Test 1 Study Guide Part 2 Flashcards
PNS includes:
- Cranial nerves, and spinal nerves
What are brain tumors in adults normally composed off? Why?
Neuroglia/glial cells
Because these cells are still dividing unlike most neurons.
General term for dendrites and axons:
Processes (extension of the cell body)
Function of neuron body/features of interest:
Metabolic center of the cell, Nissl bodies (rough ER) are localized here and in some large dendrites, they generate proteins for the cell.
A cluster of cell bodies in the CNS Is called:
A cluster of cell bodies in the PNS Is called:
Nuclei
Ganglia
Axonal collaterals:
Axonal collaterals:
extensions/splits which break off from the original axon. An axon can have as many as 200 or more Axon collaterals (collaterals can split further, innervating as many as 30 - 60 thousand neurons).
Three types of neurons
Sensory/afferent neurons:
Motor/efferent neurons:
Interneurons/association neurons:
What is the function of associative/interneurons:
They are located entirely within the CNS and serve to associate or integrate functions of the nervous system (they do all processing)
What are the two broad class of motor/efferent neurons and what do they do:
- Somatic: Regulates skeletal muscles, voluntary and involuntary
- Autonomic: Smooth muscle, cardiac muscle, glands
What are the two subdivisions of autonomic motor neurons and what do they do:
Sympathetic: Generally speeds up activities
Parasympathetic: Generally slows activities
What is the significance of autonomic ganglia and their control centers?
Autonomic ganglia: house the cell bodies of the neurons which innervate the autonomic system
Control centers: Autonomic ganglia interact with neurons which are housed in the autonomic nervous system to compose the autonomic nervous system (and make decisions as to what it should do)
Locations of the following:
- pseudounipolar neurons:
- Bipolar neurons:
- Multipolar neurons:
pseudounipolar neurons:
- Sensory neurons are pseudounipolar (synapse with brain or spinal cord)
Bipolar neurons:
- Retina of the Eyes
Multipolar neurons:
- Most common types (multiple dendrites one axon)
A bundle of axons in the CNS is called:
A bundle of axons in the PNS is called:
Tract
Nerve
Neuroglial cells of the PNS:
Satellite cells/ganglionic gliocytes: Schwann cells (neurolemmocytes):
Neuroglial cells of the CNS:
Oligodendrocytes
Astrocytes
Ependymal cells
Microglial
What makes microglial cells unique?
Derived from a hematopoietic cell line (they come from embryonic yolk sack and migrate to the developing neural tube)
How are microglia different from macrophages, how are they the same?
Because macrophages come from monocytes formed in the bone marrow.
They are the same because both are of a myeloid origin (gives rise to RBCs, many immune cells, monocytes and macrophages)
Microglial resting through activation:
Resting state: they have many processes extended probing for damage or foreign stimuli.
Infection, trauma or an altered state leads to:
- Development of amoeboid in shape
- Phagocytic motile cells
- Follow chemokines, remove damaged dendrites, axon terminals, myelin, and other debris
- Release anti-inflamatory chemokines
- Kill exogenous pathogens
What are the dangers of active microglial cells?
Overactive microglial cell can release free radicals that contribute to neurodegenerative disease.
Why are satellite cells also called ganglionic gliocytes?
Ganglionic gliocytes remove waste and give nutrients to neurons. Since the soma, the metabolic center of the cells are located in the ganglions (n the PNS) the sattelite cells are also localized there. thus ganglionic. Gliocytes is likely because they are small glial cells.
What is the size difference between myelinated and unmyelinated axons?
Axons smaller then 2 ums in diameter are usually unmyelinated
Are cells in the PNS or CNS coated in sheath of schwann?
PNS (this is where schwann cells are)
Do schwann cells rap themselves more or less times on thicker axons?
More times, so the myelin sheaths will be thicker.
What is the spacing between nodes of ranvier?
How long is each node?
1-2 mm
1-2 um
Neurilemma:
A thin sheath of schwann, a continuous layer is in all cells in the PNS (where schwann cells are located).
On myelinated neurons, the schwann cells wrap themselves repeatedly around the nerve, and then remain living outside.
On unmyelinated neurons schwann cells still live on the outside.
Neurilemma is on the outside of a myelin sheath if one is present
Oligodendrocytes:
- Function:
- Time of formation:
- Function:
Send out extensions which wrap around multiple axons, giving myelin sheaths. - Time of formation:
Postnatally into late adolecense
Gray matter in the CNS: - Location: - Composition: White matter in the CNS: - Location: - Composition:
Gray matter in the CNS: - Location: outer surface of brain - Composition: Predominately cell bodies and dendrites (lack myelin) White matter in the CNS: - Location: Interior of the brain - Composition: Myelinated axons
Gray matter in the PNS: - Location: - Composition: White matter in the PNS: - Location: - Composition:
Gray matter in the PNS: - Location: interior of the spinal cord - Composition: Predominately cell bodies and dendrites (lack myelin) White matter in the PNS: - Location: Exterior of the spinal cord - Composition: Myelinated axons
An axon in a peripheral nerve is cut. What happens next?
1: The distal portion of the axon as well as the myelin sheath is phagocytes by schwann cells and macrophages.
2-1: Schwann cells, surrounded by the basement membrane, then form a regeneration tube
2-2: The remaining axon begins to grow, utilizing amoeboid movement
3: The regeneration tube is believed to produce chemicals which attract the growth of the nerve, guiding it to its proper destination
What must be necessary for regrowth of a peripheral nerve (CNS nerves struggle to regrow, so we’re ignoring them for now)?
There must not yet be tissue death, surgery can reconnect nerves otherwise. (this is for severed digits)
What happens after a spinal cord injury:
1: some neurons die as a direct result of trauma
2: additional neurons and oligodendrocytes produce “death receptors” and die from apoptosis
3: Regeneration of axonal collaterals is possible, but the rest of the axon struggles
What makes regrowth difficult after an injury to the spinal cord?
1: Molecules inhibiting growth in the membranes of myelin sheaths.
2: the formation of a glial scar physically blocks axon regeneration
3: The glial scar induces the production of proteins which inhibit growth.
4: proteins called Nogo produced by oligodendrocytes inhibit axonal regeneration.
What experiment demonstrated the possible inhibitory nature of Nogo?
Improved regeneration in rodent models with spinal cord injury or stroke when treated with antibodies against Nogo.
Transplanted embryonic neural stem cells suspended in growth factor do what?
Produce thousands of axons and can restore hindlimb function in rats with transected spinal cords!
Do schwann cells and myelin in the PNS also inhibit axon growth?
How is this bypassed?
Yes they do.
After injury the myelin sheaths are rapidly phagocytosed by macrophages and schwann cells.
Schwann cells also stop producing inhibitory proteins after injury and quickly switch to a conducive environment for nerve regrowth.
Blood brain barrier:
- What differentiates the BBB:
- Diffusement properties:
- Function:
- What differentiates the BBB:
Tight junctions between cells lead to no pores in capillaries (no paracellular movement).
All molecules entering the brain must diffuse through the cells of capillaries (intracellular movement) - Diffusement properties:
The same as those of a plasma membrane (non-polar and small can pass)
e.g. O2, CO2, alcohol, barbiturates (organic molecules
Ions and polar molecules require channels - Function:
Filters what can enter the brain.
Enzymes within the endothelial cells and astrocytes of the BBB can inactivate potential toxins
Astrocytes:
- Function in the BBB:
- Mechanism by which this occurs:
- What induces growth of astrocytes:
- Function in the BBB:
Induce tight junctions in endothelial cells
Induce carrier proteins and ion channels
Induce enzymes that destroy potentially toxic molecules - Mechanism by which this occurs:
Produce Neurotrophins such as glial-derived neurotophic factor (GDNF) which induce changes in the endothelial cells - What induces growth of astrocytes:
Regulators secreted by the endothelial cells of the capillaries
What results from communication between astrocytes and endothelial cells in the BBB?
Dynamic structure where the “tightness” can be adjusted by a variety of regulators.
The ability to respond to stimulation changes in membrane potential:
- is called:
- Occurs in which cells:
- is called:
Excitability/irritability - Occurs in which cells:
Muscle cells, neurons
Electrochemical gradient define:
The combined concentration and electrical gradients
Ion currents:
- Define the cause:
- What dictates where they can occur?
- Define the cause:
Increased membrane permeability to ion causing it to diffuse down its electrochemical gradient - What dictates where they can occur?
The channels (which said permeability results from) exist only in certain patches of membrane.
Depolarization: - Cause: - Inhibitory or excitatory: Hyperpolarization: - Cause: - Inhibitory or excitatory:
Depolarization: - Cause: Influx of cations - Inhibitory or excitatory: excitatory Hyperpolarization: - Cause: influx of anions or efflux of cations - Inhibitory or excitatory: inhibitory
Does potassium have gated or not gated (leakage channels)?
Sodium?
Both gated and leakage channels. Only gated (though the flicker open allowing some leakage
What is the result of Na+ channel gating being imperfect?
Na channel gates occasionally flicker open. This causes a slightly more positive membrane potential then potassium equilibrium potential (which means K will leak out of the cell given the chance)
Describe the events of an action potential in terms of Na+ and K+ channels:
1: Excitatory stimuli causes the potential to cross a threshold of -55 mV (ish)
2: This opens voltage gated Na+ channels, influx of Na+ ensues
3 - 1: Depolarization from Na+ influx causes voltage gated K+ channels to open, K+ leaves the cell
3 - 2: At the same time Na+ channels become inactivated, either by ball and chain mechanism or a conformational change in the gate
4: the cell repolarizes, and has an undershoot/hyperpolarization caused be the time it takes to close voltage gated K+ channels
How is stimulus strength encoded for by action potentials
Frequency of action potentials (frequency modulated):
- The more action potential to occur within a given period of time the stronger the stimuli
RECRUITMENT:
- A larger stimuli will gradually add more and more regional axons firing.
- Different neurons will have different thresholds or different sizes resulting in differential ability to reach their potential.
What is another name for action potential?
Spike potential
What causes an absolute refractory period?
What causes the relative refractory period?
What limits the maximum frequency of action potentials?
1 millisecond
The absolute refractory period is caused by either a ball and chain mechanism or a conformational change inside the receptor (it depends on the type of voltage gated channel), during inactivation an action potential cannot occur.
1-2 milliseconds
The relative refractory period is caused because of the efflux of K+ from the cell. This hyperpolarization/undershoot followed by a lag where potassium levels have not ‘leaked’ back to equilibrium. This efflux of positive charges must be overcome by the influx of Na+ or other cations to make an action potential fire, this barrier is called the relative refractory period.
Refractory periods
True or False:
regardless of the mode of inactivation of a channel (ball and chain or conformational shift) inactivation changes after a set period of time
True
The point at which the action potential originates
Initial segment of the axon (most distal portion of the axon hillock)
L-dopa is also called?
Levadopa
