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chp 7 Flashcards

1
Q

neurons are able to divide by_____

A

mitosis

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2
Q

neurons have three principal regions:

A

cell body, dendrites, axon

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3
Q

enlarged portion of axon that contains nucleus. Contains nissl bodies (stacks of rough ER needed for synthesis)

A

cell body

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4
Q

extend from the cytoplasm to body. Transmits graded electrical impulses to cell body

A

dendrites

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5
Q

conducts action potential away from the cell body. Can produce axon collaterals branches towards their ends

A

axon

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6
Q

anterograde transport:

A

Cell body→axon→dendrites; motors of KINESIN protein are used to move material along microtubules of cytoskeleton

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7
Q

retrograde transport:

A

Axon→dendrites→cell body -Involves motor protein dynein and dynactin

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8
Q

sensory/Afferent:

A

conduct impulses from sensory receptors into the CNS

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9
Q

motor/efferent:

A

conduct impulses out of the CNS to effector organs

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10
Q

interneurons:

A

within the CNS serve integrative functions of CNS

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11
Q

two types of motor neurons are:

A

somatic and autonomic

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12
Q

Somatic motor neurons:

A

reflex and voluntary control of skeletal muscle

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13
Q

autonomic motor neurons:

A

send axons to involuntary effects; smooth muscle, cardiac muscle, glands

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14
Q

cell bodies belonging to autonomic motor neurons are ______ of the CNS in autonomic ganglia

A

outside

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15
Q

neurons are structurally classified by number of processes extending from cell body

A

true

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16
Q

motor neurons are

A

multipolar neurons

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17
Q

axons of CNS

A

lack a neurilemma

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18
Q

axons of PNS

A

have a neurilemma

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19
Q

in CNS: myelin sheath is formed by

A

oligodendrocytes

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20
Q

in PNS: myelin sheath is formed by

A

successive wrapping of schwann cells

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21
Q

myelin sheath in PNS

A

● Schwann cell wrappings are made in the SAME spot (to form MS/Myelin Sheath layer)
● # of layers of myelin sheath are greater for THICKER axons
● Cytoplasm is located on outer region of schwann cell
● **IMPORTANT, nodes of Ranvier: gaps of exposed axons between schwann cells; these
regions PRODUCE NERVE IMPULSES
**Important to know: ALL axons in PNS, both myelinated and unmyelinated are surrounded by schwann cells

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22
Q

myelin sheath in CNS

A

Myelin sheaths of CNS are formed by oligodendrocytes
● Oligodendrocytes form myelin sheath over several axons; DIFF from schwann cells,
which only forms sheath around one axon
● White matter: Areas of the CNS with ↑ concentration of axons
● Gray matter: Areas of the CNS with ↑ concentration of cell bodies and dendrites, NO myelin sheath

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23
Q

Astrocytes take up K+ from the extracellular fluid

A

k+ diffuses out of neuronal cells during nerve impulse production

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24
Q

astrocytes uptake glutamate and produce glutamine

A

ONLY astrocytes can convert glutamate to glutamine; have the glutamine synthetase enzyme
-Excitatory neurons can convert the glutamine BACK to glutamate
-Inhibitory neurons can convert glutamine produced by astrocytes into GABA (inhibitory neurotransmitter)

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25
Q

astrocyte surrounding blood capillaries from bottom uptake glucose from blood

A

-Glucose is metabolized into lactic acid/lactate
-Lactate is used as an energy source for neurons. Lactate→ CO2 + H2O → ATP

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26
Q

astrocytes release lactate; helps neurons function

A

-Neurons rely on lactate to sustain high rate of aerobic cell respiration -Astrocytes can store glycogen to make lactate; this activates neurons to release glutamate = increases glycolysis in astrocytes = more lactate (FULL CIRCLE)

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27
Q

astrocytes are needed for synapse formation, maturation, and maintenance

A

astrocytes regulate neurogenesis in the adult brain

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28
Q

astrocytes secrete glial-derived neurotrophic factor

A

-GDNF is VITAL for survival of spinal motor neurons + dopamine releasing neurons of
brain

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29
Q

astrocytes induce the formation of the blood brain barrier

A

true

30
Q

neurons communicate with astrocytes

A

-Primarily in cerebellum; glutamate binds to astrocyte receptors → influx of Ca2+ into the
astrocytes

31
Q

astrocytes release chemical transmitters that regulate neuron function

A

-Due to glutamate binding + Ca2+ influx (above function), these transmitters are gliotransmitters (eg; glutamate, ATP, D-serine, adenosine from ATP)

32
Q

**Reminder from chapter 6: In Na+/K+ pump, for every 3 Na+ ions going out of the cell (extracellular), 2 K+ ions go into the cell (intracellular;cytoplasm)

A

-↑ membrane permeability to a certain ion makes the ion diffuse DOWN its’ concentration gradient (high concentration to low concentration)

33
Q

depolarization/hypopolarization:

A

stimulation leads to POSITIVE charges flowing into the cell, the potential difference between the two “phases” is lowered

34
Q

hyperpolarization:

A

stimulation leads to NEGATIVE charges flowing into the cell OR cell interior becomes more negative than RMP (resting membrane potential)

35
Q

repolarization=

A

a return to the resting membrane potential

36
Q

depolarization =

A

excitatory

37
Q

hyperpolarization=

A

inhibitory

38
Q

ion gating in axons

A

Channel is closed at RMP
● Channel opens in response to depolarization
● Channel is inactivated after a specific time (refractory period)

39
Q

K+ has two types of channels:

A

A) Gated, and gates are closed at RMP
B) Not gated, and the gates are ALWAYS open

40
Q

Na+ channels are ALL gated and closed at RMP
● With increased stimuli, Na+ channels open briefly; leakage of Na+ into the resting cell
● Neuron at RMP is more permeable to K+ , than N

A

reminder

41
Q

important

A

-Depolarization to a threshold level causes the Na+ channels to open
-This makes membrane PERMEABLE to Na+
-Electrochemical gradient (electrical + concentration) of Na+ makes it go into the cell -for a BRIEF moment, the cell then has the equilibrium potential of Na+ (less negative charge inside the cell)
-Na+ channels close quickly because of inactivation
-Depolarization stimulus causes the gated K+ channels to open
-Membrane returns to being more permeable to K+
-Membrane moves towards K+ equilibrium potential
-Na+ and K+ channels are voltage-gated channels; stimulated by depolarization

42
Q

action potentials

A

Depolarization of an axon affects Na+ and K+ diffusion, in sequence
A) Na+gatesopen;Na+diffusesintothecell
B) Afterabriefperiod,K+gatesopen;K+diffusesoutofthecell
C) Inward diffusion of Na+ = more depolarization; more opening of Na+
gates (this is the positive feedback (+) )
D) Opening of K+ gates + outward diffusion of K+ ; cell is more negative on
the inside = negative feedback (-) on initial depolarization
● K+ is (+) charge; The cell becomes more negative/less positive when K+ leaves, the cell wants to return to its RMP (this is repolarization) and where the negative
(-) feedback loop comes from
-Gated Na+ channels open→influx of Na+ ions into the cell→ RMP of neuron changes to Na+ EP (depolarization; more positive)→inactivation of Na+ channels begins→gated K+ channels open→inactivation of K+ channel begins→gated Na+ and K+ channels close→RMP restored and is close to K+ EP

43
Q

all or none law

A

● Depolarization = or ↑ threshold value; MAXIMUM POTENTIAL CHANGE
-STRENGTH OF STIMULUS DOES NOT PLAY A ROLE IN HOW LONG THE GATES ARE
OPEN. A greater strength = more FREQUENT action potentials, but they are ALL IDENTICAL
-You can have strong stimuli activate axons with higher thresholds and lower stimuli activate
axons with lower thresholds, BUT the result is an identical action potential regardless
● ↑ intensity stimulus = ↑ axons can be activated (RECRUITMENT)

44
Q

refractory periods

A

● The axon membrane CANNOT respond to a second stimulus while producing an action potential; THIS IS ABSOLUTE REFRACTORY PERIOD
● If stimulus intensity increases, action potential frequency increases, time between each action potential production decreases BUT will never be shortened to where one action potential starts BEFORE the previous one finishes
● Inactivated state = Cannot be opened by depolarization
● Closed state = Axon can still be stimulated with strong stimulus
● **Relative refractory period: Na+ channels are recovering from inactivated state AND K+
channels are still open
-The frequency of action potentials produced DOES NOT affect the relative
concentrations of Na+ and K+ in the outer/inner cell, respectively

45
Q

conduction of nerve impulses

A

Action potential at 1st location of axon membrane > depolarization stimulus for the NEXT region of the axon membrane> this second region can then produce the NEXT action potential> The second region now acts a depolarization stimulus for the third region of the axon membrane, so on and so forth (these steps are repeated)
-Each action potential transfers positive charges (Na+) onto the adjacent region
-The region that JUST produced the action potential is refractory
-The region right after this ^^ is partially polarized
-Voltage gated Na+ channels are opened and the PROCESS REPEATS

46
Q

conduction in an unmyleinated axon

A

Action potentials are produced along the length of the entire axon
● Slow conduction rate; many action potentials taking place, each is an individual event
● Amplitude across each action potential is the SAME

47
Q

conduction in an myelinated axon

A

● Myelin sheath provides insulation for axons; Na+ and K+ movement PROHIBITED
● REMEMBER THAT MYELIN SHEATH HAS NODES OF RANVIER
● ^^ Without nodes of ranvier; ACTION POTENTIALS CANNOT BE PRODUCED
● Na+ channels are highly concentrated at the nodes
● Nodes of ranvier allow for Na+ and K+ movement in membrane; every 1 to 2 mm
● Action potentials “jump” from node to node
● ^^ THIS IS SALTATORY CONDUCTION

48
Q

important

A

Know how action potential conduction speed is increased:
A) Increased Diameter of Axon;r educes resistance to charge spread( cable properties) B) Myelination; due to saltatory conduction

49
Q

synapse

A

Synapse is a functional connection between neuron and second cell
● CNS: 2nd cell is another neuron
● PNS: 2nd cell is neuron/effector cell w/n muscle or gland
● Neuron-muscular synapses = neuromuscular synapses/neuromuscular junctions
● In most synapses: TRANSMISSION IS IN ONE DIRECTION ONLY
*Axon of first neuron (
)
● KNOW THE FOLLOWING TERMINOLOGY:
to second neuron (THIS IS
THIS IS PRESYNAPTIC NEURON)
POSTSYNAPTIC NEURON
● Axodendritic: Presynaptic neuron signals dendrite of second neuron
● Axosomatic: Presynaptic neuron signals cell body of second neuron
● Axoaxonic: Presynaptic neuron signals axon of second neuron
● MOST SYNAPSES ARE AXODENDRITIC; ONE DIRECTION
● Synapes can be electrical or chemical

50
Q

electrical synapses; gap junctions

A

● Gap junctions: adjacent cells that are electronically coupled together
● Cells must have equal size + contact in low resistance areas for COUPLING
● Gap junctions allow for the passage of ions/molecules from one cell to the other
● IMPORTANT: KNOW THE STRUCTURE OF GAP JUNCTIONS;
A) Connexin proteins from EACH side of plasma membrane for two cells make a structure
B) This structure is a hemi channel; connect the structures together, and you have a COMPLETE gap junction (TWO HEMI CHANNELS FROM BOTH CELLS LAYERED ON TOP OF EACH OTHER)

51
Q

chemical synapse

A

Synapses release neurotransmitters from axon’s terminal boutons (presynaptic endings)
● Terminal boutons are separated from postsynaptic cell by SYNAPTIC CLEFT
● KNOW CAMS (Cell-Adhesion Molecules)
A) FOUND IN PRESYNAPTIC AND POSTSYNAPTIC MEMBRANES
B) CAMS GO INTO SYNAPTIC CLEFT AND BIND TOGETHER
C) THIS BINDING IS TO MAKE SURE THE MEMBRANES (PRE AND
POSTSYNAPTIC) ARE CLOSE TO EACH OTHER FOR CHEMICAL TRANSMISSION; CAMS ACT LIKE “GLUE”

52
Q

release of neurotransmitters

A

Neurotransmitters are enclosed w/n synaptic vesicles in axon terminal **We want the neurotransmitter to be released into synaptic cleft;
● Fusion of axon membrane + vesicle membrane = exocytosis

53
Q

the process of release of neurotransmitters

A

Voltage-gatedCa2+channels open, when action potential reaches end of axon
C) ↑ action potential frequency = stimulation of postsynaptic neuron
D) Ca2+ enters cell and binds to synaptotagmin (Ca2+ sensor); COMPLEX MADE
**Synaptotagmin is located in synaptic vesicle membrane
E) Vesicles that HAVE the neurotransmitter are placed in plasma membrane by 3SNARE
complex proteins
**1 SNARE protein in vesicle membrane and 2 in plasma membrane
F) Ca2+/Synaptotagmin complex DISPLACES part of SNARE ;fusion of vesicles
G) PORE FORMATION TO RELEASE NEUROTRANSMITTER

54
Q

actions of neurotransmitters

A

Neurotransmitter = ligand
● Neurotransmitter binds to receptor protein + diffuses across synapse
● What this does is open chemically-regulated ion channels, AKA LIGAND GATES
●graded potential: There’s a change in membrane potential when the ion channel OPENS
*EPSP: Na+ or Ca2+ channels open = GRADED DEPOLARIZATION
*IPSP: K+ or Cl- channels open = GRADED HYPERPOLARIZATION

55
Q

EPSP AND IPSP

A

**MOVEMENT OF MEMBRANE POTENTIAL
-EPSP: Moves membrane potential CLOSER to threshold (action potential) -IPSP: Moves membrane potential FARTHER to threshold (no impulse)
B) Ca2+stimulates fusion of axon membrane to vesicle membrane; exocytosis of
neurotransmitter ^^
**GRADED POTENTIAL:
-There’s a change in membrane potential when the ion channel OPENS
*EPSP: Na+ or Ca2+ channels open = GRADED DEPOLARIZATION
*IPSP: K+ or Cl- channels open = GRADED HYPERPOLARIZATION
HOW MUCH IPSP AND EPSP IS PRESENT WILL DETERMINE WHETHER AN ACTION
POTENTIAL HAPPENS

56
Q

ACH AS A NEUROTRANSMITTER

A

Ach can be inhibitory ( some autonomic motor neurons) OR excitatory (CNS, all of somatic motor neurons and some autonomic motor neurons
● YOU HAVE TWO TYPES OF ACETYLCHOLINE RECEPTORS:
A) Nicotinic Achreceptors
-Stimulation through nicotine
-Nicotinic Ach receptors ; SKELETAL MUSCLE CELLS (Skeletal muscle contraction)
B) Muscarinic Achreceptors
-CNS, plasma membrane, smooth/cardiac muscle (regulate cardiovascular and digestive system)
-Stimulation through muscarine (poison mushrooms)

57
Q

**AGONISTS AND ANTAGONISTS:
-Agonists; bind + activate receptor proteins
-Antagonists; bind + reduce activity of receptor proteins -Atropine = antagonist for muscarinic receptors
-Curare = antagonist for nicotinic receptors

A

MUSCARINE IS AN AGONIST
NICTOTINE IS AN AGONIST

58
Q

CHEMICALLY REGULATED CHANNELS

A

**When neurotransmitter binds to receptor = opening of ion channels. 2 POSSIBLE WAYS:
A) Ligand-gated channels:
*
. THIS IS DIFFERENT FROM G-PROTEIN CHANNELS; NOTE THIS DIFFERENCE HIGHLIGHTED IN ORANGE BELOW ALSO
*Nicotinic ACh receptors are ligand-gated channels with two receptor sites for two AChs. *Binding of 2 acetylcholine molecules opens a channel that allows both Na+ and K+ passage.
-More Na+ flows in and than K+ flows out of the cell
● EPSP; in dendrites and cell bodies
● You can sum up EPSPs to get more depolarization; This is from having Ach
molecules bind together and totaling all that up
● This depolarization ^^ could possibly reach the threshold,for voltage-gated
channels in the axon hillock, leading to action potential

59
Q

**G-Protein Coupled Channels (What you will need to know):
RECALL THAT CHAPTER 6 BRIEFLY TOUCHED ON G-PROTEINS AS A SECOND
MESSENGER; similar concepts outlined here
● Neurotransmitter receptor is NOT CONNECTED TO PROTEIN that functions as the ion
channel (This is a MAJOR difference between ligand-gated and G-protein coupled
channels)
● Ion channels are opened indirectly by utilizing G-proteins, when binding at receptor occurs
● This is how muscarinic Ach receptors interact with ion channels
● Dopamine and norepinephrine do this also
● Muscarinic Ach receptors have five subtypes; M1-M5, each producing a different effect
in different organs

A

TRUE

60
Q

REVIEW

A

Alpha subunit dissociates from this ^^ complex when acetylcholine binds
● EITHER alpha or beta-gamma subunit will diffuse across membrane to bind to ion
channel
● ^^ What this does is open/close the channel for a SHORT period of time
● Whichever subunit bound itself to the channel will dissociate (leave) from channel + bind
back to the remaining G-protein subunit(s). GO BACK TO NORMAL
HOW G-PROTEINS ARE ACTIVATED/INACTIVATED; THIS WAS TOUCHED ON IN CHAPTER 6, A SUMMARY IS THIS:
● Remember that G-proteins exist as the three subunits (alpha,beta, gamma) .
● Alpha subunit binds GDP (This is IF there are no regulatory molecules bound to
membrane receptor)
● AGAIN, either alpha subunit OR beta/gamma subunit will move through membrane to bind to effector protein (this could be an enzyme, ion channel, etc)
● When the alpha subunit breaks down GTP to GDP, the effector protein deactivates
● SUBUNITS come back together and bind to unstimulated effector protein
- If G-proteins bind to Ach, this can open K+ channels (IPSP) OR close K+ channels (EPSP)
- The beta/gamma complex of G-proteins opens K+ channels in the heart = IPSP (hyperpolarization) + heart rate decrease
- The alpha subunit of G-proteins opens K+ channels in the smooth muscles of stomach = EPSP (depolarization) + contraction of muscle

61
Q

**ENZYME: AChE; Acetylcholinesterase: INACTIVATES ACh activity after ACh binds to
receptor
-AChE breaks down ACh to choline and acetate.

A

-This can be “recycled” and brought back to the presynaptic cell, where the process repeats.
-AChE can be inhibited by cholinesterase inhibitors, which are drugs that STOP AChE from inactivating ACh activity
-What this does is BOOST the amount of ACh in the synaptic cleft + improve synaptic transmission

62
Q

You don’t want an overstimulation of synaptic transmission. Inhibiting AChE can have negative effects

A

EP

63
Q

NEOSTigmine, physostigmine, pyridostigmine, and others are used to treat myasthenia gravis
and are important in the treatment of Alzheimer’s disease. KNOW THESE DRUGS

A

YEP

64
Q

ACh in the PNS (What you will need to know):
Somatic motor neurons form interactions called neuromuscular junctions with muscle cells (At beginning of this section)
-Motor end plate has the receptor for neurotransmitters
-EPSPs formed here are end plate potentials.
-End plate potentials open voltage-gated Na+ channels = action potential.
-This process leads to muscle contraction
-There’s drugs out there that can block neuromuscular transmission
**-CURARE: Antagonist for ACh = NO MUSCLES CONTRACT&raquo_space; paralysis + death

A

Autonomic motor neurons target cardiac muscle, smooth muscle of blood vessels.
● In this system, parasympathetic autonomic axons use ACh as their neurotransmitter
● ^^ This can have BOTH stimulatory and inhibitory (binding to muscarinic receptors) effects

65
Q

**Know the following about Myasthenia Gravis:

A

Antibodies block nicotinic ACh receptors (motor end plates in skeletal muscle cell)
● PROFOUND muscle weakness
● Neostigmine BLOCKS enzyme that degrades ACh (helpful for mitigating symptoms

66
Q

ACh in the CNS (Important Points to Know):

A

The receptor regions here ARE cell bodies and dendrites
● ACh can be used as a neurotransmitter here + neurons who use ACh synapse with
another neuron
● EPSPs and IPSPs spread to the axon hillock (BOTH graded and local)
● IPSPs will HYPERPOLARIZE membrane = NO ACTION POTENTIAL
REMEMBER: IF depolarization is above or at threshold, EPSP will stimulate an action potential to be generated
● The variation you get in the strength of EPSPs if they’re above threshold determines ACTION POTENTIAL FREQUENCY
● ^^ Remember, action potentials ALL have the same “strength” the frequency varies, but they are all the same in duration
● IF EPSP is below threshold, NO ACTION POTENTIAL

67
Q

MONOAMINES AS NEUROTRANSMITTERS

A

-Monoamines come from amino acids, you have:
A) Serotonin:ComesfromL-tryptophan
B) Histamine:Comesfromhistidine
C) Catecholamines (dopamine, norepinephrine, epinephrine): Comes from tyrosine
-Monoamines are manufactured in presynaptic axon (JUST LIKE ACh), released by exocytosis, move across synapse to get + bind to its’ specific receptors
-THEY ARE REUPTAKEN (back into presynaptic cell)
-Monoamine Oxidase degrades monoamines
**MONOAMINES UTILIZE SECOND-MESSENGER SYSTEMS, they don’t have direct ion channels
-For monoamines, they use cAMP
-A COMMON THREAD:
-We talk about G-proteins again, in the context of monoamines;
**Binding of catecholamine (as an example) to its’ receptor ACTIVATES G-protein
-G protein alpha-subunit dissociates and goes to adenylate cyclase&raquo_space; converts ATP to cAMP -cAMP activates protein kinase ; protein kinase phosphorylates proteins
-Opening of ion channel

68
Q

MONOAMINE OXIDASE INHIBITORS (KEY POINTS):

A

Block degradation of monoamines, so increases actions of dopamine, epinephrine, serotonin, melatonin (BASICALLY ALL YOUR MONOAMINES)
● MAO inhibitors help with treating depression since serotonin action is increased
● KEY MONOAMINE TO FOCUS ON IS SEROTONIN AND DOPAMINE
-Serotonin is made from L-tryptophan
-Serotonin is used by neurons in raphe nuclei
-LSD and hallucinogens can be agonists for serotonin
-Serotonin specific reuptake inhibitors can help treat depression (Prozac, Paxil, Zoloft, Lexa pro and Luvox)

69
Q

DOPAMINE

A

Biggest use for dopamine is in the midbrain (cell bodies have high concentration here)
● The two areas in the midbrain that utilize dopamine most are:
-Nigrostriatal dopamine system: Motor control
**”Transfer” of neurons from substantia nigra (basal nuclei) to corpus striatum -VITAL for control and starting movement
-Mesolimbic dopamine system: Emotional reward
**Midbrain sends neurons to forebrain, ALL part of limbic system -This system is involved in EMOTIONAL REWARD and ADDICTIONS -Having too much dopamine in the system leads to schizophrenia -Schizophrenia treated by dopamine antagonists
-PARKINSONS DIEASE happens because substantia nigra degenerates
-treatment is MAO inhibitors and L-dopa

70
Q

noreepinephrine

A

-Is in both CNS and PNS
-Used in CNS neurons for arousal
-Used in PNS sympathetic neurons for smooth muscle, cardiac muscle -Norepinephrine can be stimulated by using amphetam

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