neuro physiology Flashcards

1
Q

Skeletal Muscle Contraction
What is the sequence of events in the contraction of a skeletal muscle fibre,
starting at the motor end plate?

A

● Discharge of a motor neuron
● Release of preformed acetylcholine at the motor endplate via exocytosis
● Diffusion of Ach across the synaptic cleft
● Binding of Ach to postsynaptic nicotinic Ach receptors
● Increase Na and K conductance in the end plate membrane
● Generation of the end plate potential
● Generation of action potential in muscle fibres
● Inward spread of depolarisation along the T tubules
● Release of Ca from terminal cisterns of the sarcoplasmic reticulum and diffusion
to thick and thin filaments
● Binding of calcium to troponin C, uncovering myosin binding sites on actin
● Formation of cross linkages between actin and myosin and sliding of thin on thick
filaments, producing movement

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2
Q

What is the sequence of events in relaxation of a skeletal muscle fibre

A

● Calcium is pumped back into the sarcoplasmic reticulum
● Release of calcium from troponin
● Cessation of interaction between actin and myosin

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3
Q

How does a tetanic contraction occur?

A

● The contractile mechanism has no refractory period
● Repeated stimulation before relaxation has occurred leads to a summation of
contractions fast repeated stimulation causes a fused continuous tetanic
contraction which can be complete or incomplete

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4
Q

Smooth Muscle Contraction
Describe the sequence of events in contraction and relaxation of visceral smooth
muscle

A

● Binding of Ach to muscarinic receptors
● Increased influx of calcium into the cell
● Activation of calmodulin – dependent myosin light chain kinase
● Phosphorylation of myosin
● Increased myosin ATPase activity and binding of myosin to actin
● Contraction
● Dephosphorylation of myosin light chain phosphatase
● Relaxation or sustained contraction

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5
Q

What factors influence intestinal smooth muscle contraction?

A

● Stretch of smooth muscle causes contraction in the absence of innervation
● Cold increases the activity
● Ach decreases smooth muscle potential and increases spike frequency resulting
in more active muscle
● Adrenaline and noradrenaline increase smooth muscle potential and decrease
spike frequency causing decreased muscle activity
● Neural mechanisms

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6
Q

Cholinergic transmission
Please describe the synthesis, release and action of acetylcholine at the nerve
synapse

A

● Choline is synthesised in neurons and actively taken into cholinergic neuron
● Acetyl CoA and choline are used to form acetylcholine via choline
acetyltransferase
● This is packaged in synaptic vesicles via transporter
● When the nerve is stimulated, the vesicles execytose the Ach into the synaptic
cleft, where it binds the postsynaptic Ach receptor

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7
Q

Once released into the synaptic cleft, how is its effect terminated?

A

● Diffusion
● Catabolism by pseudocholinesterase in the circulation
● Acetylcholinesterase on the postsynaptic membrane
● Reuptake of choline into the presynaptic nerve terminal

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8
Q

Describe the differences between the two different types of acetylcholine
receptors

A

● Divided into nicotinic and muscarinic
● Muscarinic – actions mimicked by muscarine and blocked by atropine. Found in
smooth muscle, glands and brain. G protein coupled receptors.
● Nicotinic – actions mimicked by nicotine, found in the NMJ, autonomic ganglia
and the central nervous system. They are ligand gated sodium ion channels.

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9
Q

Adrenergic transmission
Which catecholamines act as neurotransmitters?

A

● Noradrenaline
● Adrenaline
● Dopamine

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10
Q

Outline the biosynthesis of adrenaline

A

● Starts with tyrosine, converted to DOPA via tyrosine hydroxylase
● DOPA is converted to dopamine byb dopa decarboxylase
● Dopamine to noradrenaline by dopamine hydroxylase
● Norad to adrenaline via phenylethanolamine methyltransferase

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11
Q

Describe the sequence of events at the noradrenergic synapse, following
stimulation of a sympathetic nerve

A

● Noradrenaline is stored in granulated vesicles in the nerve
● Released into the synaptic cleft by exocytosis once is is stimulated
● Acts on postsynaptic receptors
● Action is terminated in 2 ways:
○ Reuptake to the presynaptic neuron then metabolised by MAO to inactive
derivatives
○ Catabolised in the synaptic cleft by COMT

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12
Q

Nerve action potential
Define resting membrane potential of a neuron

A

● The potential difference across a cell at rest, as a result of separation of positive
and negative electrical charges across a cell membrane.
● Inside is negative relative to outside.
● The normal RMP is -70mV in a neuron.

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13
Q

How is the resting membrane potential generated?

A

● Main ions involved are K and Na
● The Na/K ATPase creates an electrochemical gradient by pumping out 3 Na for
every 2 K in
● Na and K diffuse down their concentration gradient across a semipermeable
membrane (K wants to go out, Na wants to come in)
● The cell membrane is more permeable to K at rest – which is why the RMP is
close to the equilibrium potential for K

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14
Q

Why is a cell more excitable in hyperkalaemia?

A

RMP moves closer to the threshold potential for eliciting an action potential (it becomes
less negative on the inside of the cell)

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15
Q

Please draw a nerve action potential and indicate the sequence of events that
occur
Key Points you must include:

A

● Starts at -70mV
● After a depolarising stimulus occurs, voltage gated Na channels become active
and Na enters the cell
● When the threshold potential is reached (-55mV) , the voltage gated Na channels
overwhelm the K channels
● Entry of Na causes opening of more voltage gated Na channels and further
depolarisation in a positive feedback loop, causing the upstroke of the action
potential (peaks at +35mV)
● Voltage gated Na channels enter an inactivated state for a few milliseconds
before returning to the resting state, this inhibits further Na movement
● The reversal of membrane potential causes opening of voltage gated K channels,
resulting in repolarisation via K efflux and the end of the AP
● Slow return of K channels causes hyperpolarisation (below -70mV)
● Over time this is corrected and the cell returns to resting membrane potential

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16
Q

Nerve Conduction
Where are ion channels distributed in myelinated neurons?

A

Concentrated in the nodes of ranvier, Na channels are flanked by K channels

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17
Q

What factors affect conduction?

A

● Myelinated is quicker than demyelinated
● Size
● Direction of conduction

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18
Q

In the synapse, where can inhibition occur?

A

● Post synaptic – via direct or indirect inhibition (i.e. refractory periods or after
hyperpolarisations)
● Pre-synaptic – mediated by neurons that end on excitatory endings (axo-axonal
synapses)

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19
Q

What mechanisms are involved in inhibitation?

A

● Increased Cl conductance (reduced Ca influx and the amount of excitatory
transmitter release)
● Voltage gated K channels – K also decreases Ca entry
● Direct inhibition regardless of Ca

20
Q

Serotonergic Transmission
What are the functions of serotonin?

A

● Regulation of the vomiting reflex
● Regulation of mood
● Control of respiration
● Platelet aggregation and smooth muscle contraction
● GI secretion and peristalsis
● Regulation of circadian rhythms

21
Q

What are the steps in the synthesis and catabolism of serotonin?

A

● Hydroxylation and decarboxylation of tryptophan to form serotonin
● Released serotonin from serotonergic neurons is recaptured by an active
re-uptake mechanism and inactivated by MAO to form metabolite 5HIAA (5
hydroxy indoleacetic acid) – which is secreted in the urine

22
Q

Hearing (from 2013)
What are the two major mechanisms of deafness?

A

● Conductive deafness – due to impaired sound transmission in the external or
middle ear, affects all frequencies. Examples: wax, perforated TM, otitis media
● Sensorineural deafness – due to loss of cochlear hair cells (most common) or
problems with CNVIII or within central auditory pathways. Only affects some
frequencies. Examples: noise exposure, aminoglycosides

23
Q

How can you differentiate between them? (sensory and conductive hearing)

A

Weber and Rinne can both be done using a 512hertz tuning fork
Weber - place on the forehead, rinne on the mastoid

24
Q

Temperature Regulation
What is the body’s response to hot and cold environments?

A

Mechanisms activated by cold (posterior hypothalamus)
- Increased heat production: shivering, hunger, voluntary activity, noradrenaline
and adrenaline release
- Decreased heat loss: skin vasoconstriction, curling up, body hair stands on
end

Mechanisms activated by heat:
- Decreased heat production: anorexia, apathy, inertia
- Increased heat loss: vasodulation, sweating, increased respiration

25
Q

What is nystagmus?

A

● Characteristic jerky movement of the eye seen at the start and end period of
rotation
● Different types - the direction of eye movement is identified by the direction of the
quick component
○ Horizontal
○ Vertical
○ Rotatory

26
Q

Why does nystagmus occur?

A

● There is a reflex that maintains visual fixation on stationary points while the body
rotates, though this is not initiated by visual impulses
● When rotation starts the eyes move slowly in the direction opposite to the
direction of rotation, maintaining visual fixation
● When the limit of this movement is reached, the eyes quickly snap back to a new
fixation point and then again move slowly in the other direction

27
Q

How is nystagmus mediated?

A

● Slow component initiated by impulses from the labyrinths
● Quick component is triggered by a centre in the brain stem

28
Q

Optic pathways
Describe the neural connections of the visual pathways

A

● Begins with the retina
● Optic nerve
● Optic chiasm
● Optic tract
● Lateral geniculate body (in the thalamus)
● Then fibres to the primary visual cortex in the occipital lobe
● Other connections
○ The lateral geniculate nucleus also sends information to the pretectal
midbrain (to control papillary reflexes, eye movements)
○ To frontal cortex (refined eye movements, near point response)
○ Optic chiasm to thalamic suprachiasmatic nucleus (endocrine and
circadian responses to the day/night cycle)

29
Q

How is visual acuity measured?

A

Using a Snellen chart viewed at a distance of 6m (20 feet)

30
Q

What does a result of 6/24 mean?

A

Reduced visual acuity. Means that at 6m this person can see something they should be
able to see from 24m.

31
Q

Why is the fovea important for visual acuity?

A

● It is the point where visual acuity is the greatest
● Fovea is the centre of the macula, a thinned out, rod-free portion of the retina
where cones are densely packed and each synapses on a single bipolar cell
which, in turn, synapses on a ganglion cell, providing a pathway to the brain.

32
Q

What factors influence visual acuity?

A

● Optical factors: state of the image forming mechanisms e.g. presence of
cataracts, keratitis, astigmatism, myopia or hyperopia
● Retinal factors: the state of the cones,, affected by retinopathies, optic neuritis
● Stimulus factors e.g. illumination, brightness of the stimulus, contrast between
stimulus and background.

33
Q

Pain conduction
Describe how pain is transmitted from the periphery to the brain

A

● Sense organ - naked nerve endings
● Transmission via type 2 fibre types - small myelinated A-delta fibres or larger,
slower, unmyelinated c fibres.
● Spinal cord - both fibre groups end in the dorsal horn of the spinal cord
● From the spinal cord, fibres go to the brain via second order neurons in the
ventrolateral system to the thalamus
● then via third order neurons on to the cerebral cortex

34
Q

How can acute pain be modulated?

A

● Gate theory – stimulation of large touch/pressure afferents causes inhibition of
pain pathways in the dorsal horn of the spinal cord
● Stress induced analgesia i.e. in trauma
● Drugs i.e. opiates
● Higher centre interpretation and modulation

35
Q

What sites do opioid medications act on?

A

● Receptors in afferent nerve fibres, in the dorsal horn of the spinal cord and in the
periaqueductal grey matter of the brain

36
Q

What is referred pain?

A

● Irritation of a visceral organ which causes pain at a somatic site other than the
location of the stimulus
● Due to the somatic structure being from the same embryonic segment or
dermatome as the structure from which the pain originates
● i.e. arm pain in a myocardial infarction, the loin to groin pain of renal colic,
diaphragmatic pain referred to the shoulder

37
Q

Spinal Tracts
What are upper motor neurons?

A

Usually refers to corticospinal neurons that innervate spinal motor neurons.

38
Q

What clinical features can be seen when they are injured? (spinal tracts)

A

Damage initially causes muscles to become weak and flaccid but eventually leads to
spasticity, hypertonia, hyperactive stretch reflexes and abnormal plantar extensor reflex
(seen as an upgoing plantar reflex)

39
Q

What is the physiological basis for clonus?

A

There is a loss of descending cortical input to inhibitory neurons (called Renshaw cells),
therefore loss of inhibition of antagonists, resulting in a repetitive sequential contraction
of the ankle flexors and extensors

40
Q

Reflexes
Describe the components of the stretch reflex

A

● A monosynaptic reflex where skeletal muscle is stretched with contraction of the
muscle as a response.
● Sense organ is the muscle spindle impulse via an afferent nerve (monosynapse
on motor neurone) effector (intrafusal fibres)
● Example of this is the kneejerk reflex

41
Q

How is the stretch reflex different from the withdrawal reflex?

A

● Withdrawal is a polysynaptic reflex
● Has afferent and efferent limbs as in the stretch reflex. But the sensory organ is a
nociceptor and responds to painful stimulus
● The central integrator (between the afferent and efferent limbs) consists of
polysynaptic connections in the spinal cord
● Efferent limbs are motor nerves to effector muscles on the ipsilateral and
contralateral sides
● Flexion and withdrawal of the ipsilateral limb and extension of the contralateral
limb

42
Q

Thermoregulation
How is heat lost from the body?

A

● Radiation and conduction (70%)
● Vaporisation of sweat (27%)
● Respiration (2%)
● Urination/defacation (1%)

43
Q

How is fever produced in the body?

A

● Endotoxins, inflammation and other pyrogens that act on monocytes,
macrophages and other cells to produce cytokines (e.g. interleukins and TNF)
● Cytokines act on the pre-optic areas of the hypothalamus. Local release of
prostaglandins raises the set point

44
Q

Where is thirst regulated?

A

Hypothalamus

45
Q

What factors increase thirst?

A

● Increased osmotic pressure in the plasma – sensed by osmoreceptors in the
anterior hypothalamus
● Decreased ECF volume (i.e. in haemorrhage) – sensed by the baroreceptors in
the heart and blood vessels, increased renin which acts on central receptors to
increase thirst
● Psychological i.e. psychosis
● Others – habitual intake of liquids when eating, other GI hormones may influence
but this is poorly understood

46
Q

In what situations may thirst be blunted?

A

● Hypothalamic disease
● Direct head trauma
● Altered mental state
● Psychosis
● Lesion of the anterior communicating artery – supplies the hypothalamus
● High protein diet – promotes diuresis