Motor Control: Reflexes Flashcards Preview

Neuroscience I Test 3 > Motor Control: Reflexes > Flashcards

Flashcards in Motor Control: Reflexes Deck (29):

motor control reflexes in the cortex

-placing reaction
-hopping reaction


motor control reflexes in the brainstem/midbrain

-righting reflex
-eye/head movements*

*these occur even with encephalic defects, so even after traumatic brain injuries, these can often be mistaken for a thing that is volitional, but that is not true


motor control reflexes in the SC

-golgi tendon reflex
-crossed extensor--withdrawal from something but then move the rest of the body to make up for the movement


difference b/w reflex and volitional motion

-precise motions in response to afferent stimuli
-mediated at all levels of CNS
-rapid initiation
-many elicited even during unconsciousness

volitional activity
-originates in cortical areas associated with judgment, initiative, and motor control
-longer onset latency due to processing
-require conscious awareness


myotatic reflex

-stretch reflex
-appearance: contraction (shortening) of the stretched muscle
-purpose: protect muscle from tearing from stretch
-initiated by muscle spindle
-monosynaptic, segmental reflex--afferent info comes into the same segment of the SC that the motor will leave


muscle spindle

-myotatic reflex
-extrafusal fibers--fibers you see when looking at a M and they are the fibers that do the work
-intrafusal fibers
-parallel to extrafusal fibers
-have an afferent sensory component in the center and an efferent motor component at the periphery/ends


sensory portion of the intrafusal M fibers of the muscle spindle

-sensory portion:
-not contractile
-portion sensitive to length
-actually 2 different afferents
1. nuclear bag fiber--nuclei are in the center in a swelling
2. nuclear chain fiber--nuclei are lined up in a row


primary afferent in the sensory portion of the intrafusal M fibers of M spindle

type 1 A fiber
-innervates both the nuclear bag and nuclear chain fiber
-large, myelinated 1a fiber
-sensitive to both:
-length of M
-how fast the length is changing
-fires a few APs per sec at rest, but fires inc APs when the muscle spindle is stretched


secondary afferent in the sensory portion of the intrafusal M fibers of M spindle

type 2 fiber
-slightly smaller than type 1A fiber
-innervates only the nuclear chain fiber
-sensitive to only the length of the M--tells us what the length of the M is RIGHT NOW, and doesn't give any info o if the M is changing
-less myelin


motor portion of the intrafusal M fibers of the muscle spindle

-same as skeletal M
-innervated by a gamma motoneuron--this neuron goes thru NMJ and releases ACh
-control the length of the sensory portion


how does the contraction of the intrafusal sensory and motor fibers

-by contracting the intrafusal Ms, we stretch the sensory portion, this renders the sensory portion more sensitive to a superimposed stretch
-the motor portion on each end is attached to ligaments/tendons that the M is attached to and as we contract the motor part the sarcomeres move closer together, and we stretch the sensory portion nuclear bag/chain
-gamma motoneurons control the sensitivity


alpha vs. gamma motoneurons

alpha motoneurons
-large, heavily myelinated fiber
-innervates (via NMJ) the skeletal M
-responsible for activating M
-activity directly leads to motion

gamma motoneurons
-slightly smaller, slower than alpha--still fast overall
-innervates the contractile component of the M spindle via the NMJ
-activity causes contraction
-controls sensitivity of M spindle
-activity does NOT lead to motion


how does the myotatic reflex work for the agonistic M

-1a afferent neuron comes into the SC and releases EAA onto the alpha motor neuron
-motoneuron is excited by the activation of the 1a afferent-->contraction relieves the stretch, returning the 1a discharge rate back to normal


how does the myotatic reflex work for the antagonistic M

-when elicit a stretch reflex on the agonistic M and contract the M, the antagonistic M is also stretched but don't get another stretch reflex
-when 1a afferent comes in, it sends a branch to an interneuron that inhibits the alpha motor neuron to the antagonist M which allow the antagonist M to relax and allow the original M to experience the reflex--RECIPROCAL INHIBITION
-anytime you contract one M, their antagonist M must relax
-there is a decrease in the activity of the alpha motoneuron innervating the antagonist M allowing it to RELAX and LENGTHEN


golgi tendon reflex

-also called inverse myotatic reflex and autogenic inhibition
-appearance: sudden (abrupt) relaxation of a contracted M
-purpose: protect M from damage due to excessive force
-initiated by the golgi tendon organ
-polysynaptic, segmental reflex--more than one synapse, but afferent and efferent come out the same segment


golgi tendon organ

-innervate tendon
-bare N ending with lots of branches
-APs increase with tension
-1b fiber goes to spinal cord


how does the golgi tendon reflex work

-1b afferent come from the golgi tendon organ and into the SC and is excitatory to so releases EAA to the interneuron in the SC
-activated by the EAA and then this interneuron releases an inhibitory NT (glycine) which inhibits the alpha motor neuron of the contraction M
-so this alpha motor neuron gets input from brain to contract and inhibitory input form the SC to relax--so when inhibition finally comes thru, it stops contraction of the alpha motor neuron
-these reflexes allow us to avoid going to the brain to get the contraction to stop

-motoneuron is inhibited by the activation of the spinal interneuron-->abrupt relaxation of the M occurs, returning the golgi tendon organ discharge rate to normal


myotatic reflex vs. golgi tendon reflex

myotatic reflex:
-initiated by M spindle
-passive stretch of the M
-monosynaptic reflex
-contraction of stretched M back to normal length

golgi tendon reflex:
-initiated by golgi tendon organ
-active contraction of M
-polysynaptic reflex
-abrupt relaxation of the contracted M to prevent damage


modification of reflexes

-occurs all the time--healthy
-a lot of the time, the influence for modification is inhibitory


spinal shock

-occurs from spinal transection--from hyper polarization of spinal neurons due to loss of excitatory input form cortex
-reflexes that are below the level of the transection, the reflex fails to occur even though the wiring is intact
-occurs right after the spinal cord is transected but usually goes away and reflexes can return, except in humans, the Ms often atrophy w/in the year and the reflex return is never noticed
-recovery results from axonal sprouting below the level of the transection--occurs due to neurons need for input b/c without input they will die
-recovery also occurs due to expression of R phenotypes that are self-activating


decerebrate posturing

results from loss of all structures rostral to the pons
-involves the whole body
-spinal reflexes are intact and hyperactive
-experience extension in all Ms, so rigid--happens instantly
-usually bilateral


rigidity vs. spasticity

-resists motion in all directions
-results from maintained M contraction; loss of cortical influence that inhibits a medullary input to the alpha motoneurons
-continual activation of alpha motoneurons
-not due to reflexes
-brainstem is activating alpha motoneurons

-resists motion in a given direction--so when move arm, the arm will spring back
-myotatic reflex is hyperactive due to inc gamma motoneuron firing
-continual activation of gamma motoneurons
-contracts intrafusal M
-lengthens nuclear bag/chain fibers
-cause: damage to cortex that abolishes activation of the brainstem inhibitory region


spasticity from alteration to what locations?

-brainstem facilitatory region
-by activating the gamma motoneurons, makes M spindle more sensitive
-region is spontaneously active
-dominates with decerebrate posturing

-brainstem inhibitory region
-inhibits gamma motoneurons, making M spindle less sensitive
-region requires activation from cortical regions
-this doesn't work in decerebrate posturing


decorticate posturing

-flexion of the upper limb joints
-extension of the lower limbs
-dependent on head position
-head motion in one direction will flex the contralateral arm and extend the ipsilateral arm
-changes as the head is moved passively
-happens often b/c it happens in pts that experience strokes in the vicinity of the internal capsule
-cause: loss of cortical inputs due to lesion of internal capsule


which of the following reflex requires cortical input?
withdrawing hand from hot stove
turning heads towards sound
hopping run
turning eyes towards motion
righting response

hopping rxn


what innervates the intrafusal M fibers?

gamma motoneuron


in order to save time, Dr. K tries to lift 47 cases of Pepsi into car in one lift. She is not up the challenge and a reflex is elicited, resulting in complete relaxation of her Ms. Activation of what produces this?

1b fiber b/c this is involved in the golgi tendon reflex which protects M from damage due to excessive force and causes abrupt relaxation of a contracted M


in order to save time, Dr. K tries to lift 47 cases of Pepsi into car in one lift. She is not up the challenge and a reflex is elicited, resulting in complete relaxation of her Ms. How many synapses in the SC are required for reflex?

1b afferent from golgi tendon--interneuron--alpha motorneuron


in order to save time, Dr. K tries to lift 47 cases of Pepsi into car in one lift. She is not up the challenge and a reflex is elicited, resulting in complete relaxation of her Ms. what R is most likely on the alpha motoneuron in this reflex?