Nakamura Human Physiology Lecture 4 Flashcards

(37 cards)

1
Q

Functional classification of neurons

A

.Based upon direction of impulse conduction
–Sensory (afferent) neurons conduct impulses from peripheral receptors to CNS.
–Motor (efferent) neurons conduct impulses from CNS to effector organ or cell
-somatic motor neurons: to skeletal muscles
-autonomic motor neurons: to smooth muscle, cardiac muscle, and glands
–Interneurons are located entirely within the CNS.

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2
Q

Structural classification of neurons

A

.Number of processes that extend from cell body.
–Pseudounipolar
•Short single process that branches like a T
–Sensory neurons
–Bipolar neurons
•Have 2 processes
–Retina of the eye
–Multipolar
•Have several dendrites on cell body and 1 axon
–Motor neurons

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3
Q

Glial cells

A

.•Six categories of glial cells:
–Schwann cells form myelin in PNS
–Satellite cells support neurons in PNS ganglia
–Oligodendrocytes form myelin in CNS
–Microglia are phagocytic (engulfs other cells. Enzyme breaks down engulfed cell and digests it) cells in the CNS
–Astrocytes regulate ECF in CNS
–Ependymal cells line the ventricles (empty cavities/areas in CNS. Contain CSF) in the CNS

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4
Q

Myelin formation in PNS

A

.•Schwann cells:
–Wrap tightly around axons in PNS
–One Schwann cell wraps around one axon
-makes myelin. Insulation
•Nodes of Ranvier are regions of unmyelinated axon between each Schwann cell wrapping.
•Segments of myelinated axon are called internodes

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5
Q

Myelin formation in the CNS

A
.Oligodendrocytes
     –Wrap tightly around axons
     –One oligodendrocyte may wrap several axons
•Nodes of Ranvier
•Internodes
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6
Q

Electrical activity of axons

A
All cells maintain resting membrane potential
•Resting potential is caused by:
–High permeability to K+
–Slight permeability to Na+
–Electrogenic Na+/K+ ATP-ase pump.
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7
Q

Electrical activity of neurons

A

Depolarization
–Potential difference reduced (become more positive)
•Repolarization
–Return to resting membrane potential (become more negative)
•Hyperpolarization
–More negative than resting membrane potential
-after action potential, Repolarize, but go more negative than resting potential.
-Causes the cell to become inactive. Keeps us from being too hyper

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8
Q

Membrane potentials and action potentials in axons

A

•Changes in membrane permeability to ions alters the membrane potential
•Specific ion channels for Na+ and K+
•Voltage-gated channels open in response to membrane depolarization
-closed during resting membrane potential
-channel inactivated during refractory period

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9
Q

Action potentials

A

.Stimulus causes depolarization to threshold potential
•Voltage gated (VG) Na+ channels open
•Upstroke of AP caused by influx of Na+ through open Na+ channels
–Na+ ions diffuse into the axon and cause a further local depolarization
–Local depolarization activates other Na+ channels: positive feedback loop.
•VG K+ channels open with a delay
•After short delay, membrane potential repolarizes because of K+ efflux through K+ channels
–K+ ions diffuse out of the axon to repolarize the membrane potential: negative feedback loop.
•These rapid changes in membrane potential are the action potential (AP)

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10
Q

Action potential characteristics for neurons

A

.All or none” characteristic
–At the threshold potential, the axon will fire a full-sized AP. If threshold is not reached then the axon will not fire an AP.
•Coding for Intensity
–Increased frequency of AP indicates greater stimulus strength.
•Na+/K+ ATPase pumps Na+ out of the cell, and pumps K+ into the cell (3 Na+ out/ 2 K+ in) to restore ion distributions

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11
Q

Refractory periods

A

Absolute refractory period:
–Axon membrane is incapable of producing another AP.
-regardless of how strong the stimulation is, the neuron will not respond
-neuron is in the middle of AP already
•Relative refractory period:
–Axon membrane can produce another action potential, but requires stronger stimulus.
-almost end of Repolarization

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12
Q

Conduction of nerve impulses

A

.Cable properties:
–Ability of neuron to transmit charge through cytoplasm
–High internal resistance (causes many potential charges leak out of the axon through its membrane)
•During the AP, the influx of Na+ at each segment of axon increases the + charge at the adjacent segment of axon and this depolarization activates the Na+ channels in that segment to propagate the AP.

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13
Q

Conduction in an unmyelinated neuron

A
  • Cable spread of depolarization with influx of Na+ depolarizes the adjacent membrane, and the AP propagates (one area to the next) down the axon.
  • gradually conducts
  • 1st area depolarizes, 2nd area still polarized
  • 1st AP stimulates 2nd one. 1st area repolarizes, 2nd area depolarizes
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14
Q

Conduction in a myelinated axon

A

.Myelin prevents movement of Na+ and K+ through the membrane.
•Nodes of Ranvier contain VG Na+ and K+ channels.
•Saltatory conduction from node to node. (Jumps from node to node over myelin sheaths)
•AP conduction is much faster than in non-myelinated axons.
•Conduction velocity

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15
Q

Synapses

A

.Functional connection between a neuron (Presynaptic) and another cell (Postsynaptic).
•Two basic types of synapses:
–Electrical
•Presynaptic and Postsynaptic cells connected by gap junctions.
-electricity delivered can go Both ways. Pre to post and post to pre
–Chemical
•Presynaptic cell releases a chemical neurotransmitter that binds to receptors on the post synaptic cell.
-only one way direction. Pre to post

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16
Q

Electrical synapses

A

.Gap junctions:
–Adjacent cells electrically coupled
–APs may be conducted in both directions across the the synapse
-Connexin proteins form gap junctions
•Examples:
–Smooth and cardiac muscle.
–Some electrical synapses in brain

17
Q

Chemical synapse

A

-Terminal bouton is separated from postsynaptic cell by synaptic cleft.
•Neurotransmitters (NT) are released from synaptic vesicles.
-Arrival of the AP at the terminal causes vesicles to fuse with the presynaptic terminal membrane and dump neurotransmitter into the synaptic cleft

18
Q

Chemical Synaptic transmission

A
  1. Depolarization of terminals opens VG Ca2+ channels
  2. AP travels down axon to synaptic terminals
  3. Ca2+ diffuses into the terminal through the Ca2+ channels
    -ca2+ binds with calmodulin
    -activate protein kinase
    -Activated protein kinase causes synaptic vesicles to move to terminal membrane
  4. Synaptic vesicles fuse with presynaptic terminal and dump NT into synaptic cleft
  5. NT (ligand) binding to receptors on postsynaptic cell membrane opens (or closes) ion channels
  6. Neurotransmitter action stops because:
    –Enzymes break down the chemical transmitter
    –Transmitter diffuses away from synapse
    –Transmitter is resequestered by the presynaptic terminal
19
Q

Post synaptic neurons and chemical synapse

A

.EPSP (excitatory post synaptic potential) excited, go through
–Depolarization
•IPSP (inhibitory post synaptic potential) inhibits, stops
–Hyperpolarization
•Whether a NT causes an EPSP or IPSP depends on the permeability change in the postsynaptic cell. (If do not reach threshold, can’t have action potential)
-EPSP and IPSP are not action potentials. They are stimulation/ electrical activity
-add EPSP and IPSP together (graded in amplitude)

20
Q

EPSP

A
.No threshold
•Depolarizes the membrane potential
     –Closer to threshold
•Graded in amplitude (slowly get bigger)
•No refractory period
•Summation of EPSPs may cause membrane potential to reach threshold and elicit an AP
21
Q

IPSP

A
.No threshold
•No refractory period
•Hyperpolarizes postsynaptic membrane potential
      –Further away from threshold
•Graded in amplitude
22
Q

Synaptic integration

A

EPSPs and IPSPs can sum (add them), producing (EPSP) or inhibiting (IPSP) production of an AP
–Spatial summation
•Numerous boutons (axon terminal) from different neurons converge on a single postsynaptic neuron (sum over distance)
–Temporal summation
•Successive waves of neurotransmitter release from the same terminal (sum over time)

23
Q

Types of receptors for chemical neurotransmitters

A

Located on post synaptic neurons
-Ligand-gated receptor/ion channel complex (directly coupled or bonded): Fast synaptic transmission
•G-protein gated (regulated) ion channel (indirectly coupled): Slow synaptic transmission

24
Q

Ligand gated receptor example

A

-Nicotinic ACh (acetylcholine) receptors
•ACh receptor is part of ion channel
•Binding of 2 ACh molecules opens the channel
•Channel opening permits diffusion of Na+ (in) and K+ (out). Na+ > K+ causes EPSP. (More sodium in, less potassium out, intracellular becomes more positive, depolarization)
•CNS and neuromuscular (btwn neuron and muscle) synapses

25
G protein gated ion channel example
- muscarinic ACh receptors | - norepinephrine one
26
Muscarinic ACh receptors
.Muscarinic ACh receptors •Ion channels are separate proteins located away from the receptors •Binding of ACh activates G protein •One or more of the G-protein subunits binds to ion channel and opens (or closes) the channel (K+/ IPSP). Hyperpolarization •CNS and heart •Atropine is a muscarinic antagonist/blocker
27
Norepinephrine receptor thingy
1. Binds to receptor 2. Causes alpha beta gamma G protein to disassociate 3. Alpha binds to adenylate cyclase (enzyme) 4. Enzyme catalyzes the conversion of ATP to cyclic AMP (cAMP) 5. Causes protein kinase to activate 6. This then causes the ion channel to open
28
Acetylcholinesterase
.Enzyme that inactivates ACh. | •Cleavage of ACh abruptly ceases synaptic transmission
29
Other neurotransmitters
.Monoamines (Ion channels indirectly coupled) g-protein receptors –Epinephrine –Norepinephrine –Serotonin –Dopamine •Amino Acids (Ion channels directly coupled) ligand gated receptors –Excitatory (EPSPs) •Glutamic Acid and Aspartic Acid –Inhibitory (IPSPs) •Glycine and GABA (-aminobutyric acid) •Polypeptides
30
Neural control of involuntary effectors
-Innervate organs not usually under voluntary control. | •Effectors include cardiac and smooth muscles (blood vessels and visceral organs) and glands
31
Autonomic nervous system actions
.Stimulation of Sympathetic Division activates organs involved with: –Fight –Flight •Stimulation of Parasympathetic Division activates organs involved with: –Feeding –Reproductive Behavior
32
Divisions of the ANS
.Sympathetic Nervous System •Parasympathetic Nervous System •In both divisions, the preganglionic neurons originate in the CNS, and the postganglionic neurons originate in ganglia outside of the CNS
33
Autonomic neurons
2 neurons in the effector pathway. •1st neuron has its cell body in gray matter of brain or spinal cord. –Preganglionic neuron •1st neuron synapses onto 2nd neuron within an autonomic ganglion. 2nd neuron synapses onto cells in effector organ. –Postganglionic neuron -adrenal gland only effector not regulated by both sympathetic and parasympathetic nerve, only sympathetic
34
Sympathetic division of neurons
-Axons of preganglionic neurons exit spinal cord in ventral roots at T1 to L2 levels (Thoracolumbar Division). Middle of back •Preganglionic fibers are short and release ACh •Postganglionic fibers are long and release norepinephrine (or epinephrine from adrenal medulla)
35
Parasympathetic division of neurons
.•Preganglionic fibers originate in midbrain, medulla, and pons; and in the 2-4 sacral levels of the spinal cord (Craniosacral Division) •Preganglionic fibers are long and release ACh •Postganglionic fibers are short and release ACh
36
Distribution and physiological effects of different adrenergic receptors (sympathetic)
.blood vessels: Alpha1 and alpha2: construction Beta2: dilation Heart: Beta1: tachycardia (increased HR); increased contractility Alpha1: increased contractility Bronchi: Beta2: relaxation Thrombocytes: alpha2: aggregation Kidneys: Alpha1 and alpha2: vasoconstriction Beta1 and beta2: Renin release; inhibition tubular sodium reabsorption Adipocytes : Alpha2: inhibition lipolysis Beta1, beta2, and beta3: lipolysis
37
Write out chart
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