Lecture 8: Neuroplasticity Flashcards
what are the 10 principles of neuroplasticity ranked from most to least important
- Salience
- specificity
- repetition
- intensity
- use it and improve it
- use it or lose it
- time matters
- interference
- age matters
- transference
what is the principle of interference with neuroplasticity
sometimes new plasticity can be delayed
definition of neuroplasticity
ability of neural circuirs to change through growth and reorganization
naturally happens with development
can be used for specific activity guided training or rehab
can be adaptive or maladaptive
describe the natural development of the nervous system
stem cells align along the ventricular wall and central canal of the spinal cord
the cells differentiate to either glioblasts or neuroblasts
for the stem cells that differentiate into glioblasts, what happens next
radial glial cells (directly merging with the pia mater) form the scaffold and the other 4 types of glia cells are in the CNS
radial glial cells are first to develop
other 4 types of glial cells develop after neurons
for the stem cells that differentiate into neuroblasts, what happens next
they mainly migrate along the radial glial scaffold; these neurons form a columnar functional unit
some migrate horizontally after climbing the glial process; these are responsible for coordinating and modulating functions
what mechanism is post natal neuroplasticity mainly through
neuroblasts that migrate horizontally after climbing the glial process (responsible for coordinating and modulating function)
what is a neurite
extension from the neuron soma/cell body
defines the neuron type and function
in the beginning, neuroblasts develop neurites without differentiation
types of neurites , where to find them/what neurons generally fall into the category
multipolar: UMNs and LMNs and most interneurons
pseudounipolar: DRG, sensory neurons
Bipolar: olfactor receptor neurons, visual pathway, some interneurons
describe how the polarity of neurons works
they have functionally distinct proteins that are attracted to neurite tips by directional stimuli
works via chemoattraction and chemorepulsion
where can you find neurotrophins/how do they work (chemoattraction factors)
peripheral process of sensory neurons in the DRG
different target cells secrete different neurotrophins (called cytokines)
these send signals to different peripheral processes that conduct specific sensory modalities
function = transported back to the somata for the survival of the neurons (block apoptosis)
purpose/function of chemorepulsion
still through different cytokines; used to avoid abnormal interactions
self avoidance = intra-neuronal repulsion (dendrites of same neuron)
tiling = inter-neuronal repulsion (dendrites of different neurons)
how do chemo- repulsion/attraction control the direction of the neuron signals
chemoattraction = direction of the neurite extension
chemorepulsion = turning point along the extension
describe how CN II is an example of the balance of chemo repulsion/attraction
axons of ganglionic cells from the temporal retina extend ipsilaterally
axons of ganglionic cells from the nasal retina cross over to form optic chiasm
both chemoattraction and repulsion are at play
what gene defines the development of external genitalia
SRY gene on the Y chromosome
if expressed = male
if female, there is no SRY gene (XX chromosomes) or the SRY is mutated and non functional (XY)
male external genitalia if SRY is inserted into the father copy of X chromosome
describe the relationship/importance of male genitalia and sec hormones related to brain development
all hormones synthesized from cholesterol
only male sex hormones surge in the fetal brain; male and female both have active hormones but only females have this fetal surge
describe the phases of sexual hormones related to brain development in males vs females
male brain has 2 phases: prenatal and puberty
females only have 1 phase: puberty phase
differentially developed brains define different behaviors in males vs females
examples of how differentially developed brains define different behaviors
sexual activities = different LMN pools for mm and reflex
violence (in amygdala) = males have fewer astrocytes to insulate and inhibit neurons thus they tend to be more violent
sexual hormones improve genesis of what
neurites
dendritogenesis for dendrites
what is spinogenesis
spine sprouting along dendrites
dendritic spines = major synaptic points
i.e. pyramidal cells, medium spiny neurons, purkinje cells, etc
stimulated by sex hormones
describe the findings of oxytocin and ADH levels in prairie voles/montane voles and how it relates to behavior
oxytocin
- prairie = found in prefrontal cortex, caudate, putamen, and nucleus accumbens
- this is NOT true of montane voles
ADH
- prairie = ventral pallidum
- montane = lateral septal nucleus
behavior
- prairie = MONOGAMY
- montane = POLYGAMY
male brain larger areas and the effects this causes
orbitofrontal cortex = analysis of results
corpus callosum = more cross talking, but harder stroke recovery
amygdala = more fights/violence
female brain larger areas and the effects this causes
limbic lobe = more emotion
olfactory system = more sensation related to smell
SMA = like to work more?
hippocampus (smaller??) = more challenge with spatial orientation
stages of synaptogenesis
early stage = axons extend to target structures under over amount of neurotrophins; axons mainly extend to dendrites, other axons, cell bodies, and target cells
synapses are formed by complex proteins (electric vs chemical)
late stage = synapse pruning if not strengthened
what are the types of receptors on the postsynaptic membrane and their functions
AMPA receptor: ligand gated ion channel pending on presynaptic stimuli intensity; depolarization of postsynaptic membrane changes NMDA receptor conformation
NMDA receptor: Ca2+ channel is blocked by Mg2+
how does ca2+ concentration in the postsynaptoc membrane affect the functions of the Ca2+
if above 5microM = activate kinase, transfer more AMPA to postsynaptic membrane; this strengthens the synapse (long term potentiation/LTP)
if below 1 microM = activate phosphatase, endocytosis of AMPA from postsynaptic membrane; pruning the synapse (long term depression/LTD)
describe the critical stage of development of synapses/myelogenesis
birth = guided extension of axons
2 years = over amount of synapses
6 years = synapses are pruned; mature neural connecting network
*myelogenesis = myelination happens until late 20s
what is the importance of pruning og synapses
spatiotemporal summation must be unified
each neuron gives off an output like morse code, each conveys a different meaning
there can be more than 1 menaing (i.e. mirror neurons and context dependent coding)
without pruning and after pruning can encode entirely different meanings
mechanisms of pruning
long term potentiation and long term depression
what is adult neurogenesis
more common in lower level animals
examples:
- regrowth of tails on lizards
- growth of eyes and brain in goldfish
- refresh caudate nucleus to learn sons in songbird
where in the brain can you find stem cells
dentate gyrus of hippocampus and subventricular zone (septal nuclei)
how do blast cells migrate
along radial glial processes then horizontal transfer
neuroblasts
- only for granule cells in hippocampus
- granule and periglomerular cells in olfactory bulb, rostral migration system
glioblasts
- mainly oligodendrocytes
concentration of 14C in individuals born in 1952 vs 1968
1952
- no 14C in neurons = limited regenerating neurons in lifespan
- slight increase in 14C in glial cells = limited gliogenesis to replace lost glia
1968
- high concentration of 14C in neurons = limited replacement of neurons in lifespan
- slight decrease 14C in glial cells = limited gliogenesis to replace lost glia
what is a diaschisis
neuropathology after nervous system injury
local injury results in both local and distant functional loss
what is a connectome
nervous system functions through circuitry called a connectomeq
MCA stroke; explain the diaschisis
whole brain functions are affected
occipital functional loss
L hemineglect
timeframe for neuroplasticity with motor functions
3 months
3 types of neuroplasticities and their prognosis **
peripheral axon injury = potential for full regrowth
in CNS, activating glia, loss of neurons and loss of function
in CNS activating glia, rarely neurogenesis for lost neurons, restoring functions
why might there be slow reparation/regeneration of axons in the CNS
disruption of blood brain barrier after CNS injury = recruits glia and lasts for weeks
invasion of immune cells that lasts months
both contribute to glial scar formation; this may completely block regeneration of axons
what is chromatolysis
death of neurons
no neurotrophins transported back to the cell bod
describe the neuroplasticity post injury/loss of BUEs when using BLEs for ADLs
functional MRI show activated regions for LE motor functions AND the motor region for BUEs (improved fine motor control of the toes)
describe the changes in brain pathways associated with blind people using Braille
braille reading in trained blind patients increased activities of the visual cortex
connections were restructured
increased connections with somatosensory cortex
decreased connections to dorsal/ventral streams and motor cortex
describe how the use it or lose it principle of neuroplasticity pertains to the use of braille
monitoring of the 1st dorsal interosseous mm of a braille proofreader showed decreased motor presentation following a 10 day break from work but then a return to normal levels after 1 week of work again
reversible principle of therapeutic exercise
describe the S1 presentation after electric stimulation of the ulnar and median nerve of untrained subjects vs skilled musicians
skilled musicians = larger representation
