Practicals Flashcards

1
Q

what is the neuromuscular junction made up of

A

the NMJ is made up of the axon terminal, synaptic cleft, and motor endplate of the muscle fiber.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

list the steps involved in neuromuscular transmission at the NMJ

A
  1. The arrival of an action potential in the axon terminal of the motor neuron opens voltage-sensitive calcium ion (Ca2+) channels
  2. This allows Ca2+ ions to enter the neuron.
  3. The influx of Ca2+ triggers vesicles that contain the neurotransmitter acetylcholine (ACh) to move to the synaptic membrane.
  4. Here, vesicles exocytose (release) ACh into the synaptic cleft.
  5. ACh diffuses across the synaptic cleft and binds to nicotinic ACh receptors (nAChR’s) on the motor end plate of the muscle membrane.
  6. As ACh binds, the ion-channel within the receptor opens and allows sodium ions (Na+) ions to flow into the muscle fiber.
  7. This influx of Na+ results in local depolarization of the motor endplate, and initiation of an action potential that flows along the muscle membrane.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is a motor unit

A

A single motor neuron, and all the muscle fibers that it innervates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe how muscle contraction is controlled by recruitment

A

Motor neurone + muscle fibre + action potential = twitch

recruitment = adjusting the number of motor axons firing
thus controlling the number of twitching muscle fibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe summation in muscle contraction

A

At stimulation intervals greater than 200 ms, intracellular [Ca2+] is restored to baseline levels between action potentials and the contraction consists of separate twitches

  • At stimulation intervals between 200 and 75 ms, [Ca2+] in the muscle is still above baseline levels when the next action potential arrives
  • Muscle hasn’t fully relaxed so the next contraction is even stronger than normal

this is an additive effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe tetanus and tetanic contraction in muscles

A
  • happens when the muscle has no time to relax between stimuli
  • leads to smooth contraction much stronger than a single twitch - tetanic contraction
  • tetanus is when muscle twitches occur so rapidly that they become indistinguishable from each other and causes smooth contraction
  • in health it is precisely controlled and graded so as to be able to lift heavy things but then also do fine things like writing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when might tetanus be bad - give some examples

A
  • In the case of poisoning by tetanus toxin, produced by the soil bacteria Clostridium Tetani, the release of inhibitory neurotransmitters in the neuromuscular junction is compromised and we get an uncontrolled tetanus
  • leads to spastic paralysis
  • symptoms of spastic paralysis:
    > rigid smile - risus sardonicus
    > lock jaw - trismus
    > arched back - opisthontus
  • spasms can be so strong that they can break bones and stop breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the symptoms of spastic paralysis

A
  • leads to spastic paralysis
  • symptoms of spastic paralysis:
    > rigid smile - risus sardonicus
    > lock jaw - trismus
    > arched back - opisthontus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe the sliding filament theory and cross bridge cycling

A
  • sliding filament theory = actin (thin) slides over myosin (thick) to produce contraction
  • actin and myosin stay same length throughout but the whole muscle shortens

Cross bridge cycling = how the myosin pulls the actin over it (the ‘sliding’ part):

  • impulse arrives at muscle
  • calcium released from sarcoplasmic reticulum of muscle fibre (The sarcoplasmic reticulum (SR) is a membrane-bound structure found within muscle cells that is similar to the endoplasmic reticulum in other cells. The main function of the SR is to store calcium ions (Ca2+).)
  • calcium binds to troponin on the actin
  • this displaces tropomyosin and exposes binding sites on the actin - myosin heads can now bind to these (tropomyosin covers the binding sites on the actin when the muscle is at rest - it is bound to troponin)
  • myosin heads covalently bind to the binding sites on the actin
  • power stroke then occurs - this is when ADP and Pi are released from the myosin head and it undergoes conformational change - this pulls the actin along
  • when ATP binds to the myosin head it releases the actin and returns to its original position
  • if there is enough calcium this process will repeat and the actin will be pulled past the myosin and muscle contraction will occur
  • when calcium concentrations decreased the tropomyosin reins to the actin and the contraction ends
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the visual range for humans

A

380 nm to 750 nm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

briefly describe the function and location of the two types of photoreceptive cells in the eye

A

CONES:

  • coloraturas differentiation
  • found in fovea ( region of highest visual acuity) ( often appears darker than surrounding retina)

RODS:

  • responsible for contrast (light and dark) resolution
  • rods not found in fovea but found everywhere else
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the optic disc

A

The optic disc where the nerves and retinal blood vessels enter and exit is devoid of receptors. Hence it is often referred to as the ‘blind spot’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is accommodation in the eye

A

Accommodation is the process in which the eyes see objects at different distances and maintain clear images of the objects by the convergence and divergence of light.

Light must pass through the pupil - its size is controlled by the iris - brighter light = smaller pupil

Then light passes through the lens - curvature controlled by ciliary muscles - adjusted so that light at diff distances can be properly focused on the retina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how far can humans see clearly

A

100m-200m - far point normally in this range too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is myopia and hyperopia

A

myopia:

  • short sightedness
  • The inability to focus light entering the eye from a distance object
  • lens is unable to flatten sufficiently to enable the light to be focused on the retina

Hyperopia:

  • long-sightedness
  • The inability of the lens to accommodate near objects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the normal near point in humans

A

30cm from the eye

17
Q

what 3 things is visual acuity dependent on

A

(i) the sharpness of the retinal focus within the eye
(ii) the health and functioning of the retina
(iii) the sensitivity of the interpretative faculty of the brain.

18
Q

how is visual acuity tested and how is it recored

A

Charts have been devised for clinical testing of VA using symbols (especially for kids) or letters of different sizes.

The tests are designed to be taken at a standard distance of 6m or 20 feet, with normal VA being signified by the abilty to differentiate a letter of a certain height (but more precisely the individual bars on that letter eg E vs B).

The number on the line of the chart equates to the distance at which someone with normal VA should be able to read the letters (eg 5-60m).

The bigger the writing, the further from the chart a person with normal VA should be able to read clearly.

So someone with normal VA should be able to read the top line at 60m and the bottom line at 5m.

VA is then expressed as a ratio of the distance from the chart (6m) divided by the number of the smallest line which is can be read eg the individual who can olny read line 18 has a VA of 6/18 while someone with normal vision would have an VA of 6/6.

19
Q

what are the three most common causes of visual impairment

A

refractive errors (43%), cataracts (33%), and glaucoma (2%)

just a reminder:
- Refractive errors include myopia (short-sightedness), hyperopia (long-sightedness), and presbyopia (inability to focus on near objects with aging), strabismus (mis-alignment of the eyes due to weakened orbital muscles) and astigmatism (blurred vision due to differences in the curvatures of the cornea or lens).

Other disorders that may cause visual problems include age related macular degeneration, diabetic retinopathy, corneal clouding, childhood blindness, and a number of infections. Visual impairment can also be caused by problems in the brain due to stroke, premature birth, or trauma among others. These cases are known as cortical visual impairment.

20
Q

what are Intrinsically photosensitive retinal ganglion cells (ipRGCs)

A

Intrinsically photosensitive retinal ganglion cells (ipRGCs), also called photosensitive retinal ganglion cells (pRGC), or melanopsin-containing retinal ganglion cells (mRGCs), are a type of neuron in the retina of the mammalian eye. The presence of ipRGCs were first noted in 1923 when rodless, coneless mice still responded to a light stimulus through pupil constriction, suggesting that rods and cones are not the only light sensitive neurons in the retina. It wasn’t until the 1980s that advancements in research on these cells began. Recent research has shown that these retinal ganglion cells, unlike other retinal ganglion cells, are intrinsically photosensitive due to the presence of melanopsin, a light sensitive protein. Therefore they constitute a third class of photoreceptors, in addition to rod and cone cells.

Compared to the rods and cones, the ipRGCs respond more sluggishly and signal the presence of light over the long term. Photosensitive ganglion cells innervate the centre of pupillary control, the olivary pretectal nucleus of the midbrain. They contribute to regulation of circadian rhythms and the regulation of pupil size.

21
Q

describe positive and negative afterimages

A
  • An afterimage is an image that continues to appear in one’s vision after the exposure to the original image has ceased.
  • An afterimage may be a normal phenomenon (physiological afterimage) or may be pathological (palinopsia).
  • Afterimages occur because photochemical activity in the retina continues even when you are no longer experiencing the original stimulus.

Negative afterimages are caused when the eye’s photoreceptors adapt to overstimulation and lose sensitivity.

Positive afterimages, by contrast, appear the same color as the original image. They are often very brief, lasting less than half a second. The cause of positive afterimages is not well known, but possibly reflects persisting activity in the brain when the retinal photoreceptor cells continue to send neural impulses to the occipital lobe.

These afterimages tell us that the process by which light is transduced in the photoreceptor is initiated much faster than it is terminated especially when the stimulus is high in intensity.

22
Q

describe the terms protan deutan and tritan

A

The term protan is used for a defect in the red cones.

  • People who have some altered sensitivity in the red cone function are referred to as having a protanomaly.
  • Complete red cone deficiency is called protanopia.

The term deutan is used for a defect in the green cones.

  • People who have some altered sensitivity in the green cone function are referred to as having a deutanomaly.
  • Complete green cone deficiency is called deutanopia.

The term tritan is used for a defect in the blue cones.

  • Altered sensitivity in blue cone function is not seen.
  • Complete blue cone deficiency is called tritanopia.
23
Q

what are the two methods of recording in an EMG

A
  1. Surface EMG; electrodes are placed on the skin surface.

2. Intramuscular EMG; needle electrodes are inserted into the muscle through the skin.

24
Q

when do we require an emg

A
  • muscle dystrophy
  • disease damage to NMJ
  • peripheral neuropathies
  • damage to upper motor neurones
25
Q

where is the cell body located in sensory and motor neurons

A

Neurons carrying sensory information to the spinal cord have their cell bodies in the dorsal root ganglia.

Neurons carrying information from the spinal cord to skeletal muscles have their cell bodies in the ventral horn of the spinal cord.