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704 > Neuroplasticity > Flashcards

Neuroplasticity Flashcards

1
Q

Definition of plasticity =

A

???

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2
Q

Hierarchical control model =

A

higher brain centers control primitvie behaviors in lower brain centers

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3
Q

Localization of function (hierarchical control model) =

A

specific brain areas control specific functions

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4
Q

Is there regeneration in CNS in hierarchical control model?

A

no, no regeneration in CNS because in inability of central axons to regenerate following lesions [they try]

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5
Q

Distributed systems model =

A

numerous reciprocal connections between and within levels of CNS. ; information and motor commands flow in all directions

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6
Q

In distributed systems model, function is a cooperative effort among regions of the CNS. Control site depends on what?

A

the task to be executed [ voluntary movement - area 4 vs automatic movement - area 6; both may be active]

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7
Q

Habituation =

A

decrease in a response due to a decrease in the synaptic effectiveness (↓ neurotransmitter released from presynaptic membrane)

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8
Q

What will habituation eventually result in?

A

decreased number of synaptic connections [synapses need activity to remain viable]

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9
Q

Sensitization =

A

enhancement of synaptic transmission.

Experience with one type of stimulus (i.e. painful) enhances responsiveness to other stimuli (i.e. nonpainful)

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10
Q

What type of synapses does sensitization involve?

A

axo-axonal synapses (presynaptic)

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11
Q

In the process of sensitization, what do facilitating neurons do?

A

(some which are serotonergic) enhance transmitter release from the sensory neurons by increasing the amount of second messenger cAMP in the sensory neurons.

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12
Q

In sensitization, the effects are short-term, but with repeated exposure to stimulus, long-term changes may occur that _______________________________________.

A

involve the synthesis of new protein and gene activation (mRNA).

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13
Q

Long-term potentiation =

A

cellular mechanism proposed for formation of consolidation of memories through hippocampal formation.

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14
Q

In long-term potentiation, cooperative and associative activation of numerous neurons in the hippocampal formation increases ___________________________________. What are the effects of the LTP?

A

the amplitude of ESPS’s (increased depolarization) on a receptive cell.

are specific to those synapses that are activated by the stimulus.

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15
Q

Long term depression =

A

cerebellar cortical circuitry proposed to be responsible for motor learning.

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16
Q

What is the essential process of long-term depression?

A

the persistent desensitization of selective glutamate receptors that mediate mossy fiber –> parallel fiber –> Purkinje cell transmission.

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17
Q

In long term depression, climbing fibers play a leading role in induction of LTD. Climbing fibers monitor the performance of a system in which the cerebellar circuitry plays a role and informs Purkinje cells about what?

A

control errors due to misperformance of the plan.

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18
Q

What is a classic example of long term depression?

A

a change in gain of VOR is a classic example of this form of plasticity.

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19
Q

What is development though to serve as?

A

a process template for later neuroplastic changes.

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20
Q

radial glial cells =

A

guidance system for neuronal migration in neural tube

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21
Q

process growth -

A

the axons and dendrites extend outward from the soma, the axon first process in vivo.

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22
Q

In process growth, in vitro (petri dish), undetermined neurite outgrowth occurs until a “guiding signal” is:

A

recognized that determines axon vs dendrite

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23
Q

What is the guidance of the process (axon and dendrites) formation governed by?

A

governed and directed by a number of external signals

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24
Q

What is a growth cone?

A

enlarged tip of growth cone with multiple filopodia or lamellipodia

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25
Q

What do growth cones contain?

A

organelles and cytoskeleton necessary for growth and addition of neuron membrane as well as movement proteins.

26
Q

What are growth cone membranes rich in?

A

rich in receptors responding to directing signals.

27
Q

What do directing signals adhesion differ dependent upon?

A

extracellular matrix

28
Q

Name 4 directing signals?

A
  1. contact inhibition
  2. growth factors
  3. calcium
  4. GAP 43
29
Q

contact inhibition =

A

can be recognition of neurotransmitters

30
Q

growth factors =

A

nerve growth factor supports and directs process outgrowth. Other growth factors may play a role: brain derived neurotrophic factor (BDNF), epidermal growth factor (EGF), fibroblast growth factor (FGF), along with cytokines and hormones

31
Q

Calcium =

A

modify growth cone motility. Thought to act by facilitating depolarizing currents as the neurite grows.

32
Q

What does too much calcium result in?

A

hyperpolarizztion effectively slowing down the growth.

33
Q

What role does Ca++ have on terminal activity specific to neurotransmiter release?

A

???

34
Q

GAP 43 =

A

found in growth cones of axons not dendrites

35
Q

(synaptogenesis and pathfinding) contact guidance =

A

membrane molecule mediated (neural cell adhesion molecule, laminin, neural cadherin)

36
Q

(synaptogenesis and pathfinding) chemotropism =

A

neurotransmiter specific, region specific

37
Q

(synaptogenesis and pathfinding) galvanotropism =

A

neurotransmiter growth toward negative pole in voltage variable environment

38
Q

(synaptogenesis and pathfinding) neurotransmiter specific =

A

postsynaptic excitability, presynaptic site formed first then postsynaptic site modifies position by becoming localized

39
Q

(synaptogenesis and pathfinding) adjustments =

A

apoptosis (programmed cell death), exuberant axons (multiple axons develop and then are reduced to a single functional axon)

40
Q

(synaptogenesis and pathfinding) competition =

A

spatial and chemospecific - functional validation or “the best suited wins” this may be spatial on any given neuron

41
Q

Recovery of synaptic effectiveness =

A

neurons at site of lesion may be temporarily affected by swelling, free radical presence, loss of blood supply, neurotoxic chemicals released in response to trauma.

42
Q

synaptic hypereffectiveness =

A

change in presynaptic event, more neurotransmitter released.

43
Q

denervation hypersensitivity =

A

in response to vacated synapses, adaptive changes occur to other synapses in the are. Increases receptor density in postsynaptic membrane is evidenced in mammalian NS.

44
Q

(denervation hypersensitivity) Originally found in PNS - in denervated muscle, ___________________ increased in density in entire length of muscle, not just motor endplate. Also known to happen in basal ganglia with Parkinson’s disease. Cells in the striatum deprived of DA input from _____________________, some receptors will increase in density in postsynaptic membrane.

A

ACh receptors

substantia nigra

45
Q

Unmasking of silent synapses =

A

some synapses exist on dendrites that are “silent” (don’t release neurotransmitter). These normally ineffective synapses become effective. May consist of strengthening dormant synapses of remaining input to a cell.

46
Q

Example in kitten studies - one eye of kitten was sewn shut for 4 months. When the eye was opened, only 10% of the cortical cells responded to light (normally 80% would - most cells are binocular). The remaining good eye was surgically removed. Immediately:

A

40% of the neurons in the cortex receiving connections from the previously sutured eye now responded to light- this suggests that the pathways were present but not being used.

47
Q

Axonal regeneration =

A

Sprouts from injured axons start growing out within several days of injury. May connect with nearer cell bodies, scarring a problem. Not a strong possibility in human CNS. Does occur in PNS, rate of 1mm/day, scarring still can be a problem. [This process is similar to axon outgrowth during development using similar signals such as growth factor guidance]

48
Q

collateral sprouting =

A

surviving neurons that innervated the same target organ are somehow stimulated (postsynaptic hypersensitivity) to send out collateral branches from their axons to reinnervate denervated target cells. Begins 4-5 days post injury. First identified in PNS but now confirmed in CNS.
Not random. New input closely related to original function (use of same neurotransmitter, although not necessarily same afferent system).

49
Q

What is the advantage of collateral sprouting?

A

may prevent dendritic atrophy and maintain functional level of excitability [but not necessarily the same function]

50
Q

What is the disadvantage of collateral sprouting?

A

may create abnormal connections - SCI - may be responsible for spasticity

51
Q

(activity dependent functional reorganization) functional reorganization of sensory cortex in monkeys with training in a ___________________________________

A

fine motor finger manipulation task

52
Q

(activity dependent functional reorganization) functional reorganization of motor cortex in monkeys with training on two different tasks, ________________________________________________

A

a finger flexion/extension task, and a forearm pronation/supination task

53
Q

What happens to the brain as a result to aging?

A

decrease in brain weight and volume

54
Q

With the decrease in brain weight and volume due to aging, the specific cortical regions =

A

frontal and temporal lobe, hippocampus and amygdala vs. primary sensory and motor regions

55
Q

With the decrease in brain weight and volume due to aging, ventricles:

A

increase in size

56
Q

With the decrease in brain weight and volume due to aging, cells loss versus?

A

neuronal atrophy

57
Q

With the decrease in brain weight and volume due to aging, axonal death?

A

loss of collateral may explain decrease in ability to “multitask”

58
Q

With the decrease in brain weight and volume due to aging, the effect of neuronal atrophy on excitability of neuron, decrease input =

A

increased time for summation –> increased processing time

59
Q

With the decrease in brain weight and volume due to aging, discuss can and does lead to:

A

atrophy and cell death

60
Q

stem cells =

A

Stem cells present in layer I and at other places such as the hippocampal formation. These are responsible for continued CNS mitotic growth well into our 20s. They can be turned on by trauma such as ischemia or traumatic denervation. Their response is to generate new neurons. This theoretically looks very promising. The problem as it exists now [current technology] is that we don’t know how to “encourage” this growth in a positive way or direct migration of new cells to area of need. The increase in new neuron number does not predict that axonal growth can or does occur.

704 (22 decks)

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