Week four Flashcards

1
Q

Development of the Nervous system

A

Human brain development is a protracted process that begins in the gestational week (GW) with the differentiation of the neural progenitor cells and extends at least through late adolescence

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2
Q

Neural System Development

A

Nervous system development starts early and finishes late.
It begins in the embryonic stage (defined as the time of life from conception until the end of the 8th week), continues throughout the fetal stage (defined as the interval from the beginning of week 9 to week 38) and continues beyond birth for several decades, at least into early adulthood (some argue for the full lifespan)

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3
Q

Milestones of the Neural System Development

A

1) Closure of the neural tube (- day 22)
2) Neurogenesis (16weeks)
3) Neuronal migration
4) Cell differentiation glial cell proliferation
5) Axonal and dendritic sprouting
6) Synptogenesis
7) Neuronal cell death (apoptosis)
8) Synaptic pruning
9) Myelination (late adolescence / early adulthood) Synaptic density in both cerebral and cerebellar cortex increass until early adult life.

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4
Q

Development of the central Nervous System

A
  • Parenchymal XNS tissues are derived from the ectodermal germ layer.
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5
Q

Two broad categories of CNS development (nature vs nurture)

A

Nature (experience expectant development)
- Resulting from “hardwired”, genetic programs that occur in a relatively tight time sequence
- Cell birth, differentiation, migration and axon guidance to target location

Nature (experience-dependent development)
- As axons reach their target locations the individuals interaction with the environment plays a role in modification of some aspects of CNS structure and function ( e.g. synapse formation, synaptic pruning and neural circuit 0creation and maintenance)

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6
Q

IQ tends to be higher in
- Babies with higher birthweight
- Children who grow taller in childhood and adolescence

A

Gale et al (2004) found full-scale IQ at age 9
increased by ~2 points for each SD increase in head circumference at 9 months and by ~2.9 points for each SD increase in head circumference at 9 years of age…They concluded that “brain growth during infancy and early childhood is more important than growth during foetal life in determining cognitive function”

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7
Q

Development of Myelination

A

What is myelinated by:
Full term: brainstem, cerebellum, posterior internal capsule, optic tract, perirolandic region

2 mo: + anterior intenal capsule
3 mo: + splenium of corpus callosum
6 mo: + genu of the corpus callosum

General myelination trend over neonatal development

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8
Q

The last brain areas to fully myelinate

A
  • anterior cingulate cortex (rational cognitive functions – error detection and conflict monitoring, reward anticipation, decision making, empathy, impulse control, emotion)
  • inferior temporal cortex (“where perception meets memory”—object identification)—the ‘ventral stream’ of the retinocortical pathway
  • dorsolateral prefrontal cortex (executive functions – decision making, working memory, social cognition) – as late as 20’s
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9
Q

Neuroplasticity

A

The ability of nervous tissue to change the mapping of neural function to change neural structure

Neuroplasticity can be inferred by changes in:
- Experience (sensation, preception)
- Behaviour
- Brain anatomy
- Functional brain maps
- Synaptic organization
- Phsyiological organization
- Molecular structure of nervous issues

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10
Q

Neuroplasticity

A
  • The human genome has 20,000 genes distributed across 23 chromosomes. Not all genes result in phenotypic expression.
  • Since you inherit 50% from each parent and each parent is a (more or less) random sample from the human genome it would be nearly impossible to genetically code for the development of a brain that would match every possible combination of somatic, metabolic and behavioural phenotypes
  • Therefore the brain must develop and maintain a calibrated relationship with the body to which it is neutrally connected and the environment in which it lives..
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11
Q

Why is neuroplasticity adaptive?

A
  • makes it possible for the brain to create and maintain high-fidelity functional relationships with the body and environment
    How does the CNS achieve this?
    • building, monitoring and modifying the brain-body interface (cortex, cerebellum, basal ganglia, etc.)
      Building, monitoring and modifying the neural representation of the environment (through sensorimotor interactions)
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12
Q

Neuroplasticity is necessary because:

A
  • The brain has to calibrate its interaction with the body because sexual reproduction prevents accurate prediction of phenotypic variation. (i.e., your brain cannot know the characteristics of your body, metabolism, etc.)
  • The brain has to recalibrate its interaction with the body during development, following injury, etc.
  • The brain has to reorganize following experience for learning and memory…

Dynamic reorganization of brain function (and to some extent, structure) occurs throughout the lifespan due to
* changing sensory inputs (development, aging, injury, etc.)
* changing motor output (behavioural demands, learned tasks, etc.)

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13
Q

Principles of Brain Plasticity

A
  • Plasticity is common to all nervous systems and
    the principles are conserved
  • Plasticity can be analyzed at many levels
  • Similar behavioural changes can correlate with
    different plastic changes
  • Experience-dependent changes interact
  • Neuroplasticity can be age-dependent and time
    dependent
  • Plasticity is related to experience frequency
  • Plasticity can be maladaptive, too…
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14
Q

Neuroplasticity and Sensitive Periods:

A
  • Brain plasticity varies as a function of a number of factors
  • Not all brain regions are equally plastic.. Most show maximum plasticity in limited time frames called ‘critical periods’ or ‘sensitive periods’..
  • e.g. binocular vision, Lorentz ‘imprinting’ in birds, language acquisition, motor skills. Etc.
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15
Q

Why is neuroplasticity Advantageous?

A

Mendel’s Second Law - the law of independent assortment; during gamete formation the segregation of the alleles of one allelic pair is independent of the segregation of the alleles of another allelic pair

Implications - Nervous system and body correlations can only be acquired by experiential, not genetic, means

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16
Q

Signaling Within the Neuron

A

The Neuron

  • The basic cellular unit of nervous tissue
  • An”irritable”*eukaryote
  • Neurons have evolved mechanisms to process information, communicate with other neurons and control other tissues (e.g., muscles and glands)
    *the excitatory ability thatliving organismshave to respond to changes in their environment
17
Q

Camillo Golgi 1843 - 1924

A
  • Invented the Golgi “black reaction” histological
    stain (1873) which opacifies 1% - 10% of the neurons in a thin tissue slice. When placed on a microscope stage and illuminated from behind the silhouettes of whole Golgi-stained neurons are visible against the brighter background.
  • Golgi incorrectly believed that the nervous system was a continuous filament of tissue, a fused “reticulum” (L. ‘little net’)
18
Q

Santiago Ramon y Cajal (1852 – 1934)

A

Made extensive drawings of Golgi-stained nervous tissue. He was a proponent of The “Neuron Doctrine” – that the nervous system was composed of elemental anatomic units – individual cells, later to be called “neurons”…

19
Q

Neurons generate signals

A
  • Neurons evolved a socialization that other eukaryotes do not have: the ability to generate and transmit signals that influence the physiology of other neurons
  • This is done by briefly varying the neuron’s membrane potential. (In all other eukaryotes the membrane potential remains fairly constant)
20
Q

Membrane potential

A

The membrane potential of a eukaryote refers to the relative difference in the electric charge across its cell membrane. It is created by differences in the concentration of various ions inside and outside the cell, created and maintained by both ‘passive’ and ‘active’ mechanisms that affect the permeability of ion channels and ion transporters in the cell membrane…The “resting” membrane potential is around -70 mV.

21
Q

Measuring a Neuron’s Electrical Activity

A
  • Oscilloscope
    • A device that measures electric potential as a function of the time
    • Used to record voltage changes on an axon
  • Unequal ion concentrations inside vs outside the cell membrane called the membrane potential

Charged particle (aka ion) movement across the eukaryote’s cell membrane results in a different electrical charge inside the cell relative to the interstitium (aka the extracellular matrix) in which the cell is bathed.
- Positively charged ions (called ‘cations’) such as sodium (Na+), potassium (K+), calcium (Ca++)
- Negatively charged ions (called ‘anions’) such as chloride (Cl−) and some protein molecules (A−)

22
Q

Maintaining the Resting Potential

A
  1. Because the membrane is relatively impermeable to large molecules, the negatively charged proteins remain inside the cell.
    1. Potassium and chloride channels are ‘ungated’ which means they allow potassium and chloride ions to pass freely through the membrane in both directions..
    2. Sodium channels are ‘gated’ which means that Na+ cannot pass freely through the membrane unless the gate Is held open..
    3. Active ion pumps located in the membrane (called NA+ – K+ pumps) export 3 Na+ ions from the cytoplasm to the interstitum and import 2 K+ ions from the interstitium into the cytoplasm with each pump cycle
23
Q

Alternating the Neurons Membrane Potential

A
  • Changing the permeability of the neuron’s plasma membrane to various species of ions causes the membrane potential to deviate from its resting level of -70mV.
  • Adding positive ions (or subtracting negative ions from) the cytoplasm with DEPOLARIZE the membrane potential while adding negative ions to (or subtracting positive ions from) the cytoplasm will HYPERPOLARIZE it.

When the neuron’s membrane potential changes from its resting level it’s called:

24
Q

When the neuron’s membrane potential changes from its resting level it’s called:
Depolarization

A
  • If the change in the membrane potential goes from -70mV to values less negative (e.g., to -50mV i.e., closer to 0V).
25
Hyperpolarization
* If the change in the membrane potential from -70 mV to values more negative (e.g., to -90 mV i.e., further away from 0V)
26
Two types of variable membrane potentials in neurons
* “Graded” potentials: found mainly in the dendrites (near the postsynaptic membranes) * Excitatory post synaptic potentials (EPSPs) * Inhibitory post synaptic potentials (IPSPs)
27
Action Potentials
found mainly in the axon and terminal boutons Post-synaptic Potentials are Graded Changes in the Membrane Potential in the Dendrites
28
Excitatory Post-Synaptic Potentials (EPSPs)
are created by neurotransmitter chemicals binding to excitatory* receptors embedded in the membrane of the neuron’s dendrites that cause the resting potential in the dendritic region to depolarize.
29
Inhibitory Post-Synaptic Potentials (IPSPs)
are created by neurotransmitter chemicals binding to inhibitory# receptors embedded in the membrane of the neuron’s dendrites that cause the cell’s resting potential in the dendritic region to hyperpolarize. *increasing the likelihood of the production of an action potential on its axon #decreasing the likelihood of the production of an action potential on its axon Note: Neurons can have BOTH excitatory and inhibitory synaptic receptors on their dendrites.
30
The Graded Potential
A brief, variable change in the transmembrane potential measured in the neuron’s dendrites and soma caused by the sum of the EPSPs and IPSPs generated by the binding of neurotransmitter molecules to receptors on the postsynaptic membrane of the receiving cell. The graded potential can take on many values depending upon this summation process…
31
Problem: Graded Potentials Aren’t Useful For Long-distance Signaling
The amplitude of graded potentials rapidly falls off with distance from the source of generation in the dendrites. This limits their effectiveness for signaling over longer neural distances.
32
Solution: The Action Potential
- A brief, ballistic (ie, all-or-none) change in the membrane potential generated in the neuron's soma and propagated without decrement along the full length a neuron's axon to its terminal boutons. - Action potentials can carry information over great distances using changes in the production rate rather than changes in amplitude (as graded potentials do)
33
What causes an Action Potential?
- All of the EPSPs and IPSPs created within a short time span are added together (integrated). The net result affects whether or not an action potential is created at the axon hillock. - The net membrane potential must be depolarized to about -55mV for an action potential to be produced. This value is called the 'trigger threshold'
34
rate law
The “rate law” demonstrated from the intracellular recording of action potentials generated in the optic nerve of the cat to (top) a weak and (bottom) a strong light stimulus... Note there are ‘spontaneous’ APs produced in the neuron both before and after the light stimulus is presented…
35
- Factors affecting the conduction velocity of Action Potential along axons...
- Conduction speed varies inversely with the cytoplasm’s electrical resistance - Cytoplasm resistance varies inversely with the cross-sectional area...so, ○ an axon with a large cross-sectional area (large caliber) has lower cytoplasmic resistance -- thus, a higher conduction velocity.
36
- Factors affecting speed of Action Potential propagation along axons
○ Conduction speed also varies inversely with the electrical capacitance of the axon membrane ○ Myelinated axons have a lower capacitance than unmyelinated axons, so... ○ a myelinated axon with a large cross-sectional area has the highest conduction velocity.
37
Myelination
conduction of action potentials through myelinated axons is faster than unmyelinated axons (>12 m/s).
38
Saltatory conduction
The action potential appears to jump from one node of Ranvier to the next.