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NEUROSci Winter > Final > Flashcards

Final Flashcards

(41 cards)

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1
Q

What do the lower motor neurons of the medial ventral horn govern?

A

posture, balance, locomotion, and orienting movements of the head and neck during shifts of visual gaze

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2
Q

describe the organization of descending motor control for the medial motor neurons

A

These medial motor neurons receive descending input from pathways that originate mainly in the brainstem, course through the anterior-medial white matter of the spinal cord, and then terminate bilaterally

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3
Q

What do the lower motor neurons of the lateral ventral horn govern?

A

The lateral ventral horn contains lower motor neurons that mediate the expression of skilled voluntary movements of the distal extremities

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4
Q

Describe the pathway of the descending motor control of lateral motor neurons

A

These lateral motor neurons receive a major descending projection from the contralateral motor cortex via the main (lateral) division of the corticospinal tract, which runs in the lateral white matter of the spinal cord.

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5
Q

What is the internal capsule

A

As the white matter of the corona radiata passes through the basal ganglia it is called the internal capsule

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6
Q

Describe the corticospinal tract

A

motor cortex  internal capsule  midbrain  pons  medullary pyramids  pyramidal decussation  lateral column of the spinal cord
terminate in the ventral horn (grey matter

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7
Q

Describe the medial and lateral vestibulospinal tracts

A

Both originate in the vestibular nuclei. The medial vestibulospinal tracts projects bilaterally down the spinal cord and activates the cervical spinal circuits that control neck and back muscles to our guide head movements.
The lateral vestibulospinal tracts projects ipsilaterally as far down as the lumbar spinal cord. It helps maintain an upright and balanced posture by facilitating extensor motor neurons of the legs.

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8
Q

Describe the tectospinal tract summary

A
  • Tectospinal tract summary: superior colliculus  decussation  contralateral termination - orienting response of head and eyes in response to primarily visual stimuli
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9
Q

Describe the pontine reticulospinal tract

A
  • The pontine reticulospinal tract (medial tract) enhances the antigravity reflexes of the spinal cord.
  • Activity in this pathway, by facilitating the extensors of the lower limbs, helps maintain a standing posture by resisting the effects of gravity
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10
Q

Describe the medullary reticulospinal tract

A
  • The medullary reticulospinal tract (lateral tract) has the opposite effect; it liberates the antigravity muscles from reflex control
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11
Q

What kind of mechanism does postural control require

A

Feedforward, anticipatory mechanism

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12
Q

What would a smashed T10 vertebra result in?

A

Bilateral leg flaccid paralysis

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13
Q

What would be the result of an anterior spinal cord lesion at C5-T1

A

Quadriplegia, bilateral hand and tricep weakness, hypotonia, and absent tricep reflexes, urinary retention, incontinences, and absent rectal tone

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14
Q

What does a lesion in the posterior limb of the right internal capsule result in

A

Pure motor hemiparesis in the left side

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15
Q

What is the function of the vestibulospinal and tectospinal tracts

A

Keep the head balanced as our body moves and to turn our heads in response to new sensory stimuli

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16
Q

What muscle helps with the maintenance of body posture

A

gastrocnemius muscle

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17
Q

How can the motor cortex influence the activity of the spinal cord

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A

Neurons in the motor cortex that supply the lateral part of the ventral horn to initiate movements of the distal limbs also terminate on neurons in the reticular formation to mediate postural adjustments that support the movement. The reticulospinal pathway terminates in the more medial parts of the ventral horn, where lower motor neurons that innervate axial and proximal muscles are located. Thus, the motor cortex can influence the activity of spinal cord neurons via both direct and indirect routes

18
Q

Describe the crossed-extensor reflex

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A

In response to pain detected by nociceptors (Chapter 7), the ipsilateral flexor muscle’s motor neuron is stimulated (withdrawal reflex).
The opposite limb is extended (crossed-extensor reflex) to support the body’s weight.
Activation of flexor muscles and inhibition of extensor muscles in ipsilateral leg.
That same stimulus causes opposite response in the contralateral leg (motor neurons to the extensor muscles are activated and flexor neurons are inhibited.
The contralateral leg supports body’s weight as the pain inflicted leg contracts

19
Q

Describe the NMDA rhythmic activity in a spinal interneuron

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A
  • Some neurons respond to the activation of NMDA receptors with rhythmic depolarization.
  • (a) In the resting state, the NMDA receptor channels and the calcium-activated potassium channels are closed.
  • (b) Glutamate causes the NMDA receptors to open, the cell membrane to depolarize, and Ca2+ to enter the cell.
  • (c) The rise in intracellular [Ca2+] causes the Ca2+-activated potassium channels to open. Potassium ions leave the neuron, hyperpolarizing the membrane. The hyperpolarization allows Mg2+ to enter and clog the NMDA channel, arresting the flow of Ca2+.
  • (d) As [Ca2+] falls, the potassium channels close, resetting the membrane for another oscillation
20
Q

What is a central pattern generator

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A

Circuits that give rise to rhythmic motor activity, flexing of one & extension of the other

21
Q

What is chronic traumatic encephalography (CTE)

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A

Consisten hits to the head/brain disease
Progressive neurodegenerative brain disease
Like alzheimer’s
Develops into progressive dementia
abnormal build-up of tau in brain
Causes tau to form around the brain’s blood vessels, interrupting normal functioning and eventually killing nerve cells

22
Q

What are the 4 stages of CTE

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A
  1. No symptoms, Isolated spots of tau build-up mostly around the frontal lobe or crown of the head
  2. Rage, Impulsivity, depression, and Symptoms begin to appear as defective tau protein affects more nerve cells in the brain’s frontal lobes
  3. Confusion, Memory loss, Tau deposits expand from the frontal section to the temporal section of the brain, the condition begins to affect the amygdala and the hippocampus, which impairs emotion and memory
  4. Advanced dementia, brain becomes deformed and brittle, and cognitive function is severely limited, Tau deposits have overwhelmed the brain, killing many nerve cells and shrinking it by roughly half its size
23
Q

Functional recovery in patients with brain injury reflects _________ of ________ circuits and not regrowth/replacement of damaged neurons

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A

Functional recovery in patients with brain injury reflects reorganization of intact circuits and not regrowth/replacement of damaged neurons

24
Q

What happens to the neuron after axotomy

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A

Injured neuron inputs and targets can atrophy and degrade
Distal axonal stump separates from cell body and undergoes wallerian degeneration
Myelin fragments
Cell body undergoes chromatolysis synaptic terminals contacting the damaged neuron withdraw

25
Describe the pathway for axon degeneration
NMNAT2 generates NAD which inhibits SARM1. SARM1 degrades NAD High NAD levels are required for energy metabolism Following axotomy, NMNAT2 levels decrease, disinhibiting SARM1, which leads to decrease in NAD and energy Proteases are activated and the axon is degraded MAPK (kinases) and a ubiquitin ligase regulates the pathway
26
What would happen if you were to delete the SARM1 gene
Resistance to degeneration
27
Why do Wlds mice axons last long following axotomy
Have a mutant form of NMNAT which mislocalizes to the axon where it substitutes for NMNAT2 after injury and prolongs survival.
28
Why do axons in the periphery regenerate better than those in the central nervous system
After injuring the peripheral nerve, the perineural sheath reforms rapidly and Schwann cells promote axonal growth in the distal stump After injuring the central nerve, the distal segment disintegrates, and myelin fragments, astrocytes and macrophages are attracted to the site which produces local inhibitory factors and a glial scar is formed
29
Describe the inflammatory response of neuronal regrowth and repair
When local damage occurs in brain tissue or BBB is disrupted, cytokines and other signalling molecules activate microglia and astrocytes. Astrocytic process increase in frequency leading to the scaffold for the local glial scar. Once the BBB is compromised, monocytes rush to the site to release pro-inflammatory cytokines to reinforce inflammation leading to a decrease in neuronal survival in potential for neuronal survival, regrowth and repair
30
how does myelin affect the regeneration of central axons
Myelin inhibits regeneration of central axons
31
What aare the myelin and glial scar components that inhibit regeneration of central axons
Myelin contains porteins Nogo-A, oligodendrocyte-myelin glycoprotein (OMgp), and myelin-associated glycoprotein (MAG), when myelin breaks and exposes them, they bind to their appropriate receptors which inhibit growth. (PirB and NogoR are bound and interact with p75 to become a growth inhibiting receptor.)
32
What is Chondroitin sulphate proteoglycans (CSPG)
major component of the glial scar and thought to suppress axon regenration through interaction with the receptor tyrosine phosphatase PTP-sigma, which activates intracellular mediators such as Rho and ROCK
33
What are the two obstacles to nerve regeneration? How could you get around these obstacles
Chondroitin sulphate proteoglycan (CSPG) and special cell-membrane-anchored proteins actively stop growing nerve fibres. Best know of these is Nogo. Bacterial enzyme chondroitinase ABC can prune the side chains of CSPGs. Nogo can be blocked by specific antibodies
34
What is a conditioning lesion and how can it be mimicked
When there is a prior peripheral lesion close to the lesion of the central axon, the prior peripheral lesion promotes regeneration of the central axon. This can be mimicked by elevating levels of cyclic adenosine monophosphate (cAMP) or of GAP-43 in the peripheral branches
35
Describe the signalling pathway in the optic nerve? describe the regeneration in SOCS3 and PTEN mutant mice
The suppressor of cytokine signalling 3 (SOCS3) prevents ciliary neurotrophic factor (CNTF) from binding its receptor GP130, thus blocking CNTF from promoting regeneration. SOCS3 and PTEN are moth mediators of growth-promoting signals, blocking either of these results in greater regenerative ability
36
Describe what happens during neuromodulation and rehabilitation training following a severe contusion
The cortex projects to the spinal cord through the corticospinal tract and to the ventral gigantocellular nuclei (vGi) in the brainstem. A motor cortex-brainstem relay underlies the benefits of neuromodulation and rehab training. The training coaxes the cortex into re-establishing connectivity with the spinal cord by enhancing circuits between the cortex and vGi, as well as the spinal cord and vGi Cortico-reticulo-spinal reorganization
37
What is the application of e-dura
Electrochemical neuroprosthesis for restoration of motor control
38
Where does neurogenesis occur
Stem cells in the dentate gyrus of the hippo campus
39
What are the stages of neurogenesis
1: Proliferation: Stem cells give rise to precursor cells that divide asymmetrically, which gives rise to a neuroblast or glioblast + another precursor cell 2. Differentiation: Postmitotic neuroblasts differentiate into immature neurons 3. Migration: Immature neurons migrate into the granule cell layer 4. Axon/ dendrite targeting: Immature neurons extend axonal projections 5.: synaptic integration: New granule neurons receive input and send outputs to the CA3 and hilus regions
40
How can loss od dopaminergic neurons in Parkinsons be treated
Grafting embryonic cells into the putamen Usually projections from the substantia nigra innervate the putamen, which activates neurons in the globus pallidus to facilitate movement The loss of dopaminergic neuron in the SN deprives the putamen globus pallidus pathways of their drive By injecting embryonic stem cell dopaminergic neuron in the putamen, it reactivates the globus pallidus output pathways
41
what can induced pluripotent cells be used for
can be reprogrammed to generate precursors of many neuronal and glial types

NEUROSci Winter (3 decks)

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