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FoM - normal function > how nerves work > Flashcards

how nerves work Flashcards

1
Q

what is the nervous system divided into?

A

Central Nervous System (CNS) → Brain & Spinal cord

Peripheral Nervous System (PNS) → Peripheral nerves

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2
Q

what is the peripheral nervous system further divided into?

A

Somatic Nervous System (SNS) → voluntary

Autonomic Nervous System (ANS) → involuntary (sympathetic & parasympathetic)

Enteric Nervous System (ENS) → innervates the gut

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3
Q

what is the cerebrum? what 4 lobes is it composed of?

A

largest part of the brain, two hemispheres connected at corpus callosum, made up of four lobes:

[1] Frontal lobe → somatosensory cortex at back

[2] Parietal lobe

[3] Temporal lobe → auditory cortex

[4] Occipital lobe → visual cortex

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4
Q

what is the cerebellum (little brain)?

A

a structure that processes sensory info and coordinates movement.

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5
Q

what is the diencephalon (between brain)? what 4 structures is it composed of?

A

is a structure that lies between the brain stem and the cerebrum, composed of:

[1] Thalamus → integrating center and a relay station

[2] Hypothalamus → neuroendocrine regulator - homeostasis and behavioural drives (e.g. hunger and thirst)

[3] Pituitary gland

[4] Pineal gland

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6
Q

what is the brainstem? what 3 structures is it made up of?

A

oldest part of brain, is made of structures that control blood pressure/respiratory rhythm, like:

[1] Midbrain

[2] Pons

[3] Medulla Oblongata

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7
Q

what is the structure of a neuron?

A

Dendrites (receives information)

Soma (contains nucleus)

Initial segment (trigger and generation of action potential)

Axon (myelinated & unmyelinated, sends action potential)

Presynaptic terminal (moving action potential through neurotransmitters)

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8
Q

there are 12 pairs of cranial nerves, what are the 31 pairs of spinal nerves in the spinal chord?

A

[1] 8 Cervical nerves

[2] 12 Thoracic nerves

[3] 5 Lumbar nerves

[4] 5 Sacral nerves

[5] 1 Coccygeal nerves

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9
Q

what is sulci and gyri?

A

grooves/valleys in the brain

Gyri (sing. gyrus) → dividing convolutions/hills in the brain

The degree of folding is directly related to the level of processing of which the brain is capable.

i.e. lower animals have a smoother cortex compared to humans

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10
Q

what are the 3 types of neurons?

A

Posterior (dorsal) root is a PNS nerve root that consists of sensory (afferent) fibers that conveys neural impusles to the CNS from sensory receptors.

afferent = in

Interneurons are CNS neurons that connect the two roots together.

Anterior (ventral) root is a PNS nerve root that consists of motor (efferent) fibers passing from nerve cell bodies in the anterior horn of the spinal cord gray matter to peripheral organs.

efferent = out

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11
Q

what are the 2 different glia cells of the peripheral nervous system?

A

schwann cells - forms myelin sheath
satellite cells - support neuron and cell bodies

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12
Q

What’s the difference between Gray matter and White matter?

Compare brain and spinal cord white/gray matter distribution

A

Grey matter contains neuron bodies/somas

White matter contains myelinated axons

Brain - white matter on the inside & gray matter on the outside (the cortex)

Spinal cord - gray matter on the inside & white matter on the outside

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12
Q

what are the 4 types of glia cells in the central nervous system?

A

astrocytes
- Maintain external environment for the neurons
- Surround blood vessels and form blood brain barrier

ependymal - produces cerebrospinal fluid

microglia - macrophages of cns, hoover up infection

oligodendrocytes - form myelin sheath

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13
Q

what is the spinal cord pathway?

A

Afferent/Sensory/Dorsal (Ascending Tract)
- PNS impulses taken from receptors into dorsal root ganglion
(cell bodies)
- Dorsal root into the dorsal horn (axons) to the CNS

Efferent/Motor/Ventral (Descending Tract)
- CNS impluses taken into → ventral horn (cell bodies) → ventral root (axons) → peripheral organ (response)

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13
Q

what are spinal tracts? what are they divided into?

A

groups of nerve fibres divided into:

Ascending Spinal Tracts (sensory) → sensory receptors to CNS

Descending Spinal Tracts (motor) → motor CNS to PNS to organs

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14
Q

what are 3 types of membrane potentials?

A

Action potentials (AP) - transmit signals over long distances

Graded potentials (GP) - decide when an action potential should be fired

Resting Membrane potential (RMP) - keeps cell ready to respond

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14
Q

How is resting membrane potential (Vm) i.e. potential difference approx -70mV maintained/generated?

A

[1] The uneven distribution of ions across the membrane i.e. Na+ & Cl- & K+

[2] Differing membrane permeability to the ions (depends on the amount of open ion channels)

  • K+ is the major ion contributing to the RMP because the membrane is much more permeable (has more open ion channels) to it than to other ions, so they have a smaller effect on RMP.

This is why the RMP is close to the K equilibrium potential.

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14
Q

what is the equilibrium potential of an ion?

A

it’s the membrane potential at which the electrical and chemical/concentration forces/gradients acting on the ion are equal and opposite.

(+) outside → (-) inside (ion pulled inside)

↑ [K+] inside → ↓ [K+] outside (ion pushed outside)

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15
Q

Why doesn’t half of the K+ move out of the cell to equilibrate as it goes down its concentration gradient?

A

Because the concentration gradient (K+ going out) develops an electrical gradient that is opposite to it (K+ going in) eventually reaching an equilibirum where they are both equal forces/gradients.

This is called the equilibrium potential

If the concentration gradient was higher, the ion movement will produce a bigger electrical potential before they are equal, leading to a higher equilibrium potential.

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16
Q

According to Nernst’s equation of K+, the equilibrium potential/RMP for neurons should be approx -90mV, but that isn’t the case in reality.

Why is that?

A

Because of the differing membrane permeability to the ions
(how many open ion channels are in the membrane)

  • K+ is the major ion contributing to the RMP because the membrane is much more permeable (has more open ion channels) to it than to other ions, so they have a smaller effect on RMP.

The other ions, in addition to the Na+ / K+ pump, also affect the RMP, but they have a smaller effect.

That’s the reason why RMP is close to -70 mV

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17
Q

Why is K+ considered the major contributing ion to the RMP?

A

Because the permeability of the cell membrane is much higher to K+ compared to other ions.

i.e. contains more open ion channels to K+ at rest.

Permeability to K+ is at least 30 times higher than other ions.

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18
Q

How does the Na+ / K+ pump contribute to the resting membrane potential?

A

[a] It is an electrogenic pump, it imports 2 K+ and exports 3 Na+ against their concentration gradients making the inside slightly move negative.

5 mV contribution to the RMP

[b] It sets up the ion concentration gradients.

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19
Q

What happens to the RMP if you poison the Na+ / K+ pump?

A

Cells will depolarise only a few mV from -70 to -65

Then there’s a gradual loss of concentration gradient until we lose the RMP

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20
Q

what do graded potentials do?

A

they generate action potentials when they depolarise the cell to reach the threshold
(from -70 mV to -55mV).

21
Q

How does hyperkalaemia cause ventricular fibrillation in the heart?

A

high [K+] in the ECF leads to a smaller concentration gradient, which then generates a small electrical gradient to oppose it, this leads to a more depolarised cell equilibrium potential/RMP.

↑ [K+] → ↓ conc gradient → ↓ elec gradient → depolarised (more positive) cell RMP → action potentials

This causes cells to fire action potentials in an irregular manner, which causes ventricular fibrillation.

21
Q

how is the K+ maintained in the brain when you have a high [K+] in the blood?

A

The blood brain barrier, made by astrocytes, prevents K+ in the capillaries from entering the brain.

So [K+] ECF in the brain does not change

22
Q

what are the 4 types of graded potentials?

A

Generator potentials - at sensory receptors e.g. the skin

Postsynaptic potentials - at synapses

Endplate potentials - at neuromuscular junctions

Pacemaker potentials - pacemaker tissues in heart

23
Q

what are the 4 properties of graded potentials?

A

Graded (small stimulus = small response & vice versa)

Decremental - (they diminish over time like throwing a pebble in a lake)

Exciting/Depolarising (excitatory postsynaptic potential - EPSP) or

Inhibiting/Hyperpolarising (inhibitory postsynaptic potential - IPSP

Summation - important for synaptic integration

24
Q

How do neurons generate graded potentials?

A

By binding certain excitatory/inhibitory neurotransmitters to ligand-gated ion channels on the postsynaptic cell or through closing the channels.

Through this we can control which ions go in or out depending on their concentration gradients, to generate a graded potential.

Ion channels open:

K+ going out OR Cl- moving in → IPSP

Na+ or Ca2+ moving in → EPSP

Ion channels close:

K+ closing → EPSP

Na+ closing → IPSP

25
Q

why are IPSP/EPSP fast/ slow? what are they known as?

A

Fast IPSPs/EPSPs are fast because they are mediated by ion channels. Fast → begins quickly and the effect lasts milliseconds

Known as ionotropic receptors

Slow IPSPs/EPSPs are slow because they are mediated by G protein-coupled receptors. Slow → begins slowly by response of 2nd messenger and the effect lasts seconds to minutes.

Known as metabotropic receptors

26
Q

what is GABA (Gamma-aminobutyric acid)?

A

the principle fast inhibitors neurotransmitter in the brain.

27
Q

what is glutamtate and glycine?

A

Glutamate is the principle fast excitatory neurotransmitter in the central nervous system.

Glycine is the principle fast inhibitory neurotransmitter in the spinal cord

28
Q

what happens due to a decremental property of a graded potential?

A

A synapse that is closer to the initial segment (axon hillock) will generate a graded potential that is greater than a synapse that is farther away from the initial segment.

29
Q

what is synaptic integration?

A

the process of summing all inputs from presynaptic neurons, whether inhibitory or excitatory, at the axon hillock, it generates an action potential if threshold is reached (-55 mV).

29
Q

when graded potential reacheds threshold (-55mv) what 3 things does this cause?

A

[1] Depolarization

opening of Na+ voltage gated channels

(due to change in membrane threshold)

Na+ moves in → depolarization (-55 mV to +40 mV, which is close to the equilibrium potential for Na+)

Then the Na+ channels close.

[2] Repolarisation

opening of K+ voltage gated channels

(due to change in membrane threshold but they are slower and last longer)

K+ moves out → repolarization (+40 mV to -90 mV due to hyperpolarization)

[3] Hyperpolarization

occurs due to K+ voltage gated channels staying open a little longer than needed to and sending the cell towards K+ equilibrium potential -90mV

then the K+ channels close

30
Q

what are the 3 types of synaptic connections?

A

Axo-dendritic synapse → a (usually excitatory synapses e.g. Glutamate)

Axo-somatic synapse → c (usually inhibitory synapses e.g. GABA)

Axo-axonal synapse → b & d
(can be excitatory or inhibitory - by regulating the amount of neurotransmitter released)

31
Q

what 2 methods is synaptic integration done through? can be excitatory or inhibitory

A

Temporal Summation - occurs when two graded potentials from one presynaptic neuron occur close together in time.

Spatial Summation - occurs when the currents from nearly simultaneous graded potentials combine.

32
Q

what is the absolute refractory period?

A

At the start of an action potential propagation the excitability of the cell is high, but once the action potential fires it drops to zero, and no action potential can be generated

33
Q

Why does the cell permeability to Na+ increase more than usual as voltage gated Na+ channels open?

A

Because there is a positive feedback mechanism

Entry of Na+ leads to depolarization, which causes more voltage gated Na+ channels to open, increasing the cell permeability to Na+ even more.

This is why there is a massive influx of Na+ into the cell.

33
Q

what are some properties of an action potential?

A

Properties of an action potential:

[1] They have a threshold at -55 mV

[2] All-or-none - you never get a half action potential!

[3] Encode stimulus intensity in their not their amplitude

i.e. they encode a stronger stimulus by firing more action potentials.

[4] Self-propagating & travel slowly 1 m/s (without myelin sheath)

[5] Mediated by voltage-gated channels

34
Q

what is the relative refractory period?

A

Once the action potential passes through a location, it goes through a phase where the excitability of the cell slowly rises and the Na+ gated channels slowly recover and open

34
Q

Why can’t an action potential be generated both ways as it propagates through the cell?

A

Because the area behind an action potential is in a phase called an absolute/relative refractory phase where the Na+ voltage gated channels are either closed or they are recovering from generating the action potential.

35
Q

How can action potentials be delivered across long distances without decaying?

A

Because they are able to self-propagate across an axon by

depolarization - repolarization - hyperpolarization

The previous area then is in a absolute refractory period (Na+ channels are closed & cell excitability is at zero) and they both slowly recover over in a relative refractory period.

36
Q

There are two ways to speed up action potential conduction velocity:

A

[1] Large axons

→ Axial resistance is lower in larger axons than smaller axons, so the electric current flows more easily.

→ Allows the Na+ channels to be wider spaced along the membrane

[2] Myelination

→ formed by Oligodendrocytes in CNS & Schwann cells in PNS around axons

→ Myelin increases membrane resistance, and reduces membrane capacitance, so less current is wasted

→ Allows the action potential to spread passively from one node of Ranvier to another, called {{c2::saltatory conduction}} - dancing/jumping from one node to the next.

→ Allows big increase in conduction velocity

→ Metabolically good as it only allows ions to cross at nodes, and saves space & energy.

37
Q

what are the consequences of demyelination?

A

CNS → Multiple sclerosis

PNS → Guillain-Barre syndrome

These are both demyelinating diseases, they cause a:

  • Decrease in membrane resistance and an Increase in membrance capacitance

→ leads to loss of current between nodes and saltatory conduction fails.

38
Q

what is a subthreshold graded potential?

A

a graded potential starts above threshold at its initaition point but decreases in strength and therefore does not initiate an action potential

39
Q

what is a suprathreshold graded potential?

A

a stronger stimulus at the same point on the cell body created a graded potential that is still above thresholdby the time it reaches the trigger zone, so an action potential results

40
Q

what are the functions of 5 different axons? Aalpha, Abeta, Agamma, Adelta, C

A

Aalpha (largest myelinated)
- velocity - 70-120m/sec
- proprioception, motoneurones

Abeta (large myelinated)
- velocity - 30-70m/sec
- touch, pressure

Agamma (small myelinated)
- velocity -15-30m/sec
- motoneurones of muscle spindles

Adelta (smallest myelinated)
- 12-30m/sec
- touch, could, fast pain

C (unmyelinated)
- 0.5-2m/sec
- warmth, slow pain

41
Q

how does the motor neurone stimulate contraction in skeletal muscle?

A

by evoking an action potential in the sarcolemma, the muscle membrane.

42
Q

Why does the neuromuscular junction contain no synaptic integration?
i.e. how does a healthy NMJ have a high safety factor?

A

Because the post-junctional folds pack voltage-gated Na+ channels close to where the graded potential is evoked, so it will ALWAYS be big enough to reach threshold and make an action potential.

If the motor neuron fires an action potential, the muscle will always fire an action potential.

42
Q

what is the neuromuscular junction?

A

a synapse between a motor neuron and a skeletal muscle.

43
Q

Why would administration of a drug that inhibits acetylcholinesterase improve muscle function in patients with a deficiency of ACh receptors on their skeletal muscles?

A

Because inhibition of acetylcholinesterase means that ACh sticks around longer in the synaptic cleft and generates a stronger stimuli in the postsynaptic membrane i.e. more action potentials.

Therefore it improves muscle function in the patients.

44
Q

what are nonspecific monovalent cation channels?

A

e.g. when glutamate binding to receptor that opens up a channel which allows Na+ to go inside and a little K+ goes outside, this generates a fast EPSP.

45
Q

what is a a divergent pathway?

A

a type of synaptic connectivity where one presynaptic neuron branches to affect a larger number of postsynaptic neurons

45
Q

what are the different types of synaptic connectivity?

A

Convergence

Divergence

Feedback inhibition
- stimulus causes a response that counteracts the stimulus.
- Neuron fires AP → axon → axon collateral (branch) → activates inhibitory neuron → hyperpolarization

Monosynaptic pathway - simplest reflex, sensory neuron directly activates a motor neuron

e.g. patellar tendon reflex

Polysynaptic pathway - complex reflex, synaptic integration either excitatory or inhibitory

45
Q

what is a convergent pathway?

A

convergent pathway is a type of synaptic connectivity where many presynaptic neurons provide input to influence a smaller number of postsynaptic neurons.

46
Q

what is synaptic plasticity?

A

Synaptic plasticity is the ability of the nervous system to change activity at synapses.

Occurs primarily in the CNS

e.g. enhancing activity → potentiation/facilitation

e.g. decreasing activity → depression

If either persists for a significant period of time, they are called long-term potentiation/ depression.

47
Q

what happens when a graded potential increases in strength?

A

they trigger more frequent action potentials, releasing more neurotransmitter.

FoM - normal function (20 decks)

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