nervous system 2 Flashcards

1
Q

TYPES OF MOTOR NEURONS:

A

Upper motor neurons – motor neurons that synapse either with another upper motor neuron (CNS) or with a lower motor neuron.

Lower motor neurons – motor neurons that directly stimulate effector organs in response to signals from the UMN.

Summary
Usually a command from the CNS will pass from an UMN to a LMN before stimulating the muscle or gland (effector organ).

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2
Q

Electrical signals in the Neuron

A

Neurons are electrically excitable (like muscle cells) and conduct signals (action potentials) to target cells => muscles or glands.

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3
Q

Neurons communicate using two types of signals…

A

1) Graded potentials (short distance only)
2) Action potentials (longer distances)
Remember muscle APs? Now we have
nerve APs

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4
Q

Membrane Potential:

A

The production of nerve impulses (graded potentials and action potentials) depends on two features of the cell membrane:

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5
Q

Resting membrane potential

A

– electrical difference (voltage) across the cell membrane (when the neuron is at rest).

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6
Q

Ion channels

A

– the flow of ions across the membrane makes up the electrical current.

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7
Q

*Graded potentials and action potentials both occur due to

A

the opening and closing of ion channels which creates a flow of ions (current).

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8
Q

Membrane potential – exists due to

A

the electrical difference (separation charge, or voltage) across the cell membrane. Measured in millivolts (mV). In neurons it is -70mV (it is slightly different in other types of cells.)

The buildup of positive ions along the outside of the cell membrane, and the negative ions on the inside of the membrane creates a form of potential electrical energy.

The greater the difference in charge, the greater the membrane potential (voltage).

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9
Q

Resting membrane potential is due to:

A

Unequal distribution of ions in the ECF and ICF

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10
Q

ECF has a higher concentration of

A

Na+ ions,

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11
Q

ICF has a higher concentration of

A

K+ ions.

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12
Q

K+ has more

A

leakage channels to diffuse down its concentration gradient compared to Na+ (the membrane is more permeable to K+).
This movement of K+ makes the ECF side of the membrane more positive.

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13
Q

Anions that can’t leave the cell

A

The presence of amino acids and ATP (phosphate) which are negatively charged. These molecules are unable to leave the cell and therefore make the inside of the cell membrane more negative.

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14
Q

Electrogenic nature of Na+/K+ pump

A

Na+/K+-ATPase pumps 3 Na+ out of the cell and 2 K+ in each cycle. This means one more cation (1+) is pumped out than in, making the inside of the cell relatively more negative. This helps to maintain the neuron’s resting membrane potential of -70mV.

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15
Q

Na+/K+ pump

A

Ubiquitous (found in all cells)
Pumps 3 Na+ OUT for every 2 K+ IN to help establish this resting membrane potential.
ACTIVE transport (pushing these ions against their concentration gradients).

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16
Q

Na+ & K+ are the most

A

important electrogenic ions – I.e. their movement contributes to establishing the resting membrane potential.

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17
Q

Na+/K+ pump:

A

Three Na+ OUT of the cell for every two K+

IN

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18
Q

Because the ECF has a higher

A

[Na+], this ion tends to “leak” into the cell (down its concentration gradient).

.

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19
Q

Because the ICF has a higher

A

[K+], this ion tends to “leak” out of the cell (down its concentration gradient)

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20
Q

Sodium and potassium are considered

A

electrogenic. I.e. they contribute to establishing the resting membrane potential.

 The Na+/K+ pump actively pumps these 2 ions AGAINST their concentration gradients. This costs ATP!!!

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21
Q

Ion channels

A

– ion channels are embedded in the cell membrane. When open they allow specific ions into and/or out of the cell, down their electrochemical gradient.
As ions move they create electrical current which changes the membrane potential.

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22
Q

The main ions involved are:

A

Sodium (Na+) – carries a positive charge; concentrated higher OUTSIDE the cell. It wants to leak into the cell, down its concentration gradient. [This is the most abundant cation/ion in extracellular fluid]

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23
Q

Potassium (K+)

A

– carries a positive charge; concentrated higher INSIDE the cell. It wants to leak out of the cell, down its concentration gradient. (There are also MORE K+ leakage channels than Na+ channels) [This is the most abundant cation in intracellular fluid.]

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24
Q

Chloride (Cl-)

A

– carries a negative charge; concentrated outside the cell. [Most prevalent anion found in extracellular fluid.]

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25
Q

Calcium (Ca2+)

A

– carries a highly positive charge; concentrated outside the cell. [Most abundant mineral/cation in the body although NOT in the ECF!]

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26
Q

Phosphate (PO4-)

A

– large and highly negative – concentrated inside the cell; don’t move too much because of size and lack of channels.

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27
Q

Amino acids (aa)

A

– large and mostly negative; concentrated inside the cell and don’t move too much because of size and lack of channels.

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28
Q

Electrical signals rely on 4 types of ion

channels to allow the flow of ions

A

Leakage channel

Voltage-gated channel

Ligand-gated channel

Mechanical-gated channel

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29
Q

Leakage channels

A

– alternate between open and closed positions. Most membranes tend to have more K+ ion channels making them more permeable to this ion.

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30
Q

Voltage-gated channels

A

– open & close as a response to a change in the membrane potential. These ion channels play a key role in action potentials.

31
Q

Ligand-gated channels

A

– open & close in response to chemicals/molecules (be it a hormone, neurotransmitter, etc.). Involved in graded potentials.

32
Q

Mechanically-gated channels

A

– open & close in response to a mechanical stimulus. E.g. vibrations, pressure, and stretch. Involved in graded potentials.

33
Q

Potentials: 1) Graded potentials

A
Graded Potentials (GP) – involve ligand-gated & 
mechanically gated channels.

Small deviations from the membrane potential (-70 mV) that makes the inside of the membrane either less negative (depolarizing) or more negative (hyperpolarizing).

May vary in amplitude (depending on the strength of the stimulus). Hence the term ‘graded’.

The effects of GPs are restricted to a smaller/localized area of the membrane (dendrite and cell body). They only last a short distance unlike action potentials.

Not subject to refractory period.

34
Q

Spatial graded potential

A

– summation of GP in response to stimuli that occur at different locations in the membrane of a neuron at the same time.

35
Q

Temporal graded potential

A

– summation of GP in response to stimuli that occur at the same location in the neuron’s membrane but at different times. I.e. Same location firing several times in quick succession.

36
Q

Action Potentials

A

– an all or none electrical
impulse that occurs when a stimulus causes a
sufficiently large depolarization in the membrane
potential (reaches the AP threshold).

37
Q

AP -Arises from

A

the trigger zone at the axon hillock
Conducts AP down the axon to axon terminals
Involves voltage gated channels.
Works on the all or none principle (no summation) – like dominoes falling
2 key phases=
1) depolarization
2) repolarization

38
Q
  1. Depolarization
A

– when a depolarizing GP causes the membrane of the axon to reach threshold, Na+ channels open and Na+ rushes into the cell. This makes the inside of the cell more positive. (-70 mV  - 55mV  0 mV  +30 mV)

39
Q
  1. Repolarization
A

– when the membrane potential returns to resting state (i.e. becomes negative/polar again).
K+ channels open and K+ rushes out of the cell which causes the membrane potential to return to its normal resting electrical potential (-70mV)

40
Q

Related principles (action potentials)

A

All or None Law – when depolarizing stimulus reaches a threshold, the action potential is generated and is always the same size & amplitude (i.e. dominoes – pushing of the first chip faster or harder will not alter the speed or the size of the toppling effect).

41
Q

Threshold

A

– the minimum amount of voltage needed to generate an action potential. Approximately -55 mV in a neuron. (I.e. at -60, no AP will be generated.)

42
Q

Refractory period

A

– the period following an AP in which no other AP can be generated.

43
Q

Absolute

A

– this coincides with the period of Na+ channel activation and inactivation (you can think of this as the Na+ channels being open). NO amount of stimulation can cause a 2nd AP during this time.

44
Q

Relative

A

– coincides with the time that the Na+ channels have closed (returned to their resting state) but the K+ channels are open. A stronger than normal stimulus is required to generate a 2nd AP during this time.

45
Q

Propagation (conduction) of APs:

2 main types:

A

Continuous – nerve impulse travels along the membrane due to opening of each subsequent and adjacent ion-channel. This occurs in unmyelinated axons and is (relatively) very slow

Saltatory – nerve impulses “jump” along the axon at the Nodes of Ranvier (remember these are the gaps between myelin sheaths where there are concentrated amounts of voltage gated channels).This is not only a LOT faster (usually 10 fold), it’s also a lot more energy efficient!

46
Q

Speed of transmission also depends on size/diameter of the axon; there are 3 types of axon fibers found throughout the body.

A
  1. A fibers – 100 % myelinated, speeds up to 130 m/sec. Found in sensory nerves of touch, temp & pressure, & motor neurons of skeletal muscles. VERY FAST!
  2. B fibers – moderately myelinated, speeds up to 15 m/sec. Found in ANS & visceral organs. MODERATELY FAST!
  3. C fibers – No myelination, slowest of the 3 fibers. Found in reproductive, urinary, excretory, digestive neurons, nociceptors from skin and viscera. SLOW!
47
Q

Signal Transmission between neurons:

A

Synapse: the site of communication between two neurons or a neuron and effector cell (mm/gland)
Synapses allow information to be filtered and integrated – they can be electrical or chemical.

a. pre-synaptic neuron – the neuron before the synapse
b. post-synaptic neuron – the neuron after the synapse
c. axo-dendritic – connection b/w an axon & a dendrite
d. axo-somatic – connection b/w an axon & cell body

48
Q

2 types of synapses:

Electrical

A

– uses gap junctions & found in the ANS, smooth muscle & cardiac muscles. The signal passes through tubes made of connexon proteins.
Advantageous for faster communication & synchronization of signals (e.g. heart/digestive organs).
FAST!!!

49
Q

Chemical

A

– involves the transmission of an AP across a synapse. This is slower!!!

50
Q

1) AP signal arrives at the synaptic end bulb of the pre-synaptic neuron.
2) Depolarization phase opens voltage gated Ca2+ channels that allow Ca2+ to flow in.
3) Stimulates the exocytosis of synaptic vesicles. Neurotransmitters from within the vesicles are released into the synaptic cleft.

A

4) The released neurotransmitters diffuse across the synapse and attach onto corresponding receptors on the post-synaptic membrane.
5) Binding of the neurotransmitter to the receptor (AKA ionatropic receptors-specific to NTs) opens the channel and thus triggers a graded potential (post synaptic potential).
The post synaptic potential may be excitatory (EPSP) or inhibitory (IPSP).

51
Q

If the neurotransmitter causes an opening of Na+ channels,

A

an excitatory post synaptic potential occurs (EPSP) – if that potential reaches threshold (-55mV), we get an action potential in the post synaptic neuron.

52
Q

If the neurotransmitter released causes hyperpolarization,

A

then we get an inhibitory effect (IPSP). In this case Cl- ion channels open and the cell membrane becomes more negative/hyperpolar (making an AP less likely to occur).

53
Q

Neurotransmitters cause graded potentials (post synaptic potentials) that are either a:

A

Excitatory post synaptic potentials (EPSP) – depolarizing, bringing the membrane closer to threshold.
Inhibitory post synaptic potential (IPSP) –hyperpolarizing, membrane becomes more negative, further away from threshold and therefore the generation of an AP becomes more difficult.

54
Q

Ionotropic receptors

A

– neurotransmitter receptor connected directly to an ion channel. I.e. An acetylcholine receptor at a NMJ is connected to a sodium ion channel

55
Q

Metabotropic receptors

A

– uses a messenger protein to open certain ion channels. These are usually inhibitory.
NB: ACh can be excitatory at some synapses (ionatropic) and inhibitory at others (metabotropic).

56
Q

Post synaptic neurons receive input from numerous pre-synaptic neurons.

A

Some release excitatory NTs, others inhibitory.
The total post synaptic potentials (the total excitatory effects vs the inhibitory effects) must reach threshold in order for an AP to be generated.

57
Q

Neurotransmitters (NTs): Two types:

Small molecule NTs

A
Acetylcholine (Ach)
Excitatory NT at NMJ, inhibitory NT in cardiac muscle in response to PSNS.
Amino Acids
Excitatory:
Glutamate and aspartate
Inhibitory: 
GABA – Gamma-aminobutyric Acid (CNS)
Glycine (inhibitory effects at NMJ)
58
Q

Biogenic Amines

A

Epinephrine (adrenaline) – released by adrenal glands and also as a NT in a small amount of neurons in the brain.
Norepinephrine (NE) (noradrenaline)
Dopamine (DA) – E.g. mood & pleasure centers.

Serotonin (5-HTP) – E.g. sensory perception & mood.

59
Q

Parkinson’s disease

A

=> not enough DA

60
Q

Nitric oxide (NO)

A

– vasodilator, relaxes blood vessel smooth muscles but also an important excitatory NT in the brain.

61
Q

Neuropeptides: large molecules

A

Found in CNS and PNS – both excitatory and inhibitory (depending on the receptor).
Bind to metabotropic receptors and many also play a role as hormones.

Certain neurons in the brain have receptors for opiate drugs which led to the discovery of the first neuropeptides:

Endorphins and enkephalins – natural painkillers – 200x stronger than morphine!
Substance P – also a neuropeptide – enhances the perception of pain.

62
Q

Removal of the NTs from the synaptic cleft is necessary for proper communication. If they aren’t cleared away they will continue to have an effect on the neuron/mm/gland. 3 ways:

A

Diffusion – NTs diffuse out of the cleft

Enzyme degradation – i.e. acetylcholinesterase at the NMJ.

Uptake by cells (reuptake) – NTs are actively transported back to the neuron that released it.

63
Q

Modifying the effects of NT

A

Delaying NT reuptake – cocaine delays reuptake of dopamine by blocking its active transporters.
NT synthesis can be inhibited – patients with Parkinson’s produce less dopamine.
NT release can be inhibited or enhanced –amphetamines enhance the release of dopamine and norepinephrine.
NT receptors can be blocked or activated, enhancing or inhibiting their effect – usually by drugs or toxins.

64
Q

Neural Circuits:

A

Functional groups of neurons that process specific types of information.
Types of neural circuits:

65
Q
  1. Simple
A

– simplest of all – 1 neuron stimulates another which in turn stimulates another (very rare).

66
Q
  1. Diverging
A

– a single neuron stimulates a few neurons, which then in turn stimulate more (signal amplification).
Sensory signals, and some neurons in the brain that are responsible for certain body movements will stimulate numerous motor neurons.

67
Q

Converging

A

– multiple neurons will stimulate 1 single neuron, which will allow for summative effects (reverse of diverging circuits). E.g. a single motor neuron receiving numerous signals from the brain.

68
Q
  1. Reverberating
A

– similar to simple circuits – neurons will reverberate backwards to stimulate earlier neurons. E.g. coordinated movement, short term memory, breathing.

69
Q
  1. Parallel after-discharge
A

– a single pre-synaptic cell stimulates multiple neurons which all synapse back to a common post-synaptic cell. E.g. precise activities like solving mathematical equations

70
Q

Damage and Repair of Nervous Tissue:

A

Plasticity – the capability to adapt/change based on experiene.

Neurogenesis – the birth of new neurons from undifferentiated stem cells.

Epidermal growth factor (EGF) – in 1992 it was discovered that this chemical can trigger mitosis in neuronal cells.

71
Q

CNS damage:

A

Our current understanding is that damage to
axons and cell bodies within the CNS (brain
& spinal cord) will result in permanent
damage. It is suspected that this is due to
the formation of myelin sheaths from
oligodendrocytes and NOT Schwann cells.
Research is ongoing.

72
Q

PNS damage:

A

Mild to moderate damage to neurons of the PNS will still permit good recovery of nerve function. This is b/c most cells of the PNS are covered with a protective sheath called a neurolemma (from Schwann cells).

73
Q

Chromatolysis

A

– degranulation of nissl bodies within the neuron as part of the repair process.

74
Q

Wallerian degeneration

A

– degeneration of the distal portion of the axon and myelin sheath as part of repair.