Neuroscience and Mental Health Flashcards

1
Q

Outline the organisation of the Central Nervous system.

A

Central Nervous System

Peripheral Nervous system

 - Autonomous Nervous system
      - Sympathetic nervous system
      - Parasympathetic nervous system
 - Somatic PNS
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2
Q

Define the central nervous system.

A

Brain and spinal cord

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3
Q

Define the peripheral nervous system.

A

Nerves and ganglia (clusters of neuronal cell bodies) outside the brain and spinal cord.

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4
Q

What to the branches of the PNS do?

A
  • Somatic PNS: controls motor and sensory function for the body wall e.g. skin, skeletal muscles
  • Autonomic NS: regulates function of the viscera (internal organs, smooth involuntary muscle, pupils, sweating, blood vessels, bladder, intestin, glands etc and controls heart and contraction rate. It had two arms (sympathetic and parasympathetic)
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5
Q

What are the different types of neurones with regard to direction of information flow?

A
  • Afferent axons propagate action potential towards the CNS, away from PNS e.g. sensory neurones
  • Efferent axons propagate action potentials from the CNS to the PNS e.g. motor neurones
  • Inter-neurones are CNS neurons that synapse with other CNS neurons within the brain or spinal cord
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6
Q

Outline the parts of the brain.

A
  • Cerebral cortex: two hemispheres. Each receives sensory info from and control movement of the opposite side of the body
  • Cerebellum: Controls coordination of movement
  • Brain stem: Primitive, densely packed fibres, regulates vital functions e.g. consciousness, breathing. Damage is usually serious and could be fatal
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7
Q

Where does the CNS end in the spinal cord?

A
  • Ends at the margins of the spinal cord

- Dorsal and ventral roots that emerge are part of the PNS

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8
Q

Outline axon packing in nerves.

A
  • Spinal nerves contain both afferent and efferent axons
  • They’re bundled into fascicles surrounded by a perineurium
  • Whole nerve encased in tough epineurium capsule
  • Individual axons wrapped in myelin and endoneurium, though some are unmyelinated e.g. nociceptive (pain) neurons
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9
Q

What is the function of a neuron?

A

To transmit and receive action potentials, or stimulate target tissue e.g. contraction of smooth/skeletal muscle, secretion from gland.

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10
Q

What is the difference between PNS and CNS with respect to regeneration?

A
  • Axons in PNS can regenerate after injury. Though recovery is often compromised by non-specific target re-innervation and aberrant axon sprouting. It can leave to neuropathic pain.
  • Axons in CNS are unable to regenerate over long enough distance to be useful.
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11
Q

Why can’t axons in the CNS regenerate?

A
  • Inhibitory molecules in CNS not PNS e.g. myelin differences
  • Absence of guidance cues that stimulate axon growth during development
  • Some loss of intrinsic axon growth capability by neurons
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12
Q

What is white and grey matter?

A

White matter - Ascending and descending axons

Grey matter - Neuronal cell bodies

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13
Q

What is the difference in the action potential pathways between a reflex response and conscious registering?

A
  • Reflex: Only somatic sensory input to inter-neurons and motor output from spinal cord are required NO communication with sensorimotor cortex
  • Conscious registering: Sensory inputs activate sensory neurons in spinal cord grey matter that transmit action potentials upward to sensory cortex of brain. Similarly neurons of motor cortex transmit action potentials downward to synapse with spinal motor neurons for voluntary movement
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14
Q

What is considered when diagnosing neurological problems?

A
  • Presenting signs and symptoms to identify underlying anatomy and characterise the syndrome
  • Mode (and speed) of onset to determine underlying aetiology (pathological cause)
  • History: previous medical problems, family history, social history, other symptoms
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15
Q

List common causes of neurological problems in order of speed of onset.

A
  • Trauma
  • Vascular
  • Toxic/metabolic
  • Infectious
  • Inflammatory/autoimmune
  • Genetic-congenital
  • Neoplastic
  • Degenerative
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16
Q

Give some features of stroke.

A
  • 80% are infarct
  • 20% haemorrhage (often related to high bp)
  • Can affect any part of brain including brainstem
  • Problems in opposite side of lesion (contralateral)
  • Risk factors include smoking, family history, diabetes, alcohol
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17
Q

What are the common areas affected by stroke and the syndromes they cause.

A
  • Middle cerebral artery: most common, results in weakness and loss of sensation on the other side (contralateral)
  • Posterior cerebral artery: often affect occipital lobe, result in visual loss on contralateral side
  • Anterior cerebral artery: often cause contralateral leg weakness
  • Brainstem: problems with balance, eye movemetns, speech and swallowing, breathing
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18
Q

What treatments are available for stroke?

A

Acute:
- intravenous thrombolysis to dissolve clot
- intra-arterial thrombectomy to remove clot
Treat complications:
- neurosurgery for haemorrhage or dangerously high pressure
Prevent further stroke:
- thin blood with aspirin
- treat diabetes and high cholesterol
- treat dangerously narrow carotid arteries

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19
Q

What are the examinations performed to diagnose neurological problems?

A
  • Cognitive/thinking abilites: e.g. mini mental state examination
  • Cranial nerves: smell, vision, eye-movements, facial sensation and movements
  • Limbs: power, coordination, reflexes and sensation
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20
Q

Describe the mini mental state examination?=.

A
  • Orientation e.g. what year is it?
  • Registration e.g. ask patient to recall 3 things you just said (like items)
    Trials:
  • Attention and calculation e.g. spell world backward, or count back in 7s
  • Recall e.g recall 3 objects
  • Language e.g. follow a 3 stage command
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21
Q

Outline the features of Parkinson’s disease.

A
  • Slowly progressinve degenerative diseas affecting the basal ganglia
  • Clinical features; rigidity, tremor, bradykinesia (reduced movement)
  • Loss of neurons from substantia nigra to the caudate and putamen
  • Dopamine is associated neurotransmitter
  • Treated with levodopa which can cross blood brain barrier
  • Also with deep brain stimulation
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22
Q

What is Spastic Parapaesis?

A
  • Axonal degeneration that affects the spinal cord and leads to rigidity and weakness in the leg muscles which gets progressively worse
  • Causes include: Trauma, inflammatory/autoimmune, neoplastic, degenerative, vitamin deficiency (B12), vascular
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23
Q

What is multiple myeloma?

A
  • tumour of plasma cells (b cells)

- treated with radiotherapy and chemotherapy

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24
Q

What is stocking and glove distribution?

A
  • Peripheral nervous disease
  • Around the hands approx up to wrist
  • Around the feet approx up to mid-shin

(Where you’d wear gloves and socks)

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25
Q

What is Acute Polyneuropathy?

A
  • Peripheral nerve damage

Can be caused by

  • Infections e.g. diptheria, autoimmune (e.g. Guillain Barre)
  • Drugs (chemotherapy)
  • Exposure to toxins (organophosphate insecticides)
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26
Q

Outline Guillain-Barre syndrome and Acute inflammatory demyelinating polyneuropathy.

A
  • Common cause of acute neuromuscular weakness
  • Progressiv ascending sensorimotor paralysis with areflexia, affectin 1 or mor limbs and reaching nadir (the worst point) within 4 weeks
  • Patients may progress to almost complete paralysis and require ventilation
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27
Q

What treatment is available for Guillain-Barre and Acute Inflammatory demyelination polyneuropathy (AIDP)?

A
  • Immunotherapy: Plasma exchange or intravenous immunoglobulin
  • Supportive including ventilation if necessary
  • Cardiac monitoring
  • Anticoagulation to prevent leg clots (and subsequent pulmonary emboli)
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28
Q

What are the investigative methods of diagnosing a neurological problem?

A
  • Brain scans: CT and MRI
  • Cerebrospinal fluid: Lumbar puncture
  • Nerve conduction studies and electromyography (EMG)
  • Electroencephalogram (EEG) and Evoked potentials
  • Brain pathology: damage to cells or larger structures
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29
Q

Where is a Lumbar puncture performed?

A

Between L3 and L4 or L4 and L5

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30
Q

What is a neuron?

A
  • Basic structural and functional unit of the nervous system
  • information processing unit
  • responsible for generation and conduction of electrical signals
  • communicates with other neurons via chemicals at the synapse
  • supported by neuroglia, comprising of different types
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31
Q

Describe the structure of a neuron.

A
  • cellular structure of all neurons are similar
  • diversity achieved by differences in number and shape of processes
  • usually made up of cell body, axon and dendrites
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32
Q

What are the adaptions of neutrons inside the cell?

A
  • large nucleus
  • prominent nucleolus
  • abundant rough ER
  • well developed golgi
  • abundant mitochondria
  • highly organised cytoskeleton

Highly organised, metabolically active, secretory cell.

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33
Q

Outline the features of dendrites.

A
  • major area of reception of incoming information
  • spread from cell body, branching frequently
  • greatly increase surface area
  • often covered in protrusions called spines
  • dendritic spines receive majority of synapses
  • large pyramidal neurons may have up to 30,000/40,000 spines
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34
Q

Describe the structure of pyramidal cells.

A
  • triangular (isosceles)
  • primary dendrite from each corner
  • one large axon from bottom
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35
Q

How are Purkinje cells specialised?

A
  • enormous number of spines on dendrites (>80,0000 per cell)

- human cerebellum has about 15 million Purkinje cells

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36
Q

Outline the features of axons.

A
  • conduct impulses away from cell body
  • emerge at the axon hillock
  • usually one per cell
  • may branch after leaving cell body and at target
  • prominent micro-tubules and neurofilaments
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37
Q

Describe the properties of axons.

A
  • contain abundant intermediate filaments and micro-tubules
  • can be myelinated or unmyelinated
  • axonal membrane in only exposed at node of Ranvier, ion channels at node and juxtanode, not paranode
  • cable properties
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38
Q

Describe the features of axon terminals.

A
  • Axons often branch extensively close to target (terminal arbor)
  • Form synaptic terminals with target
  • Boutons (typical synpaptic knob) OR
  • Varicosities ( -O-O-O- )
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39
Q

Outline the ways the synapse is adapted for its function.

A
  • Synaptic vesicles, packaged in Golgi and shipped by fast anterograde transport to synapse
  • specialised mechanisms for association of synaptic vesicles with the plasma membrane
  • abundant mitochondria about 45% of total energy consumption is required for ion pumping and synaptic transmission, sensitivity to O2 deprivation
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40
Q

Describe organisation of the synapse.

A
  • neurons receive multiple synaptic input
  • neurons use a range of chemical transmitters, excitatory and inhibitory
  • competing inputs are integrated in the post-synaptic neuron (neuronal integration)
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41
Q

What are the types of synapses?

A
  • Axo-dendritic (often excitatory)
  • Axo-somatic (often inhibitory)
  • Axo-axonic (often modulatory)
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42
Q

Describe the neuronal cytoskeleton.

A
  • In adult humans axons range in length from micrometres to a metre
  • Highly organised cytoskeleton required (microfilaments, intermediate filaments, microtubules)
  • neurofilaments play a critical role in determining axon caliber (diametre)
  • microtubules are very abundant in the nervous system
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43
Q

Outline axonal transport.

A
  • transport of membrane associated materials
  • vesicles associated motors are moved down the axon at 100-400mm per day
  • different membrane structures targeted to different compartments
  • retrograde moving organelles are morphologically and biochemically distinct from anterograde vesicles
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44
Q

What is the primary cause of Multiple Sclerosis?

A

Immune system attacking and destroying the myelin sheath of CNS neurons, and therefore their axons.

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45
Q

What are the different morphological sybtypes of neurons?

A
  • Pseudounipolar (one axon) e.g. sensory neurons
  • Bipolar (two axons) e.g. retinal bipolar cells
  • Golgi type I multipolar (highly branched dendritic trees, long axons) e.g. pyramidal cells, Purkinje cells, retinal ganglion cells
  • Golgi type II multipolar (highly branched dendtritic trees, short axons) e.g. stellate cells in cerebral cortex and cerebellum
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46
Q

What are Neuroglia?

A
  • Support cells of the nervous system
  • Astroglia, oligodendroglia, microglia, immature progenitors, ependymal cells, Schwann cells, satelite glia
  • many and varied functions
  • essential for correct functioning of neurons
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47
Q

What are the features of Astroglia?

A
  • Multiprocessed star-like shape
  • Most numerous cell type
  • Numerous intermediate filament bundles in cytoplasm of fibrous astroglia
  • Gap junctions suggest astroglia-astroglia signalling
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48
Q

What are the functions of astroglia?

A
  • Scaffold for neural migration and axon growth during development
  • Formation of blood brain barrier
  • Transport of substances from blood to neurons
  • Segregation of neuronal processes (synapses)
  • Removal of neurotransmitters
  • Synthesis of neurotrophic factors
  • Neuronal-glial and glial-neuronal signalling
  • Potassium ion buffering
  • Glial scar formation
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49
Q

What are the features of Oligodendroglia?

A
  • the myelin forming cells of the CNS: interfasicular (peripheral white matter), perineuronal (CNS grey matter)
  • Small spherical nuclei
  • Few thin processes
  • Prominant ER and Golgi
  • Metabolically highly active
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50
Q

What are the functions of Oligodendroglia?

A
  • Production and maintenance of the myelin sheath

- Each cell produces multiple sheaths (1-40)

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51
Q

What are the features of myelin?

A
  • a lipid rich insulating membrane
  • up to 50 lamellae (layer)
  • dark and light bands seen in EM images
  • loss of oligodendroglia and myelin has disastrous consequences:
    e. g. Multiple Sclerosis (MS), Adrenoleucodystrophy
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52
Q

What are Microglia?

A
  • derived from bone marrow during early development
  • resident macrophage population of CNS
  • involved in immune surveillance
  • present antigens to invading immune cells
  • first cells to react to infection or damage
  • role in tissue modelling
  • synaptic stripping
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53
Q

What are Schwann cells?

A
  • myelin producing cells of the PNS
  • each Schwann cell produces only on myelin sheath
  • surrond unmyelinated axons
  • promote axon regeneration
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54
Q

Define flux.

A

The rate of transfer of molecules.

The number of molecules that cross a unit area per unit of time

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55
Q

What are the properties that affect excitable cells?

A
  • Voltage/Potential difference: Generated by ions to produce a charge gradient (volts)
  • Current: Movement of ions due to a potential difference (amps)
  • Resistance: Barrier that prevents the movement of ions (ohms)
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56
Q

What is an electrochemical equillibrium?

A

When electrical forces balance diffusion forces, and prevent further movement.

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57
Q

What is the equilibrium potential?

A

Potential that prevents diffusion of the ion down its concentration gradient.

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58
Q

Which ions are the most important for maintaining resting potential?

A

Na+ and K+

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59
Q

What Is Ek and ENa? Why isn’t resting membrane potential eaqual to either?

A
Ek = -90mV
ENa = +72mV

Membranes have mixed K+ and Na+ permeability (but at rest K+»Na+)

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60
Q

Which ions contribute to the membrane potential?

A

K+, Na+ and Cl-

The size of each ion’s contribution is proportional to how permeable the membrane is to the ion.

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61
Q

What equation is used to calculate the resting memrbrane potential (Em)?

A

Golman-Hodgkin-Katz equation.

Takes into account the concentration of ions and the membrane’s permeability to them.

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62
Q

Name the stages of an action potential.

A
  • Resting potential
  • Depolarizing
  • Overshoot
  • Repolarizing
  • Hyperpolarizing
  • Resting potential
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63
Q

What differences in stimulus can be seen when measured?

A
  • Depolarisation causes positive deflection, hyper-polarization causes negative negative deflection
  • Weak stimulus causes smaller potential than stronger stimulus
  • The further from the stimulus site the smaller the potential
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64
Q

What is a graded potential?

A
  • Changes in membrane potential that vary in size, rather than being all or none.
  • Can be less than threshold
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65
Q

Where do graded potentials occur and why?

A

Occur at synapses and sensory receptors

Function: contribute to initiating or preventing action potentials

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66
Q

Describe the process of an action potential.

A
  1. Resting Potential
    - Permeability K+» Permeability Na+
    - Membrane potential nearer EK+ than ENa+
  2. Stimulus
    - Depolarizes the membrane potential
    - Moves it in the +ve direction towards threshold
  3. Depolarization
    - Na+ permeability increase greatly, Na+ enters down electrochemical gradient
    - K+ permeability slowly increases, K+ leaves cell down electrochemical gradient but less than Na+. Membrane potential shifts to ENa+
  4. Repolarization
    - Na+ permeability decreases, Na+ entry stops.
    - K+ permeability increases as more channels open. Membrane potential shifts to EK+
  5. After Hyperpolarization
    - K+ continues to leave electrochemical gradient. Membrane potential shifts to EK+. Some K+ channels.
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67
Q

Outline when during an action potential there is and isn’t possibility for a new action potential.

A

Absolute refractory period: Start of repolarization

  • Inactivation gate closed, no new potential even if strong stimulus
  • Later in repolarization activation gate also closes

Relative refractory period: After hyperpolarization
- Inactivation gate is open, but stronger than normal stimulus required to trigger an action potential

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68
Q

What are the features of neurons and action potentials?

A
  • Once threshold is reached action potential is released
  • All or nothing nature
  • Refractory state where it is unresponsive to threshold depolarization
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69
Q

What restores the electrochemical equilibrium?

A

Non-voltage gated channels (fast) and sodium-potassium pumps (slow)

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70
Q

What is the difference between passive and active propagation?

A

Passive: Only resting K+ channels are open, resistance alters it, both directions

Active: Na+ channels involved, different areas are at different stages of the action potential, unidirectional

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71
Q

What is Saltatory conduction?

A
  • Myelin sheath around axon with nodes of Ranvier allow the depolarisation to ‘jump’.
  • Voltage-gated channels mostly at nodes creating a circuit
  • Faster impulses
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72
Q

What factors affect conduction velocity?

A
  • Axon diametre: velocity increases with axon diameter as there is less resistance
  • Myelination: Faster with myelination
  • Conduction is slowed by cold, anoxia (lack of oxygen), compression and drugs e.g. some anaesthetics
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73
Q

What are the divisions of the brain?

A
  • Forebrain: Cerebral hemispheres, diencephalon
  • Midbrain
  • Hindbrain: Pons, medulla, cerebellum

(Brainstem: Midbrain, Pons and medulla)

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74
Q

What are the different parts seen in a cross section of the spinal cord?

A
  • White matter: axons
  • Grey matter: Cell bodies
  • Dorsal horn: (posterior) Contains sensory neurones
  • Ventral horn: (anterior) Contains motor neurones
  • Dorsal root ganglion: (posterior) Contains sensory neuron somas/bodies
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75
Q

Identify the different structures of vertebra.

A
  • Inter-vertebral foramen: Openings between verterbrae
  • Body of verterbrae
  • Arch of verterbrae
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76
Q

What are the spinal and vertebral levels?

A
  • Cervical vertebrae C1-C8 and Cervical nerves C1-C7
  • Thoracic vertebrae T1-T12 and Thoracic nerves T1-T12
  • Lumbar vertebrae L1-L5 and Lumbar nerves L1-L5
  • Sacral Vertebrae S1-S5 and Sacral nerve S1-S5
  • Coccygeal nerve
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77
Q

Where does the spinal cord end?

A

L1/L2

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78
Q

What is the relationship between spinal segments and nerves their corresponding vertebrae?

A

Lumbar and sacral spinal segments are higher that their corresponding vertebrae.
Spinal nerves run below their vertebrae

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79
Q

What is the Peripheral nervous system?

A
  • Peripheral nerves

- Ganglia

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80
Q

Describe the structure of a ganglion.

A
  • Connective tissue capsule on outside
  • Many neurons inside, but no dendrites
  • Satellite cells support neurons
  • Axons (appear dark, corrugated) in different planes
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81
Q

Describe the structure of a nerve.

A
  • Neuron axons grouped in bundles called fascicles
  • Fascicles grouped together with blood vessels into nerves
  • Packaged with layers of connective tissue which give protection
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82
Q

What are the layers of connective tissue in a nerve?

A
  • Epineurium: Outer layer, thick layer of loose connective tissue around whole nerve
  • Perineurium: Dense layer of connective tissue capsule around fascicles
  • Endoneurium: Delicate connective tissue around individual axons
83
Q

What are the two types of axons in the peripheral nervous system?

A
  • Myelinated: Row of Schwann cells along axon wrapped around it forming concentric rings of adjacent cell membranes full of myelin protein. Between adjacent Schwann cells there is the node of Ranvier.
  • Unmyelinated: Surrounded by Schwann cell, but only a single membrane. This means one cell can accommodate several axons. Usually small axons, up to 1-1.5µm.
84
Q

Why is there a limit to the axon diameter?

A

The larger the diameter the more maintenance required.

85
Q

What are the different neurons involved in the PNS?

A
  • Somatic motor neurons: CNS -> Skeletal muscle
  • Autonomic motor neurons: CNS -(preganglionic)-> Autonomic ganglion -(postganglionic)-> e.g. glands, viscera
  • Sensory neurons: Receptors –(sensory (Dorsal root) ganglia)–> CNS
86
Q

Describe the organisation of nerves in the spinal cord.

A
  • Both somatic autonomic neurons
  • Spinal nerves on either side feed in sensory neuron to dorsal root ganglion
  • Synapses in the grey matter
  • Motor neurons exit through the ventral root
  • For autonomic motor nerve they go through the White ramus communicans, then either back into the spinal nerve or further into the sympathetic trunk
87
Q

What do the spinal nerves supply?

A

Each spinal nerve innervates muscles (mytome) and skin (dermatome) in a particular part of the body. (only somatic)

88
Q

Describe the innervation of the upper limbs.

A
  • By C5, C6, C7, C8, T1
  • Converge to form the Brachial plexus
  • Axons from different spinal nerves mix forming a new mix of axons in the diverging nerves
89
Q

What two ways can skin from the upper limbs be considered to be innervated?

A
  • By dermatome: axons from one spinal nerve

- By peripheral nerve e.g. radial nerve, medial etc

90
Q

By what two mechanisms can disorders of the PNS come about?

A
  • Injury

- Disease

91
Q

What is the process of repair after peripheral nerve injury?

A
  • Damage to axon (crushed) within endoneurium
  • Axon degeneration in distal part (away from cell body)
  • Macrophages clear debris
  • Cell division of Schwann cells
  • This encourages the proximal stump (part closest to cell body) to grow axonal sprouts
  • One of the sprouts with suitable synapse with the target, causing others to retract.
  • The axon grows wider and myelin sheath forms
  • Regenerated axon but normally with smaller gaps between nodes of Ranvier leading to slower conduction velocity
92
Q

What factors affect a neuron’s ability to regenerated?

A
  • If the damage is close to the cell body it may not try to regenerate
  • If damage is a long distance to target chances of successful regeneration is reduced
  • Type of injury; if endoneurium is intact there is guidance for axonal growth if not it could be dangerous
93
Q

What medical techniques can be used for nerve damage?

A
  • Microsurgery - Suturing fascicles together
  • Grafts - take nerve from a patient and replace the part lost, or man-made material
    In case of neuroma (knot of axon endings) there is pain
94
Q

What are the features of peripheral nerve disorders caused by disease?

A
  • Progressive degeneration of nerves
  • Usually distal to proximal
  • Cause may be metabolic (e.g. diabetes), infectious (leprosy), hereditary
  • Affects sensory/and or motor axons
  • May initially affect myelin or axon
95
Q

What is segmental demyelination?

A

Where Schwann cells die, leaving gaps in the myelination. This would slow conduction velocity.

96
Q

What is Axonal degeneration?

A

Damage to the axon, causing a complete conduction block.

97
Q

How do you diagnose peripheral nerve disorders?

A
  • Neurological examination
  • Conduction velocity test
  • Nerve biopsy to look at histology
98
Q

What is the neuromuscular junction?

A

Specialised synapse between a motor neuron and a muscle fibre

99
Q

What is the contact ratio for synapses?

A

Ranges from 1:1 for muscle, to 10,000:1 in CNS

100
Q

Outline the features of the structure of a neuromuscular junction?

A
  • Incorporates the distal axon terminal and the muscle membrane that allows for the unidirectional chemical communication between peripheral nerve and muscle
  • Main structures: Pre-synaptic nerve terminal, synaptic cleft, post-synaptic endplate region on the muscle fibre
  • Acetyl choline serves as the neurotransmitter for voluntary striated muscle
101
Q

Describe how contraction in muscle is initiated.

A
  • Action potential opens voltage-gated Ca2+ channels
  • Ca2+ enters, and triggers exocytosis of vesicles
  • Acetyl choline diffuses into cleft
  • Acetyl choline binds to receptor-cation channel and opens channel
  • Local currents flow from depolarizes region and adjacent region; action potential triggered and spreads along surface membrane
  • Acetyl choline broken by acetyl choline esterase. Muscle fibre response stops
102
Q

What are miniature end-plate potentials?

A

Depolarization at rest caused by individual vesicles releasing Acetyl choline at a very low rate causing miniature end-plate potentials (MEPPs)

103
Q

Outline the structure of skeletal muscle.

A
  • Myofibril made up of myofilaments
  • Myofibres made of myofibrils; surrounded by Sarcolemma and capillaries
  • Muscle fibres made up of myofibrils, surrounded endomysium
  • Muscle fasciculus bounded by perimysium
  • Muscle surrounded by epimysium
104
Q

What are the features of Myofibres?

A
  • Covered by plasma membrane (sarcolemma)
  • T-tubules tunnel into centre
  • Cytoplasm called sarcoplasm, contains myoglobin and mitochondria
  • Network of fluid filled tubules; sarcoplasmic reticulum
  • Composed of myofibrils
105
Q

Outline some features of Myofibrils.

A
  • 1-2µm in diameter
  • Extend along entire lenth of myofibres
  • Composed of two main types of protein: Actin and myosin
106
Q

Outline the features of Myofilaments.

A
  • Light and dark bands give muscle striated appearance
  • Do not extend along the length of myofibres
  • Overlap and are arranged in compartments called sarcomeres
  • Dense protein Z-discs separate sarcomeres
  • Dark bands: A-band (thick- myosin)
  • Light bands: I-band (thin- actin)
  • Myosin and actin filaments overlap
107
Q

What observations can be made during muscle contraction.

A
  • I-band becomes shorter
  • A-band remained same length
  • H-zone narrowed or disappeared
108
Q

Describe how muscle is stimulated and then relaxes

A
  1. Action potential propagates along surface membrane and into T-tubules
  2. Dihydropyridine (DHP) receptor in T-tubule membrane senses the the change in voltage and changes shape of the protein link to Ryanodine receptor, opening the Ca2+ channels in the sarcoplasmic reticulum. Ca2+ is released from SR into space around the filaments
  3. Ca2+ binds to Troponin, so tropomyosin moves allowing
  4. Crossibridges attach to actin
  5. Ca2+ actively transported into SR continuously while action potentials continue. ATP-driven pump (uptake rate = release rate)
  6. Ca2+ dissociates from Troponin when free Ca2+ declines; Tropomyosin moves blocking new crossbridge formation. Active force decline due to net crossbridge detachment
109
Q

What can disorders of the neuromuscular junction lead to ?

A

Can lead to muscle weakness

110
Q

Give examples of disorders of the neuromuscular junction.

A
  • Botulism: Botulinum toxin produces an irreversible disruption in stimulation-induced acetyl choline release by the pre-synaptic terminal
  • Myasthenia gravis (MG): Autoimmune disease caused by antibodies against Acetyl choline receptor
  • Lamber-Eaton myastenic syndrome (LEMS): Associated with lung cancer, but an autoimmune disease caused by antibodies directed against the voltage-gated calcium channel
111
Q

Outline the features of Myasthenia Gravis.

A
  • Autoimmune disorder, with antibodies for neuromuscular junction proteins
  • May be family history of other autoimmune disease
  • Causes fatigable weakness (more pronounced with use) and may affect the occular, bulbar (related to medulla oblongata), respiratory or limb muscles
  • Antibodies detected in 90% of cases, electromyography (EMG) will confirm diagnosis
  • Enlargement of thymus is often seen in younger patients, and a tumour in older ones.
  • Symptomatic treatment with Pyridostigmine, immune suppression with steroids. In sever cases plasma exchange removes antibodies from blood allowing rapid improvement
  • Thymectomy is therapeutic for younger patient and removal of tumour for old
112
Q

What is Neurotransmission?

A

Information transfer across the synapse requires release of neurotransmitters and their interaction with post-synaptic receptors.

113
Q

What is the size of the synaptic cleft?

A

About 20-100 nm

114
Q

What are the 3 stages of Synaptic transmission?

A
  1. Biosynthesis, packaging and release of neurotransmitter (T)
  2. Receptor action
  3. Inactivation
115
Q

Describe how neurotransmitters are diverse.

A
  • Varied transmitters and receptors
  • Most important: Amino acids (e.g. glutamate, GABA, glycine)
  • Amines: noradrenaline, dopamine
  • Neuropeptided: opiod peptides
  • May mediate rapidly ( µs-ms) e.g. amino acid or slower (ms)
  • Vary in abundance from millimolar (amino acid), micromolar (amines) to nanomolar (peptides) CNS tissue concentrations
  • Receive multiple transmitter influences which are intergrated to produce different functional responses
116
Q

Describe the pathway of neurotransmitter.

A
  • Action potential causes depolarization in the pre-synaptic neuron
  • Causes voltage-gated calcium channels to open, and Ca2+ to enter
  • This causes vesicles to fuse with membrane and release neurotransmitters
  • Binds to receptors and opens Na+ channels resulting in depolarization in post-synaptic neuron
  • Transmitter must be removed through transporters in the pre-synaptic membrane which takes it up. (Or for acetyl choline, acetyl choline esterase breaks it down in the cleft)
  • Transmitter is then stored in vesicles to be used again
117
Q

What are the essential components of synaptic transmission?

A
  • Only take place at synapse (localised)
  • Fast: within ms (200 µs)
  • Increase in intracellular Ca2+ is essential for release
  • Synaptic vesicles provide the source of neurotransmitter (4000-10,000 molecules per vesicle)
118
Q

Describe the rapid release of neurotransmitters.

A
  • Vesicles have vesicular proteins in their membrane
  • Presynaptic membrane also contains proteins
  • Interaction between these proteins allowed docking of the vesicles in the active zone, ready to be released
  • Ca2+ channels and vesicles lined up together
  • Ca2+ entry activates a Ca2+ sensor in the protein complex of the vesicles
  • Exocytosis of the vesicle
119
Q

Name toxins which target Vesicular proteins.

A
  • Tetanus toxin C. tetani causes paralysis. It degrades a protein, inhibiting transmitter release.
  • Botulinum toxin causes flaccid paralysis (weakness).
  • α-Latrotoxin (from a black widow spider) stimulates transmitter release until depletion.
120
Q

What is needed for transmitter release within the cell?

A
  • Transmitter containing vesicles must be docked on teh pre-synaptic memrane
  • Protein complex formation between vesicle, membrane and cytoplasmic proteins to enable both vesicle docking and a rapid response to Ca2+ entry leading to membrane fusion and exocytosis
  • ATP and vesicle recycling
121
Q

Describe the receptor action of neurotransmitters.

A

Defined by receptor kinetics

  • Ion channel receptors: Fast (ms), mediate all fast, excitatory and inhibitory transmission, e.g. Na+
    e. g. CNS - Glutamate, GABA. NMJ - Acetyl choline at nicotinic receptors
  • G-protein coupled receptors: Slow (secs/mins), effectors may be enzymes (adenyl cyclase, phospholipase C, cGMP-PDE) or channels (e.g. Ca2+ or K+)
    e. g. CNS+PNS - Acetyl choline at muscarinic receptors, dopamine, noradrenaline, 5-hydroxytryptamine (5HT) and neuropeptides e.g. enkephalin
122
Q

Give some features of Ion channel-linked receptors. (with examples)

A
  • Rapid activation
  • Diverse and rapid information flow
  • Multiple subunit combinations-distinct functional properties
    Examples: Nicotinic cholinergic receptors (nACh), glutamate - Na+ (GLU), GABA - Cl-, glycine - Cl-
123
Q

What are the two effects of neurotransmitter?

A
  • Excitatory: depolarization

- Inhibitory repolarization/hyperpolarization

124
Q

What are the types of Glutamate receptors?

A
  • AMPA receptors: majority of fast excitatory synapses, rapid onset, offset and desensitisation. Na+ channel.
  • NMDA receptors: Slow component of excitatory transmission. Serve as coincidence detectors which underlie learning mechanisms. Na+ and Ca+ channel therefore increase chance of depolarization.
125
Q

What is glutamate made from?

A

Glucose (α-ketoglutarate from TCA cycle)

126
Q

How is glutamate inactivated at the synapse?

A
  • Taken up by transporter proteins (excitatory amino acid transporters) in the membranes of the pre-synaptic neuron and nearby glial cells.
  • Glial transporter removes about 80% of transmitter
  • Glutamate is made inactive by Glutamine synthetase to produce Glutamine
127
Q

What is the relationship between epilepsy and glutamate?

A
  • Excess glutamate is associated with epilepsy

- Abnormal and frequent cell firing

128
Q

What is epilepsy?

A

Common neurological condition characterised by recurrent seizures due to abnormal neuronal excitability (leads to elevated glutamate release).

129
Q

Describe the inhibitory effect of GABA.

A
  • Gamma amino butyruc acid (GABA)
  • Released into cleft
  • Binds to GABA receptor, causes Cl- influx into post-synaptic neuron
  • Taken up by GABA transporter (GAT)in the membranes of the pre-synaptic neuron and glial cells
  • GABA trans-aminase (GABA-T) Produces Succinate semialdehyde which is neurologically inactive

Used pharmacologically to inhibit excitation of neurons e.g. in treating epilepsy or anxiety.

130
Q

How do drugs which target GABA receptors work?

A

Two main types: Barbiturates and Benzodiazepines

  • GABA receptors are made up of 5 sub-units
  • The drugs target allosteric sites which modulate the activity of the channel
  • Benzodiazepines increase the frequency of the Cl- channel opening
  • Barbiturates increase the duration that they’re open
131
Q

Describe the treatment of epilepsy.

A
  • Focussed on lessening excitatory activity be facilitating inhibitory transmission
  • Main: act through Na+ channel and modulate the release of glutamate
  • New: target GABA synapse
132
Q

What are the functions of the brainstem?

A
  • Controls vital functions e.g. respiration, cardiovascular function
  • Cranial nerves provide sensory and motor innervation to the head
  • Ascending and descending pathways connect the spinal cord with the forebrain
133
Q

What are the functions of the cerebellum?

A
  • Coordinates movement

- Involved in learning motor skills

134
Q

What are the functions of the diencephalon?

A
  • Contains several nuclei with different functions
  • Thalamus acts as a relay station for the cerebral cortex
  • Hypothalamus coordinates homeostatic mechanisms e.g. appetite centre to provoke hunger if low blood glucose
135
Q

What are the functions of the diencephalon?

A
  • Basal ganglia: involved in control of movement
  • Cerebral cortex: involved in all functions
  • Corpus callosum: interconnects corresponding parts of 2 hemispheres acros midline
136
Q

What are the cortical lobes?

A
  • Frontal lobe (anterior)
  • Parietal lobe
  • Occipital lobe (posterior)
  • Temporal lobe (sides)
137
Q

Which Sulci are seen in every brain, and have an important role?

A

Sulci (crevices) are used to divide the brain into lobes.

  • Central sulcus separates frontal and parietal lobe
  • Lateral sulcus separates frontal and temporal, and parietal and temporal
  • Parieto-occipital sulcus separates parietal and occipital
138
Q

What are the two functional divisions of the cortex?

A
  • Primary cortex: Normally small areas, with tight organisation of cells which relate to a specific function in the body.
  • Association cortex: Organised differently to primary cortex, involved in higher levels of analysis e.g. perception, learning, decision making etc
139
Q

Give some examples of primary cortical areas.

A

Bilateral areas (same on both hemispheres):

  • Primary motor cortex: Anterior to central sulcus (in frontal lobe). Along the strip each area is responsible for voluntary motor control of different muscles with a contralateral relationship
  • Primary somatosensory cortex: Posterior to central sulcus (in parietal lobe). Along the strip each area receives sensory information from different parts of the body with a contralateral relationship.
  • Primary auditory cortex: In temporal lobe. Receives information from the ears and analyses it to perceive it as sound.
  • Primary visual cortex: Posterior, in occipital lobe. Recieves input from retina and produces an image.

Only on left hemisphere: not technically primary areas

  • Wernicke’s area: Important for understanding language
  • Broca’s area: Important for formulating speech
140
Q

Describe the ventricular system in the brain.

A
  • Inter-connective spaces which contain cerebrospinal fluid
  • Can be divided into parts which supply the different parts of the brain
  • ‘C’ shaped lateral ventricle, each lies in one of the hemispheres
  • Third ventricle bisects the diencephalon
  • Aqueduct goes through midbrain
  • Fourth ventricle goes into the pons
  • In the medulla it narrows to form the central canal and then continues into the spinal cord.
141
Q

What is the function of the ventricular system?

A
  • Contain vascular glands called the Choroid plexus
  • Filters blood; takes most of the cells out and changes the ionic content to produce CSF
  • Continuous process in all of the ventricles
  • CSF then circulates through ventricular system and sub-arachnoid space between membranes covering the brain (meninges)
  • CSF exits through the holes in the fourth ventricle and goes around the outside of the brain
  • The fluid protects the brain from damage inside the skull
  • It is reabsorbed into the venous sinuses via arachnoid villi
142
Q

What are the layers of the meninges?

A
  • Dura mater: very tough connective tissue, attaches to the inside of the bone
  • Arachnoid mater: finer membrane
  • Pia mater: very fine, attaches to surface of the cortex

Between the Arachnoid mater and the pia mater there is the sub-arachnoid space which is where the CSF flows through.

143
Q

Describe the reabsorption of the CSF into the venous sinuses.

A
  • On the surface of the brain there are venous sinuses which feed into the venous system
  • Pockets of arachnoid membrane which push through the dura mater into the sinuses
  • CSF is reabsorbed into the venous system
144
Q

What is hydrocephalus? How could it be caused?

A
  • Build up of fluid in the cranial cavity
  • A blockage in the ventricular system or of the reabsorption (e.g. due to infection) would raise the pressure in the cranial cavity
145
Q

What is an electromyography (EMG)?

A
  • Recording of the action potentials occurring in skeletal muscle fibres
  • Extracellular recording: Both electrodes are outside muscle fibres
  • Record the emf (potential) between 2 locations, both outside the cells
146
Q

Give examples of extracellular recording.

A
  • ECG/EKG (electrocardiogram): recording action potentials from the hear. Electrodes on limbs, or chest
  • EEG (electroencephalogram): recording action potentials from the brain. Electrodes on the scalp.
147
Q

What is an intracellular recording?

A
  • When one electrode is inside the cell

- The measurements is of emf (potential) between the inside and out.

148
Q

What is an extracellular recording?

A
  • When both electrodes are outside the muscle fibres
  • The measurement is of emf (potential) between 2 sites outside the fibres
  • There is a deflection at the first electrode, and inflection at the 2nd
149
Q

What are the parts of the body which are involved in an EMG?

A
  • Muscles: Thenar group (used in thumb movement) to record activity.
  • Nerves: Ulna, medial (middle of arm) and radial. A stimulus of the medial nerve at the elbow will cause the thumb to twitch.
150
Q

What would be seen in the EMG for voluntary contraction in the hand?

A

Increase in EMG and force then decrease when it stops.

151
Q

What is the relationship between stimulus, EMG and twitch force?

A

As stimulus increases both EMG and twitch force increases.

152
Q

What factors affect the length of time between the stimulus and the twitch in an EMG?

A
  • The nerve conduction velocity

- The distance between the place of stimulus and electrode

153
Q

What is tetanus? How does it appear in a EMG?

A
  • Tetanus: A repeated increase in force/maintenance of force due to repeated stimuli
    /~~~~~| increase which is sustained due to summation
154
Q

Define twitch.

A

An increase in force produced from a single stimulus.

155
Q

Define summation.

A

The process of adding single twitches together, where one twitch does not stop before the next starts. Leads to tetanic contraction.

156
Q

What are the types of tetanus?

A
  • Unfused: Can see ‘ripples’ as there is some relaxation between twitches
  • Fused: Smooth sustained contraction, no relaxation between twitches
157
Q

How does the frequency of a stimulus affect contraction?

A

Increased frequency mean increased contraction, until a point where you get summation causing tetany.

158
Q

What is the difference in EMG for voluntary contraction and during electrical stimulation?

A
  • In electrical stimulation there is relaxation between stimuli whereas in voluntary contraction it is continuous and from different nerves
  • Voluntary contraction is irregular/asynchronous as it’s lots of action potentials from lots of nerves
159
Q

What are the branches of the autonomic nervous system?

A

Sympathetic: Fight and flight

Parasympathetic: Rest and digest

160
Q

List some actions of the sympathetic nervous system.

A
  • Pupil dilation
  • Trachea and Bronchiole dilation
  • Glycogenolysis and Gluconeogenesis in the liver
  • Lipolysis of adipose
  • Increased renin secreteion in the kidney
  • Relaxes detrussor; constriction of trigone and sphincter in ureters and bladder
  • Stimulates thick, viscous secretion in salivary gland (immune system)
  • Piloerection, increased sweating in skin
  • Increased heart rate and contractility
  • Decreased motility and tone, sphincter contraction (gastrointestinal)
  • Dilation of blood vessels to skeletal muscle
  • Constriction of blood vessels to skin, mucous membranes and splanchnic area
161
Q

List some actions of the parasympathetic nervous system.

A
  • Pupil constriction, contraction of ciliary muscle
  • Constriction of trachea and bronchioles
  • Contraction of detrussor; relaxation of trigone and sphincter
  • Stimulates copious, watery secretion (digestion)
  • Decreased heart rate and contractility
  • Increased motility and tone, secretions of intestines
162
Q

Outline the organisation of the parasympathetic nervous system.

A
  • Originate from either the cranial region i.e. brainstem or sacral region of the spinal cord
  • Cranio-sacral outflow
  • E.g Occulomotor, Facial, Glossopharyngeal Vagus, Splanchnic
163
Q

Describe the general organisation of neurons in the Parasympathetic nervous system.

A
  • Pre-ganglionic fibres: Exit spinal cord. Usually very long and myelinated.
  • Synapse at ganglion. Usually close to the target.
  • Post-ganglionic fibres: Exit ganglion and synapses with effector organ. Usually very short.
164
Q

What neurotransmitter is associated with the PNS?

A

Acetyl choline, released from both post-ganglionic and pre-ganglionic neurons.

165
Q

Outline the organisation of the sympathetic nervous system.

A
  • Nerves originate from the thoracolumbar region (T1 - L1/2)
  • Thoracolumbar outflow
  • Originate from lateral horn of the grey matter in the spinal cord
  • Join together in the sympathetic trunk found either side of the vertebra
166
Q

Describe the general organisation of neurons in the Sympathetic nervous system.

A
  • Pre-ganglionic fibres: Exit spinal cord. Usually very short. Tend to branch out and influence many post-ganglionic fibres.
  • Synapse at ganglion, in the sympathetic trunk.
  • Post-ganglionic fibres: Synapse with effector organ, usually has many branches. Usually very long.
167
Q

What neurotransmitter is associated with the SNS?

A
  • Pre-ganglionic releases Acetyl choline.
  • Post-sympathetic releases Noradrenaline

Exceptions:

  • Adrenal gland only has one nerve (no ganglion). The Adrenal medulla then releases Adrenaline.
  • Some sympathetic nerves have post-ganglionic fibres release acetyl choline e.g. sweat gland
168
Q

What is the difference between the actions of the PNS and SNS?

A
  • PNS is localised i.e. one nerve stimulates on effector organ
  • SNS is coordinated response i.e. more that one effector organ stimulated (e.g. stress response)
169
Q

Describe the autonomic control of blood pressure.

A
  • Sensory input by baroreceptors (in carotid sinus and aortic arch)
  • An increase in BP means more stretch, so increased firing through afferent nerve
  • The information is sent to the brainstem
  • Parasympathetic nerve is stimulated more to decrease the heart rate and contractility.
  • Sympathetic nervous system is inhibited more, generalised vasodilation
  • A decrease in BP means less stretch, so decreased firing through afferent nerve
  • Parasympathetic nerve is stimulated less
  • Sympathetic nerve is inhibited less to increase heart rate and contractility, and stimulates arterioles to constrict and stimulates the release of adrenalin from the adrenal medulla
170
Q

In what ways are blood pressure changed by the ANS?

A
  • Ionotropically: force of muscular contraction
  • Chronotropically: change heart rate
  • Change total peripheral resistance by contriction or dilation

BP=COxTPR and CO=HRxSV

171
Q

Describe the exceptions to the control of the ANS and vasodilation of blood vessels.

A
  • Increased sympathetic activity to some blood vessels in skeletal muscle (either cholinergic fibres, or have adrenergic β-receptors
  • Local vasodilation (e.g. Co2, increased [H+], nitric oxide, histamine etc.)
  • Increased parasympathetic stimulation to certain blood vessels to discrete glands, organs (e.g. penis)
172
Q

Describe the autonomic control of the Gastrointestinal tract.

A
  • Enteric nervous system: Submucosal and myenteric plexus acts as a ‘brain’
  • Autonomic nervous system can influence it, but it is very complex so other factors are important in its control e.g. sensory neurons inside lumen
  • Sympathetic decreases motility and tone, stimulated contraction of sphincters and inhibits secretory activity
  • Parasympathetic increases motility and tone, causes relaxation of sphincters and stimulated secretory activity
173
Q

Describe the autonomic control of the lungs.

A
  • Parasympathetic nerve innervates it but no sympathetic
  • Nerve projects into the bronchioles, and causes constriction when acetyl choline is released
  • Sympathetic nervous system stimulates dilation via noradrenalin/adrenaline from the adrenals which pass through the blood and bind to receptors
174
Q

Describe the autonomic control of the Eyes.

A
  • Iris muscles controls the amount of opening of the pupil
  • Circular muscle is under parasympathetic control, so when it stimulates contraction the pupil constricts
  • Radial muscle under sympathetic control, so when it stimulates contraction the pupil dilates
  • Important for modifying pupil diameter as a reflex reaction to light
  • Ciliary muscle under parasympathetic control. Contracts the muscle, allowing lens to bulge for near vision. For far vision PNS stops/slows firing to relax ciliary muscle.
175
Q

Describe the autonomic control of the Bladder.

A
  • Parasympathetic nerve from sacral region, which controls the detrussor muscle. Wants to empty bladder. (main influence)
  • Sympathetic nervous system innervates the internal sphincter. Want to keep bladder shut,
  • Voluntary motor nerves innervate external sphincter
    Reflex response:
  • Pressure builds, micturition reflex activates parasympathetic nerve, causing contraction of detrussor muscles (contraction of bladder), inhibits sympathetic nerve causing internal sphincter to relax and open.
  • Voluntary control allows emptying of bladder.
176
Q

What neurotransmitters are used by the ANS?

A
  • Acetyl choline
  • Noradrenaline (norepinephrine)
  • Adrenaline (epinephrine) (By adrenal gland only)
177
Q

What are the receptors in the the ANS for acetyl choline?

A
  • Muscarinic: within the target organ. Binding of ACh to a G-protein coupled receptor. Response within seconds.
  • Nicotinic: within the ganglion. Binding of ACh causes opening of an ion channel and activates the post-ganglionic receptor. Response within milliseconds.
178
Q

What are the receptors in the ANS for noradrenaline?

A

Adrenoceptors: On effector organs.

  • α1, α2, β1, β2 subtypes
  • Present on different tissues and binding leads to different actions
  • G-protein coupled receptor
179
Q

Describe the synthesis, release and metabolism of amine transmitters.

A
  • Precursor molecule enzymatically converted to neurotransmitter
  • Load transmitter into vesicles
  • Vesicles dock at membrane
  • Action potential causes Ca2+ influx
  • Allows exocytosis of vesicle; fuses with membrane and deposits transmitter in synapse
  • When transmitter binds to receptor it’s activated
  • Removal of transmitter; breakdown
180
Q

Describe the synthesis, release and metabolism of Acetylcholine.

A
  1. Acetyl Co A and choline form ester bond (enzyme choline acetyl transferase)
  2. ACh packaged into vesicles
  3. Action potential causes vesicle exocytosis
  4. ACh in cleft binds to receptor
  5. Acetylcholinesterase breaks down ACh into Choline and acetate
  6. Uptake into pre-synaptic neuron
181
Q

Describe the synthesis, release and metabolism of Noradrenaline.

A
  1. Tyrosine to DOPA (by tyrosine hydroxylase), then DOPA to dopamine (by DOPA decarboxylase).
  2. DOPA is put into vesicles and converted to Noradrenaline by Dopamine β-hydroxylase
  3. Action potentia causes Ca2+ influx and allows exocytosis of vesicle
  4. Noradrenaline acts on receptor producing response
  5. 2 uptake methods: Uptake 1: protein which transports NA from cleft to pre-synaptic neuron, Uptake 2: protein which transports NA from cleft to other cells.
  6. Broken down after removal from synapse by Monoamine oxidase A (MAO-A) in the pre-synaptic neuron, and COMT (chatecholomethyl transferase) in other cells
182
Q

Describe the synthesis, release and metabolism of Adrenaline.

A
  • Produced by Chromaffine cells when stimulated by ACh from sympathetic ‘pre-ganglionic’ fibres in the Adrenal gland, secreted into blood
  • Same as Noradrenaline process except Noradrenaline is released from vesicle and enters another vesicle with Phenylethanolamine methyl transferase which converts it to Adrenaline.
  • Secreted into the interstitial space, and then adrenaline diffuses into the nearest capillary
183
Q

What does the adrenal medulla produce?

A

80% adrenaline

20% noradrenaline

184
Q

What is the effect of cortisol on the adrenal medulla?

A
  • Cortisol produced by the adrenal cortex diffuses through medulla
  • Upregulates the phenylethanolamine methyl transferase, therefore increases Chromaffine cell ability to produce adrenaline
185
Q

What type of effect does the sympathetic and parasympathetic response?

A

Sympathetic:

  • Diffuse system which allows stimulation of multiple body parts (MASS DISCHARGE)
  • Can also have more discrete effects

Parasympathetic:
- Relatively discrete system innervating individual target tissues via specific nerves

186
Q

Describe the Sympatho-adrenal system in the response to acute stress.

A

Stress perceived by hypothalamus, sends impulses through sympathetic nerves to…
- Adrenal medulla: produces adrenaline
- Sympathetic nerve terminals: produce noradrenaline
Causes:
- increased heart rate and contractility (increased CO)
- increased stimulation and vasodilation to brain, more activity so more alert
- constriction of blood vessels in skin and kidneys, dilation of blood vessels to muscle and brain to allow for more activity e.g. running
- glycogenolysis to raise blood sugar level (for energy)

187
Q

Outline the mechanism for transient postural hypotension.

A
  • When gaining upright posture gravity causes pooling of blood in veins of lower limbs (due to its compliance)
  • Decreased venous return (therefore lower CO, and decrease BP)
  • Decreased stimulation of baroreceptors, means decreased inhibition of sympathetic nervous system
  • Sympathetic activity increases heart rate, contractility, and vasocontriction
  • Blood pressure return to normal
188
Q

What impairs the postural hypotension reflex?

A

Age: the older you get there is intolerance to the reflex
Some individuals have intolerance due to hormonal imbalance at puberty
Disorders such as parkinson’s

189
Q

What happens in postural hypotension?

A
  • Sympathetic nervous activity is not enough to increase the cardiac output
  • Low BP
  • Decreased cerebral blood flow
  • Can cause dizziness and fainting
  • Once supine (horizontal), blood flow to the brain is restored, and conciousness is regained
190
Q

Outline the parasympathetic control of the pupil.

A
  • Through occulomotor nerve (CN III), cillary ganglion and shorter post-ganglionic fibre
  • Parasympathetic activity decreases pupil diametre
  • Activation of parasympathetic (e.g. drug pilocarpine) decreases pupil size (miosis)
  • Blocking parasympathetic receptors (e.g. drug atropine) increases pupil size (mydriasis)
191
Q

Outline the light reflex.

A
  • Stimulus e.g light in eye
  • Sensory input by optic nerve (CN II) detects level of light
  • Pre-ganglionic fibre originates from Edinger-Westphal nucleus (Occulomotor nerve)
  • Ciliary ganglion is where post-ganglionic nerve originates
  • PNS stimulation causes miosis (pupil constriction)
192
Q

Outline the consensual reflex.

A
  • A light reflex initiated in one eye will cause a response in both
  • Sensory information relayed to the brain, activates the Occulomotor nerve to both eyes
193
Q

Describe the central control of the autonomic nervous system.

A
  • Higher brain centres (e.g. cortex) and homeostatic changes feedback to hypothalamus
  • Hypothalamus stimulated medulla
  • Medulla outputs to the PNS and SNS
194
Q

What is the difference between the position of the ganglia in the ANS?

A
  • PNS: ganglia close to and even on target organs

- SNS: ganglia in sympathetic trunks, either side of vertebrae

195
Q

What are the possible pathways of a pre-ganglionic fibre entering the sympathetic trunk?

A
  • Synapse within the ganglion
  • Send fibres up or down to other ganglia
  • Go through ganglia (through splanchnic nerves) to disperse into the body to subsidiary ganglia

Post-ganglionic fibres distributes to effector organ via grey rami communicantes

196
Q

Describe the distribution of the sympathetic trunks.

A
  • Goes from base of the skull to coccyx
  • 3 ganglia in the cervical region
  • 11/12 ganglia in the thoracic region
  • 4/5 ganglia in the lumbar region
  • 4/5 ganglia in the pelvis
197
Q

Describe the sympathetic innervation in the cervical and thoracic region.

A

Cervical:

  • plexus around pharynx
  • cardiac plexus
  • thyroid plexus
  • pulmonary plexus

Thoracic:

  • plexus around thoracic aorta
  • splanchnic nerve originate then travel to and through thee diaphragm
198
Q

What is the distribution of the SNS cervical ganglia?

A
  • Follow the main blood vessels

- Superior, middle and inferior ganglia

199
Q

Describe the distribution of the SNS lumbar ganglia.

A
  • 4 lumbar ganglia

- Lumbar splanchnic nerves take part in all plexi of sympathetic nerves in abdominal and pelvic regions

200
Q

Describe the distribution of the PNS in Sacral outflow.

A
  • Anterior rami of S2-4
  • Visceral branches passing directly to pelvic viscera i.e. pelvic splanchnic nerve
  • Minute ganglia in wall of viscera giving rise to post-ganglionic fibres
201
Q

Describe the innervation of the PNS Pelvic splanchnic nerves.

A
  • Motor fibres to rectum
  • Motor fibres to bladder wall
  • Inhibitory fibres to bladder sphincter
  • Erection of penis/clitoris via vasodilator fibres
  • Fibres also pass superiorly to supply large part of the gut with visceromotor innervation.
202
Q

Describe the parasympathetic nerves which originate in the cranial region.

A
  • Oculomotor nerve (CN III):
    Ciliary ganglion - post-ganglionic fibres to sphincter pupillae and ciliary muscle inside eye. (Involved in constriction of pupil)
  • Facial nerve (CN VII):
    Sub-mandibular ganglion - post-ganglionic fibres to sub-mandibular and sub-lingual salivary glands. (promotes salivation)
    Pterygopalatine ganglion - post-ganglionic fibres to paranasal sinuses and lacrimal glands. (promotes tearing)
  • Glossopharyngeal nerve (CN IX):
    Otic ganglion - post-ganglionic fibres to parotid gland. (promotes salivation)
  • Vagus nerve (CN X):
    Enters neck and thorax via carotid sheath
    Branches to lungs, heart, oesophagus, stomach and intestines
203
Q

Outline the features of the Enteric nervous system.

A
  • In wall of alimentary tract
  • Sensory: monitoring of mechanical, chemical and hormonal activity of the gut
  • Motor: gut motility, secretion, vessel tone
  • Can be overridden by sympathetic and parasympathetic systems but has some autonomy