6 - neurophysiology Flashcards

1
Q

compare the effects of the sympathetic vs parasympathetic nervous systems on cardiac muscle

A

PARASYMPATHETIC
• in cardiac muscle, there are M2 receptors
• activated by ACh released from vagus nerve
• causes activation of G(l) protein —> inhibits adenyl cyclase —> inhibits production of cAMP —> activation of K+ channels —> K+ out of cell (hyperpolarisation) —> takes longer to reach threshold —> lower HR

SYMPATHETIC
• noradrenaline from sympathetic nerve activates beta-1 receptors
• activates G(s) protein
• different second messenger to increase HR

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2
Q

using a diagram, describe the effect of sympathetic and parasympathetic activation on the following organs: heart, brain, lungs, blood vessels, urinary bladder, liver.

A

redraw that diagram he used a billion times in the leccys

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3
Q

draw the structure of the ANS

A
CNS
pre-ganglionic fibre
autonomic ganglion (neurotransmitters + modulation of signal)
post-ganglionic fibre
varicosity (neurotransmitter)
effector organ
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4
Q

using a diagram, describe how specific receptors control

heart rate

A

:P

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5
Q

what is the function of the autonomic ganglia

A

to either enhance or reduce a signal

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6
Q

list the different forms of motility in the GIT and with one sentence for each describe the functional importance.

A

1) gastric mixing

2) segmentation
– move chyme in both directions which allows greater mixing with the secretions of the intestines

3) peristalsis
– propulsion of bolus

4) migrating motor complex
– moves undigested remains to large intestine in between meals to empty stomach for next meal
– responsible for the rumbling experienced when hungry

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7
Q

describe the mechanism of defecation

A

parasympathetic nerve involved in contraction of smooth muscle (internal sphincter) which results in defection —> automatically controlled (early development)

later in development, gain control over external sphincter using skeletal muscle and motor neurons —> voluntary control

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8
Q

using a simple diagram explain how stress affects the sympathetic nervous system and the HPA axis

A

XD

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9
Q

using a diagram explain how olfaction affects different structures within the brain

A

B~D

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10
Q

justify this statement: the sympathetic nervous system and pituitary gland maintain homeostasis

A

hypothalamus and pituitary gland function to maintain homeostasis

they respond to changes in the body by releasing hormones and activating sympathetic/parasympathetic NS

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11
Q

how does negative feedback fail during chronic stress?

A
  • more and more cortisol release
  • neg. feedback begins to fail
  • glucocorticoid receptors on hippocampus

• hippocampus logically controls stress response —>
suppresses cortisol

  • over-excitation due to cortisol = suppression form hippocampus fails
  • chronic stress leads to destruction of hippocampus —> memory loss + alzheimers + dementia
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12
Q

draw and described in order - the molecular events from motor neuron action potential generation through to the generation of a muscle action potential

A

1) AP arrives at motor nerve terminal
2) AP triggers the opening of VG Ca2+ channels = entry of Ca2+
3) Ca2+ dependant release of acetylcholine (ACh) from synaptic vesicles (exocytosis)
4) ACh traverses the synaptic cleft to bind to its receptor a ligand gated Ion channel (AChRs)
5) binding causes opening of this ion channel = large movement of Na+ in and a small movement of K+ out of the muscle cell = depolarisation
6) current flow between the depolarised post-synaptic membrane and adjacent membrane of muscle
7) local current flow opens voltage gated Na+ channels in the adjacent membrane
8) the resulting entry of Na+ causes the resting MP to rise from ~ -70 mV to -60mV = generation of a muscle action potential
9) ACh is subsequently destroyed by acetylcholine-esterase (enzyme in synaptic cleft)

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13
Q

what is the latent period?

A

muscle APs last for only 1 to 2 ms, whereas the muscle contraction that results can last about 50 ms

latent period = time delay between stimulation and contraction

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14
Q

what is myasthenia?

A

disease which causes the drop in the number of post-synaptic AChRs to such a level that causes muscle weakness

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15
Q

what is lambert-eaton syndrome?

A

auto immune self antibodies to the pre- synaptic voltage gated calcium channels

poor pre-synaptic release of neurotransmitter - leads to neuromuscular block

causes muscle weakness

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16
Q

what is spinal muscular atrophy ?

A

an autosomal recessive disease caused by a genetic defect in the SMN1 gene, which encodes SMN, a protein
widely expressed in all eukaryotic cells

SMN1 is apparently selectively necessary for survival of motor neurons

causes muscle weakness

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17
Q

what is the consequence of a mutation in the dystrophin gene

A

mutation in the dystrophin gene = no dystrophin (anchors muscle fibre to extracellular matrix)

dystrophin supports muscle fibre strength

absence of dystrophin reduces muscle stiffness, increases sarcolemmal deformability, and compromises mechanical stability

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18
Q

what is a motor unit?

briefly compare small and large motor units

A

motor unit = 1 motor neuron the number of muscle fibres it innervates

small motor units = fine control but weaker muscle contraction

large motor units = larger muscle contraction

19
Q

state and explain henneman’s size principle

A

for a given synaptic input, motor neurons with the smallest cell bodies are activated 1st & large motor neurons are activated last

smaller neurons have higher membrane resistance and require lower depolarising current to reach spike threshold

small motor-neurons innervate small motor unit
large motor-neurons innervate large motor unit

20
Q

compare the three types of motor fibres

A
TYPE I:
– small MN
– slow twitch
– fatigue resistant
– slow oxidative
– low myosin ATPase activity
TYPE IIA:
– medium MN
– fast twitch
– fatigue resistant
– fast oxidative
TYPE IIX:
– large MN
– fast twitch
– fatigable 
– fast glycolytic 
– high myosin ATPase activity
21
Q

how does chronic denervation–reinnervation of muscle lead to fibre type grouping, type I in particular?

A

chronic denervation re-innervation events lead to type 1 fibre predominance

fast motor neurons die first

de-inervated tissue pumps out GFs

∴ local sprouting and expansion of surviving slow MNs

type I now dictates fast-twitch fibres

22
Q

what do muscle spindles detect?

how are muscle spindles kept taut?

A

muscle spindles detect ∆length of muscle

spindle must always remain taut to maintain sensitivity to ∆length

gamma MN act on spindles to maintain their sensitivity during muscle contraction

23
Q

what are golgi tendon organs and what do they detect?

A

golgi tendon organs are located in the tendinous insertions of muscle

detect changes in muscle tension

activated by increases in muscle tension and thus measure the degree of tension/load that the muscle is under

24
Q

draw and briefly describe five types of interneuronal circuits

A

DIVERGENCE
black MN excite inhibitory MN —> no firing
white MN excite excitatory MN —> firing
withdrawal reflex

CONVERGENCE
many motorneurons excite the same MN
brain stem / cortex inputs

REVERBRATING
excited for longer by exciting self

FEED FORWARD INHIBITION
interneuron does not allow MN to fire
rhythmic activity

GATING
excitation and reciprocal inhibition
stretch reflex

25
Q

draw a diagram of the patella reflex

A

:P

26
Q

draw a diagram of how the crossed extensor and withdrawal reflex work together during locomotion

A

:^O

27
Q

why is a patient with a spinal cord injury and supported by a harness able to walk on a tread mill ?

A

i don’t actually know the answer to this can any1 help :(

28
Q

name and briefly describe two mechanisms used for postural adjestments

A

feed forward:
– anticipatory
– preprogrammed from experience
– unlike reflexes

feedback:
– compensatory 
– stereotyped 
– show a space time organisation
– like reflexes
29
Q

describe the reflex(es) controlled by the vestibular nuclei

A

vestibular nuclei receive afferents which signal head postion WRT gravity

signals via vestibulospinal tract to control multiple relfexes

lateral nuclei = controls proximal limbs to maintain stance

medial + superior = coordination of eye with head movements

inferior = integrates afferents + cerebellum to higher areas

30
Q

describe the reflex(es) controlled by the reticular formations

A

maintaining posture via feed-forward mechanisms

medullary (lateral) reticular formation = inhibitory to extensor muscle tone

pontine (medial) reticular formation = facilitates extensor muscle tone

31
Q

describe the reflex(es) controlled by the superior collucli

A

receives visual input

outputs to reticular formation then to motoneurons of ocular motor nucleus + outputs to cervical motoneurons of head and neck (tectospinal)

controls saccadic eye movements

32
Q

describe the reflex(es) controlled by the red nuclei

A

red nuclei increases flexor muscle tone to facilitate grabbing behaviour

33
Q

describe the function of the cerebellum

A

Functions as a COMPARATOR

compares intended movement with performance of movement and makes adjustment

1) internal feedback (corollary discharge)
2) external feed back (reference)
3) input to lower motor neurons
1 & 2 allow for comparisons, 3 for correction

34
Q

list the functional lobes of the cerebellum (function, input, output)

A
VESTIBULOCEREBELLUM
• structural = folcculonodular lobe
• input: vestibular apparatus
• output: lateral vestibular nucleus
function: maintenance of balance, control of eye movements

SPINOCEREBELLUM
• input: spinal cord
• output: back down to spinal cord via fastigial nucleus (proximal muscles) or interposed nucleus (distal muscles)
• function: regulation of muscle tone, coordination of skulled voluntary movement

CEREBROCEREBELLUM
• input: cerebral hemispheres (motor cortices)
• output: back to hemispheres
• function: planning and initiation of voluntary activity, storage of procedural memories

35
Q

what fibres control the deep cerebellar nuclei?

are they inhibitory or excitatory?

A

climbing fibres (excitatory)

mossy fibres (excitatory)

purkinje fibres (excitatory)

36
Q

what is hypotonia?

A

diminished resistance to passive limb displacements

e.g. after knee-jerk reflex, leg may oscillate 6-8 times before coming to rest (compared to immediately in healthy patients)

37
Q

what is ataxia

A

lack of coordination

errors in the range of movement

errors in the rate and regularity of movements

38
Q

what is the main difference between an upper and lower motor neuron lesion?

A

LMN lesion = flaccid paralysis (reflexes lost)

UMN lesion = spasticity (reflexes intact)

39
Q

what is the function of the premotor cortex?

from where does it receives inputs?

what are the consequences of a lesion in the PMC?

A

function:
– setting up the motor programs for learned sequences
– coordination of bilateral movements
– active when told to dream movement (planning)

inputs:
– sensory cortex
– visual inputs

lesion:
impaired ability to execute purposeful movements

40
Q

what is Broca’s area?

where is it located?

what are the consequences of a lesion to this area?

A

function:
– production of speech

location:
– inferior frontal gyrus in frontal cortex

lesion:
– speech = non-fluent, effortful
– comprehension = preserved for single words and sentences
– repetition = impaired

41
Q

what is Wernicke’s area?

where is it located?

what are the consequences of a lesion to this area?

A

function:
– comprehension of language

location:
– left posterior, superior and middle temporal cortex

lesion:
– speech = fluent
– comprehension = impaired
– repetition = impaired

42
Q

what in conduction aphasia?

A

conduction aphasia = damage to left supramarginal gyrus

speech = fluent with some articulatory defects

comprehension = intact / largely preserved

repetition = impaired

43
Q

TRUE OF FALSE

NPY, NA and ATP are all released from same nerve terminal

A

TRUE

NPY, NA and ATP are all released from same nerve terminal

All act to increase contractility of smooth muscle by acting on ⍺-1 (NA +NPY) and P2X (NPY + ATP) receptors → induce calcium release