 Neurophysiology (10 decks)

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