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CNUP > Muscles, Unit 3 > Flashcards

Muscles, Unit 3 Flashcards

1
Q

what distinguishes nicotinic and muscarinic receptors?

A

Where they are localized; the parasymp has musc, the nmj has nic

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2
Q

what is the physiology of an NMJ good for?

A

High gain system; contracts reliably; one nt, shape of synapse

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3
Q

what is the mechanism of action of curare and botulinum toxin

A

block ach release

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4
Q

what do glycogen depletion experiments show?

A

that muscle fibers innervated by the same MN are scattered uniformly through a muscle, not clustered

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5
Q

what are characteristics of fast fatiguing muscle fibers?

A

white, few capillaries, little myoglobing, but are supplied with glycolytic enzyemes

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6
Q

what is the histochemical profile of a red muscle fiber?

A

myoglobin etc, cannot metabolise, resist fatigue

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7
Q

which type of muscle fiber shows more variety in fatigue indexes?

A

White fibers

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8
Q

for what type of muscle is rheobase the smallest?

A

for s-type (red)

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9
Q

what is type-grouping

A

the clumping of type of fiber innervated by a mn after cutting and reinervatting

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10
Q

evidence that the mn specifies the type of muscle fiber?

A

after transection, type grouping occurs, and you restore the properties to the muscle fiber that it had earilier; more heterogeneous

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11
Q

evidence muscle can influence the mn

A

if a transected mn is redirected to a muscle that has no vacant end plates, mn will remain undiff, f forced to connect to s type muscle will not change muscle, mn properties change

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12
Q

how does exercise increase muscle size?

A

hypertrophy; increase in muscle size. hyperplasia does not occur

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13
Q

during training, how is efficiency improed?

A

first sign is how quickly a pluse of ach can be delivered (e stem can produce up to 30% greater muscle tension)

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14
Q

how does exercise effect mn types? fiber types?

A

mn type does not change, but proportion of muscle fiber type can

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15
Q

what is the arrangement/function of muscle spindles?

A

lie in parallel with extrafusal muscle fibers, stretch when muscle stretches

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16
Q

nuclear and afferent charicteristics of bag1.intrafusal fiber

A

nuclei are clustered in center, innervated by !A (large) fibers, which terminate near center.

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17
Q

bag2 and nuclear chain properties

A

nuclei scattered throughout, !a and II afferents, terminations more distally

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18
Q

What do Bag1 fibers respond best to, why?

A

during stretch movement, sensor is at elastic middle, affects IA (velocity detectors)

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19
Q

What do Bag2 fibers respond best, why

A

the length of muscle stretch, will affect group II fibers. (length detectors)

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20
Q

when a muscle is released from stretch, primary afferents will be—–, secondary afferents willl—–

A

be inhibited, ;fire less

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21
Q

what unwanted situation occurs when muscle shortening happens, and is prevented by contraction of he intrafusal muscle fibers

A

unloading

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22
Q

why does.a cut muscle have less activity in the spindle afferents?

A

you have removed motor drive, B mn come from sc ventral horm

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23
Q

What class of mn innervate each type of intrafusal fiber?

A

gammaD - Bag1 and gammaS -bag2 and chain.

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24
Q

Gogli tendons (Ib) do this?

A

are stimulated whe when a tendon stretch (its muscle contracts)– prevents antagonist from contracting.–smooth, not protection

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25
Q

what type of movement recruits a Gamma d/gammaS mn?

A

fast and big/slow

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26
Q

what does stimulation of free nerve endings in muscle cause?

A

exercise pressor responses

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27
Q

what is wrong with the gamma loop hypothesis

A

too fast for feedback? no accounting for load?

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28
Q

What is servo length hypothesis?

A

do not depend on load, intrafusal fibers receive feedback from muscle to maintain at optimal length

29
Q

What does an Ib afferent respond to?

A

muscle contraction (ie tendon stretch)

30
Q

why are Ib inhibitory interneurons called non-reciproal?

A

because they don’t affect the antagonist muscle

31
Q

Type III (Agamma) nerve endings are important for what?

A

physiological response to exercise; metabolites from muscle contraction trigger, bring more o2 and nutrients to a muscle

32
Q

why are goldi tendon organs slow to resopond to stretch?

A

change in length occurs mostly in the extrafusal fibers

33
Q

muscle spindle lies in —- with respect to muscle fibers, golgi tendon is in —–

A

parallel,(fire with muscle stretch), series fire with muscle contraction)

34
Q

what happens during a contraction if the ventral root is cut?

A

this means no gamma mn firing– so primary and secondary afferents will stop firing during muscle contraction

35
Q

Describe the sc connections of Ia afferents:

A

heavily to to lamina IX, (terminate on MN,) agonist and inhibiotyr interneuron ie antagonist, eg myostatic reflex, passive stretch due to load

36
Q

secondary afferents make this type of sc connection

A

barely any IX connections, intermediate grey

37
Q

where do group Ib afferents connect in the sc?

A

intermediate gray only

38
Q

define myotatic reflex?

A

contraction of a stretched muscle by a monosynaptic proprioceptive input ot a alpha motoneuron innervating the muscle being stretched (holding a glass that’s being filled)

39
Q

reciprical inhibition?

A

Ia inhibitory interneurons responsible for this, turn on agonist and turn off antagonist. (reflex hammer)

40
Q

role of renshaw cells?

A

recurrent inhibition of mn that excited them; negative feed back to stablize contractions.

41
Q

what is the only type of interneuron know to receive renshaw inhibition?

A

type 1a inhibitory interneuron, may serve to regulate strength of receprocal inhibition to antagonist ;mn

42
Q

what give input to a renshaw cell?

A

an alpha mn, or descending input

43
Q

to make a more powerful reflex, Ia inputs can do what?

A

produce inhibition of mn of antagonists, this is disynaptic

44
Q

many pathways provide inputs to motoneurons also send signals to Ia inhibitor interneurons. this is an example of

A

conserfation within the central neural circuitry

45
Q

Group Ib fibers make this kind of inhibition

A

no reciprocal; inhibition of the muscle being stretched

46
Q

what is antidromic response?

A

stimulating at axon, therfore anti to the direction, will pass collision test (ie cancel out)

47
Q

what is orthodromic response?

A

stimulating across a synapse; stimulating at soma, recording across synapse at soma, will fail collision test

48
Q

propriospinal neurons connect segments of the sc to integrate movement. medially —— range axons supply—– muscles, and —– range axons supply —- muscles.

A

long, axial; short; distal

49
Q

are supraspinal structures necessary to generate locomotion?

A

no, in a spinalized cat, still have basic pattern–alternation of flexors and extensors;stimulating afferents by putting on a treadmil

50
Q

how do supraspinal structures contribute to locomotion?

A

MLR (mesencephalic locomotor region) initiates and controls speed

51
Q

does the MLR provide input directly to the SC?

A

NO! reticular formation, inputs integrated with other inputs from vestibular, cerebellar, cortical etc

52
Q

what are the inputs to the MLR?

A

bg, limbic system, lateral hypothalamus, inhibition from STN

53
Q

what happens when you stimulate MLR?

A

find responsive neurons in lamina VIX of the spinal cord (ventral horn)

54
Q

are peripheral inputs needed for walking? how do you know?

A

no, cutting the DR does not abolish walking

55
Q

afferent feed back is important for what in walking?

A

reinforcing the step cycle, and in posture

56
Q

what is odd about the locomotor reflex pathway?

A

the convergent input of extensor muscle Ia, II and Ib spindle afferents during stance do not shut off extensor, instead, the allow extensor to stay active.

57
Q

how could cutaneous stimulation be important in gait?

A

eg the stumble response, a prolonged swing face stimulated by sensation on the dorseum of the foot

58
Q

what role do Ia inhibitory interneurons play in walking?

A

they ensure that flexors and extensors are not active at the same time

59
Q

Features of LVST; Arises-, descends- crossed or not? role in movement?

A

LVN, terminates in VIII and VII travels in ventrolateral funiculus, effects neck movements may be direct, indirect to other,ipsi

60
Q

MVST: how does this differ from LVST?

A

medial longitudinal fasciculus, and travels bilaterally, mainly in cervical sc, neck.

61
Q

how does the LVST influence limbs on the opposite side?

A

through commisural internuerons

62
Q

what is LVST good for?

A

can influence alpha and gamma mn on both sides, maintain posture when falling

63
Q

when is LVST most likely to be activated, why?

A

for ear-down movement, because they receive convergent otolith and canal signals that are activated by this– think quadrupeds!

64
Q

what part of the reticular formation sends fibers to the spinal cord, where?

A

Gigantocellular- medial, descending, mainly indirec, some direct a and g activation

65
Q

where do medullary reticulospinal axons go?

A

lateral funiculus

66
Q

where do pontine reticulopsinal axons go?

A

ventral funiculus

67
Q

descending monoaminergic pathways originate from the—- with serotonin and —– with noradrenergic

A

meullary raphe, locus coeruleus

68
Q

evoloution of rubrospinal tract:

A

most important in rats, in cats activates flexors and inhibits extensors, in primates ends at cervical

69
Q

two cortical spinal pathways:

A

dirct-ducusssates at pyramid-direct contact w mn, indirect goes to reticular formation,

CNUP (3 decks)

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