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1 Unit III- Nervous System Marieb, 8th Edition Chaps 11-12; skim 14 pages 385-483; 491-493, 510- 519 skim; skim 525-539 Book and CD-ROM CD-ROMS in SLC Rm 1214

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Unit III- Nervous System

• Marieb, 8th Edition– Chaps 11-12; skim 14

– pages 385-483; 491-493, 510- 519 skim; skim 525-539

– Book and CD-ROM• CD-ROMS in SLC Rm 1214

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• Nervous System

• I. A. Introduction– 1. Homeostasis - maintain internal life

functions within a normal range– 2. Communication an important component

• Detect a problem - sensory system

• Correct the problem with an adjustment

• Communication between two components involves the nervous system and its principles

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• I. B. Organization of the Nervous System– 1. Central Nervous System (CNS)

• Brain• Spinal cord

– 2. Peripheral Nervous System (PNS)• a) Somatic Nervous System

– Voluntary system that controls skeletal muscles attached to limbs / bones

• b) Autonomic Nervous System (ANS)– Involuntary system that controls cardiac and smooth

muscles (stomach, uterus, blood vessels, etc.) and glands– Sympathetic and Parasympathetic Divisions

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• I. C. Cellular Neuroanatomy– 1. Nerve Cell = Neuron

• Cell body = nucleus, Rough ER, neurotubules, Golgi, etc.

• Dendrites = processes which receive input to cell body

• Axon = longer process which communicates with other neurons

• Terminal Branches / End Terminals = end of axon that communicates with next neuron or muscle or gland

– How can we protect this long axonal process?

Fig. 11.4

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• I. C. Cellular Neuroanatomy– 2. Glial Cells - supportive cells of the CNS

• Protective, metabolic, phagocytosis, transport nutrients & wastes between neurons & blood vessels

• Schwann cells in the PNS and a glial cell in the CNS produce myelin sheath - phospholipids membranes of cell wrapped around neuronal axon, function:

– protection - regeneration

– Speed up rate of conduction down axon (node to node)

Fig. 48-5

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8Fig. 11.3

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Fig. 48-5

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Fig. 11.5

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11Fig. 13-4

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12Fig. 48-4 and Table 11.1

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• I.C. Cellular Neuroanatomy– 3. Types of Neurons

• a) Sensory / Afferent Neurons - carry information about the environment (internal and external) towards the CNS

• b) Motor / Efferent Neurons - carry information away from the CNS towards the periphery & effectors (muscle or gland)

• c) Interneuron / Association Neurons – Only within the CNS

– Connect two other neurons together, any combination

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14Fig. 48-1

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•I. C. 4. Synapsespace or gap between a neuron and a neuron or a neuron and an effector

• I. C. 5. Stimulus Response Mechanism– a) Stimulus

• Change in the environment– b) Response

• Reaction by the organism in response to the original stimulus

– c) Basis of all functioning of the nervous system, communication directed at stimulus - response mechanisms basis of behavior, learning, etc.

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II. Impulse conduction

• A. Introduction– 1. 1930s - at Woods Hole Mass., work on the

giant squid axon - nonconducting cell• Large enough to isolate from animal and remove the

cellular/axonal cytoplasm and chemically analyze

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1a. Ionic Distribution

• EXTRACELLULAR INTRACELLULAR• SODIUM - Na+ Na+

• HIGH LOW

• POTASSIUM - K+ K+

• LOW HIGH

• CHLORIDE - Cl- Cl-

• HIGH LOW

• HIGH PROTEINS-

SEMI-PERMEABLE MEMBRANE

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1b. CHANGES BASED UPON NORMAL NET DIFFUSION

• EXTRACELLULAR INTRACELLULAR• SODIUM - Na+ Na+

• HIGH LOW

• POTASSIUM - K+ K+

• LOWHIGH

• CHLORIDE - Cl- Cl-

• HIGH LOW

• HIGH PROTEINS-

SEMI-PERMEABLE MEMBRANE

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1c. CHANGES BASED UPON NORMAL NET DIFFUSION OPPOSED BY ACTIVE TRANSPORT AND ELECTROSTATIC CHARGES

• EXTRACELLULAR INTRACELLULAR• SODIUM - Na+ Na+

• HIGH LOW• PASSIVE• ACTIVE

• POTASSIUM - K+ K+

• LOW HIGH• PASSIVE• ACTIVE

• CHLORIDE - Cl- Cl-

• HIGH LOW• ELECTROSTATIC

• NEGATIVE• HIGH PROTEINS-

SEMI-PERMEABLE MEMBRANE

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•2. Summary of Above Ionic Behaviors

• 2a. Against maintaining the neuronal ionic gradient

– Passive diffusion (high to low)

• 2b. Favors maintaining the neuronal ionic gradient

– Active transport of the Na+ - K+ pump– Electrostatic forces due to intracellular protein

negative charge• Keeps chloride out• Binds to positive K+ to keep intracellular

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Figure 48.6Negative Intracellular Electrical Charge

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Fig. 48-7

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QuickTime™ and aCinepak decompressor

are needed to see this picture.

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II. A. 3.Terms:• a) potential difference - difference in electrical

charge• b) polarized membrane - potential difference

across membrane due to combination of membrane permeability and ionic concentrations

• c) resting potential - non-conducting neuron with a potential difference across the membrane equal to -70 to -90 millivolts (mV) inside compared to outside

• d) action potential or nerve impulse or spike a brief transient change in resting potential

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Fig. 48.6 & 11.7

II.B. Action Potential

1. Stimulating and recording setup

stimulator

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• ACTION POTENTIAL

• +

• -

• -50

-70

TIME msec

2

34

5

6

7

8

9

10

0 mV

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• B. Action Potential– 2. Electrode enters the axon– 3. Excitatory stimulus - below threshold– 4. Threshold stimulus - (outside) sodium gates suddenly open and

the Na-K pump OFF– 5. Depolarization - sodium continues to enter past 0mV (loss of

polarization)– 6. Sodium inactivation around -35mV as (inside) gate closes - too

much positive charge inside– 7. Repolarization - potassium out since Na+ gates closed & K+ no

longer attracted to positive protein– 8. Hyperpolarization - pump actively back on as K+ exit

overshoots resting potential– 9. Equilibrium or normal resting potential– 10. Inhibitory stimulus - a hyperpolarizing stimulus, harder to

excite neuron during this time period

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Fig. 11.6

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29Fig. 11.8Copyright © 2010 Pearson Education, Inc.

Figure 11.8 Resting Membrane Potential

Finally, let ’s add a pump to compensate for leaking ions.Na +-K + ATPases (pumps) maintain the concentration gradients, resulting in the resting membrane potential.

Suppose a cell has only K + channels...K + loss through abundant leakagechannels establishes a negativemembrane potential.

Now, let ’s add some Na + channels to our cell...Na + entry through leakage channels reducesthe negative membrane potential slightly.

The permeabilities of Na + and K + across the membrane are different.

The concentrations of Na + and K + on each side of the membrane are different.

Na+

(140 mM )K+

(5 mM )

K+ leakage channels

Cell interior–90 mV

Cell interior–70 mV

Cell interior–70 mV

K+

Na+

Na+-K+ pump

K+

K+K+

K+

Na+

K+

K+K

Na+

K+K+ Na+

K+K+

Outside cell

Inside cell Na+-K+ ATPases (pumps) maintain the concentration gradients of Na+ and K+

across the membrane.

The Na+ concentration is higher outside the cell.

The K+ concentration is higher inside the cell.

K+

(140 mM )Na+

(15 mM )

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FIG. 48.8, 11.9

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31FIG. 48.9

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32FIG. 48.9

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33FIG. 48.9

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34FIG. 48.9

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35FIG. 48.9 or 11.12

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• 11. All - or - Nothing Phenomenon

– Once threshold is reached, no variation in strength of response

– How does stronger stimulus manifest itself?

– Increase in frequency - not change in magnitude or height of action potential

• 12. a) Absolute Refractory Period - impossible to stimulate a neuron a second time while the Na - K pump turned off, from threshold to repolarization (while K+ moving inwards)

– b) Relative Refractory Period - can stimulate a neuron with a stronger stimulus, to reach threshold, while neuron in hyperpolarization

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37Fig. 11.13

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• 13. Propagation– Signal does not die out before

reaching the end of the axon, nor does it have to boosted

– Each area act as stimulus for the next portion of the membrane

– Depolarizing region with its positive charge moves into the adjacent negatively charges “sink”

– Why doesn’t action potential go BOTH ways in the axon??

Fig. 48-10 & 11.12

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Fig. 11.14

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• 14. Factors influencing conduction velocity– Size of axon - larger diameter means faster conducting

velocity

– Temperature - higher temperature means faster conduction velocity

• Cold block on axon stops conduction

– Myelin sheath faster conduction than non-myelinated axon

– Fig. 11.16

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Copyright © 2010 Pearson Education, Inc.

Figure 11.15 Action potential propagation in unmyelinated and myelinated axons.

Size of voltage

Voltage-gatedion channel

Stimulus

Myelinsheath

Stimulus

Stimulus

Node of Ranvier

Myelin sheath

(a) In a bare plasma membrane (without voltage-gatedchannels), as on a dendrite, voltage decays becausecurrent leaks across the membrane.

(b) In an unmyelinated axon , voltage-gated Na+ and K+

channels regenerate the action potential at each pointalong the axon, so voltage does not decay. Conduction is slow because movements of ions and of the gatesof channel proteins take time and must occur beforevoltage regeneration occurs.

(c) In a myelinated axon , myelin keeps current in axons(voltage doesn’t decay much). APs are generated onlyin the nodes of Ranvier and appear to jump rapidlyfrom node to node.

1 mm

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III. Synaptic Transmission

• 1. Synapse = space or gap between two neurons or a neuron and an effectors (muscle or gland)– Electrical synapse - smaller gap where

electrical charge (action potential) of a neuron jumps the gap to stimulate second neuron (electric eel)

– Chemical synapse - larger space or gap where a chemical diffuses across synapse

– Large number of synapses on a neuron’s cell body and dendrites

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Fig. 48-13

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45Fig. 11.16

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• 2. Anatomy of a synapse– Pre-synaptic unit - end terminals of axon that

comes before the synapse, has action potential invading the end terminal where synaptic vesicles are located

– Synaptic vesicles contain neurotransmitters which will be released into the (chemical) synapse

– Post-synaptic unit - dendrites or the cell body (possibly the axon) of the next neuron in the sequence, after the synapse, or could be an effectors

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Signal travels from pre-synaptic, across synapse, to post-synaptic unit

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• 3. Neurotransmitter chemicals– a) Synaptic vesicle of the pre-synaptic side are

membrane bound vesicles that contain specific chemicals = neurotransmitters

– b) There are dozens of different types of neurotransmitters

– c) Norepinephrine (norepi/NE)• Found in the CNS and the Autonomic NS

• Stimulates different parts of the CNS

• Can stimulate OR inhibit the ANS (see VI)

• Often similar action to Epinephrine

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• 3. Neurotransmitters (continued)– d) Acetylcholine (Ach)

• Found in the CNS and the Peripheral NS

• Stimulates in the Somatic NS - skeletal muscles

• Can stimulate OR inhibit the ANS (see VI) - involuntary muscle and glands

– e) Serotonin• Found only in the CNS

• Inhibits a variety of neurons

• Anti-depressants (Prozac) work on serotonin

– f) GABA - inhibitory in the CNS

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• 3. Neurotransmitters (continued)– g) Dopamine

• Found primarily in the CNS

• Can stimulate or inhibit different areas

– h) Nitric Oxide (NO)• Gas molecule released as a local regulator

peripherally

• NO causes smooth muscle to relax

• Work on blood vessels, smooth muscle of penis, etc.

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51A&P - Table 11.3

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• 4. Actions at the synapse– a) pre-synaptic unit fires / depolarizes / is active as an

electrical charge is propagated down the axon (remember Na+/K+ changes of part II)

– b) the electrical signal invades the pre-synaptic area of the terminal branch and the electrical signal dies - Why might signal die in this area?

– c) Calcium channels open and Ca++ enters the pre-synaptic area from the extracellular environment

– d) Ca++ causes the synaptic vesicles to migrate towards the pre-synaptic membrane and fuse with the membrane = exocytosis

– e) the vesicle contents - neurotransmitter - is released into the synaptic space and starts to diffuse across to the post-synaptic side

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Fig. 48-12

A&P Flix

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QuickTime™ and aCinepak decompressor

are needed to see this picture.

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• 4. Actions at synapse (continued)– f) as chemical reaches post-synaptic membrane, it

reacts with specific receptors on this side to trigger a response by the post-synaptic unit due to a change in post-synaptic membrane permeability

– g) if the post-synaptic membrane is now more permeable to Na+ by opening sodium channels,

• this neuron becomes excited and depolarizes

– h) if the post-synaptic membrane is now more permeable to K+ or Cl-

• this neuron becomes inhibited and hyperpolarizes - WHY?

– A single post-synaptic neuron will have different types of receptors on its membrane - like a door with several locks - each receptor can be activated by a different chemical

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Fig. 48-14 or (11-19)

EPSP = excitatory postsynaptic potential (depolarizing)

IPSP = inhibitory postsynaptic potential (hyperpolarizing)

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Fig. 11-6

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• 5. Summary– a) Excitation or Depolarization

• due to increase in positive charges intracellular which brings membrane potential towards threshold which allows sodium gates to open and neuron fires

– b) Inhibition or Hyperpolarization• Due to an increase in negative charges intracellular

or positive charges leaving (K+) which brings the membrane potential away from threshold, making it HARDER to fire this neuron

– c) How do we turn off the neurotransmitter?

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• 5d) As long as neurotransmitter is present in the synapse, it will keep reacting with post-synaptic receptors and keep the gates/channels open or closed and the reaction continues.– 1. Norepinephrine and Epinephrine are

transported AWAY from synapse or transported back into the pre-synaptic unit to be recycles

– 2. Acetylcholine has specific enzyme in the synapse - Acetylcholinesterase - which cleaves the Ach into Acetyl plus Choline to be recycled

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• 6. Summation and Integration– Number of excitatory vs. inhibitory synaptic

inputs determine post-synaptic response– Time course of inputs– Examples

• Car - brake and gas pedal

• Preying Mantis

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• 7. Effect of Drugs on Synaptic Activity– a) Insecticide or nerve gas

• What is behavior of animal exposed to this poison?• Block the action the enzyme which destroys Ach• Acetylcholinesterase = rigidity of muscles

– b) Curare• Derived from plants• Blocks receptors on skeletal muscle • Prevents Ach from working - muscle flaccid/relaxed

– c) Stimulants / Amphetamines• Mimic action of Norepi in brain• Stimulate release of Norepi in brain• Dependency• What over counter pill a stimulant, but not used to keep you

awake?

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• 7. Drugs (continued)– d) Depressants / Anesthetics

• Inhibit many centers in the brain

• Base of brain and higher up

• Overdose = depresses respiratory centers

• Alcohol?

– e) LSD / Hallucinogenic Drugs• Normally - there is inhibition between the different sensory

inputs

• Smell goes to one place, sight another region

• These drugs cause overspill of one input to different areas of the brain, so you see a sound, taste a light

• Yellow Submarine experiment

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IV. Spinal cordA. Definitions

• 1. Grey Matter - collection of neuron cell bodies and dendrites within the CNS

• 2. White Matter - collection of myleinated axons within the CNS

• 3. Nucleus - a cluster or collection of related neurons within the CNS

• 4. Ganglion - a collection of related neuron cell bodies outside the CNS, in the periphery

• 5. Interneuron or Association neuron - connecting neuron within the CNS

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Fig. 12.31/33

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• 6. Ascending tracts - related sensory axons within the white matter of the CNS

• 7. Descending tracts - related motor axons within the white matter of the CNS

• 8. Meninges - three membranes that cover the entire CNS (brain and spinal cord)– Dura Mata - tough, fibrous outer membrane that

protects– Arachnoid membrane - middle layer that supports the

blood vessels in a sub-arachnoid space (web like appearance)

– Pia Mata - inner most membrane, (gentle) tissue paper thin but helps shape CNS, which normally has a jell-like consistency

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Fig. 12.24

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• 9. Cerebral Spinal Fluid - CSF– a) Formed in ventricles of brain as a filtrate of blood,

CSF circulates through ventricles and central canal• Stabilize extracellular environment

• Tight junctions between capillary cells plus glial cells

• Selective, not absolute permeability - varies in different parts of the brain (hypothalamus, vomit center)

– b) Ventricles - fluid-filled spaces of brain (large lateral, 3rd, 4th ventricles)

– c) CSF carries nutrients, hormones, white blood cells and acts as shock absorber

– d) After circulating in the CNS, CSF returns to veins on the surface of the brain, carrying wastes

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Fig. 12.26

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Fig. 12.26b

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• 9. CSF (continued)– e) Meningitis - inflammation of the meninges,

bacterial or viral, can spread to the nervous tissue of the CNS

– f) Encephalitis - brain inflammation– g) Hydrocephalus - water on the brain - CSF

forms normally, but there is an obstruction to flow and it accumulates in ventricles

• New born - enlarged head since skull bones not fused

• Adult - compresses blood vessels and crushes soft nervous tissue

• Remove obstruction or insert shunt to drain CSF

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• 10. Spinal Puncture– Removal of CSF below L1 where spinal cord has ended

– Nerves exiting at this point drift away from needle

– Fluid removed from subarachnoid space and analyzed

– Look for infection, excessive white blood cells, proteins, removal of hydrostatic pressure on the CNS

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IV. B. Spinal cord anatomy• 1. Spinal cord runs from base of brain to L1 segment with

enlargements in cervical and lumbar areas for serving arms and legs and 31 pairs of mixed spinal nerves

• 2. Dermatome - area of skin that has sensory innervations from a specific spinal nerve, there is some overlap

• 3. Spinal cord cross-section: Identify– Deeper anterior/ventral median fissure– Shallow posterior/dorsal median sulcus– Central canal in middle of grey matter– Surrounding white matter– Dorsal and ventral horns connecting to a spinal nerve

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Fig. 48-16

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IV. B. Spinal Cord anatomy (continued)• 4. Trace the following pathway: (use diagram in notes)

– Sensory receptor or dendrites (stimulus)– Myelinated dendrite passes through spinal nerve– Travels up dorsal root– Dendrite finds its own sensory cell body in dorsal root ganglion– Central process/axon exits ganglion and travels in dorsal root to

spinal cord– Enters dorsal horn proper of grey matter and synapses with an

interneuron– Interneuron sends branch to brain AND branch to ventral area of

grey matter and– Synapses with motor cell body in ventral horn– Motor axon exits spinal cord via ventral root and enters same

spinal nerve (mixed)– Motor axon innervates an effector and a response occurs

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• 5. There are synapses -– One between incoming sensory axon and dendrite/cell

body of interneuron– Second between the terminal branch of the interneuron

and the dendrite/cell body of the motor neuron– Third between the motor terminal branch and the

effector (neuromuscular junction)– Why is there not a synapse in the dorsal root ganglion?

• 6. Injections:– Epidural - outside the dura mater and outside the spinal

cord (more sensory in effect)– Subdural - into the CSF area of the middle arachnoid

membrane and penetrates the spinal cord (both sensory and motor in its effects)

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IV. C. Spinal Cord Reflexes• 1. Reflex - innate, automatic response to a

given stimulus

• 2. Reflex arc - functional unit of the stimulus-response mechanism, highly specific neural pathway involving above (B.4.)

• 3. Two types of reflexes– Inborn / inherited– Learned / acquired / conditioned

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Copyright © 2010 Pearson Education, Inc.

Figure 11.23 A simple reflex arc.

1

2

3

4

5

Receptor

Sensory neuron

Integration center

Motor neuron

Effector

Stimulus

ResponseSpinal cord (CNS)

Interneuron

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80Fig. 48-3& A&P Flix

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81Fig.13.18

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• 4. Inborn or inherited or 2 neuron reflex– Pupillary eye reflex to light, heart rate– Patellar knee reflex, respiration– 2 neuron reflex - sensory synapses directly with motor

output, monosynaptic– No interneuron - no involvement of brain– No conscious control over response

• 5. Learned or conditioned or polysynaptic or 3 neuron reflex

– Finger on hot stove– 3 neurons - sensory, interneuron, motor, multisynaptic– Interneuron involves the brain which adds a conscious

control over the motor response– Can you leave your finger on a hot stove for 30

seconds?

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• 6. Crossed Reflex– Interneuron crosses to opposite side of the spinal cord as well

– Reflex excites extensor on one side and flexor on the other side

– Think of balancing on see-saw or stepping on a sharp tack

Fig. 13.19

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Figs. 12.1/2

V. BRAIN

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V. Brain• A. Cerebrum or Cerebral Hemispheres

– 1. Mammals - grows over other, older parts of the brain, assumed functions or control over older portions

• Furrows and convolutions of surface to increase surface area of gray matter

• White matter of cortex = ascending and descending tracts plus interneurons within cortex

• Left - Right Hemispheres connected via the Corpus Callosum - band of connecting interneuron axons

• Ventricles and CSF

• Function of the left brain?? Anatomical control??

• Function of the right brain?? Anatomical control??

• Lobes = frontal, parietal, occipital, temporal

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Fig. 12.5

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Fig. 12.4

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Fig. 12.10

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• Figs. 12.6

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Fig. 48-24

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91Fig. 28-25 or 12.9

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• A. Cerebrum (continued)– 2. Function and locations

• Controls learned behavior

• Highest reflection of sensory input (parietal)– Vision - occipital

– Hearing - temporal

– Olfaction - temporal

• Highest origin of motor output (frontal)

• Integrative functions for both

• Intelligence

• Memory

• Language and speech (frontal & temporal)

• Emotions (see limbic system)

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Fig. 12.8

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Fig. 12.8

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Fig. 28-20

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96Fig. 28-27 or 12.18

Copyright © 2010 Pearson Education, Inc.

Figure 12.18 The limbic system.

Corpus callosum

Septum pellucidum

Olfactory bulb

Diencephalic structuresof the limbic system•Anterior thalamic nuclei (flanking 3rd ventricle)•Hypothalamus•Mammillary body

Fiber tractsconnecting limbic system structures•Fornix•Anterior commissure

Cerebral struc -tures of the limbic system•Cingulate gyrus•Septal nuclei•Amygdala•Hippocampus•Dentate gyrus•Parahippocampal gyrus

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• A. Cerebrum (continued)– 3. Cut corpus callosum = split brain– 4. Limbic System

• Emotion due to interactions with sensory input and association centers

• Memory - Hippocampus• Frontal lobotomy

– 5. Basal Ganglia• Conscious and unconscious movements• Movement sequencing• Parkinson’s and Huntington’s diseases• Dopamine involvement (Awakenings)

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Fig. 12.11b

Basal Ganglia

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• B. Cerebellum– 1. Under cortex, above medulla– 2. Convoluted surface with internal axons

– 3. Communicates with many other areas (F4.)• Sensory and motor areas

– 4. Monitors and corrects motor activities• Posture

• Muscle coordination

• Error control compares intention with performance

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Fig. 12.12

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Fig. 12.13

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• C. Thalamus– 1. Collection of nuclei bordering the third ventricle– 2. Communicates with other areas (see F4 below)– 3. Relay for sensory input to the cerebrum– 4. Conscious recognition

• D. Hypothalamus– 1. Below the thalamus, above the pituitary gland– 2. Communicates with other areas (see F4 below)– 3. Psychosomatic disorders ??

• Endocrine functions - produces different hormones that control the pituitary and other body organs and functions

– 4. Nuclei controlling Autonomic Functions• Food intake Fluid balance• Temperature regulation Sex Drive• Pleasure - Pain

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• E. Pons– 1. Posterior to the hypothalamus, part of the

Brain Stem– 2. Communicates with other areas (F.)– 3. Influences other breathing centers of brain

• F. Medulla (oblongata)– 1. Part of the Brain Stem, connects the brain to

the spinal cord– 2. Conduction pathway for incoming sensory

axons and outgoing motor axons– 3. Nuclei that control Vital Reflexes

• Cardiac Respiratory centers• Swallow Cough Vomit centers

– 4. Origin of the Reticular formation

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Fig. 12.16a/b

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Fig. 12.16c

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107Fig. 28-21 or 12.19

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F. Medulla 4. Reticular formation (continued)

– Ability to facilitate or inhibit incoming sensory and outgoing motor activities

• Aids in ignoring certain stimuli as brain processes other inputs

– Responsible for normal arousal of the higher centers of brain

– Patient in coma

– Muscle jerk as one falls asleep

• Response???

• G. EEG or Brain Waves

– External detection of depolarizations and hyperpolarizations over brain

– Alpha = quiet rest Beta = active

– Theta = stress Delta = sleep

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Fig. 48-22

Fig. 12.20

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110Fig. 13.5

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• H. Cranial Nerves– 1. 12 pairs exiting/entering from the brainstem– 2. Olfactory (#1) - sensory– 3. Optic (#2) - sensory to optic chiasm– 4. Trigeminal (#5) - mixed - chewing and facial

sensations– 5. Vagus (#10) - mixed from.to all over body

including cardiac, visceral and skeletal

• I. Neural Disorders– 1. Polio - viral degeneration of ventral horn motor cell

bodies of spinal cord– 2. Cerebral palsy - voluntary muscles are poorly

controlled due to brain damage during fetal development or birth (oxygen deprivation)

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• I. Disorders (continued)– 3. Parkinson’s Disease - degeneration of

dopamine producing cells of the substantia nigra, which target Basal Ganglia cells of the inner cerebrum

• Tremors• Slow in initiating and executing voluntary motion• L-dopa compounds, fetal tissue, genetically

engineered adult cells

– 4. Multiple Sclerosis - autoimmune loss of myelin from motor and sensory neurons causes short-circuiting of signals

• Since axon healthy, variable remissions occur

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• 5. Alzheimer’s Disease - progressive degeneration of the brain resulting in dementia (genetic factors)

– Ach problems

– Structural changes in cerebrum and hippocampus

– Protein bound to beta amyloid protein plus neurofibrillar tangles in cell body

• 6. Stroke or CVA - blockage of blood circulation to brain and brain tissue dies

– Caused by clot, compression by hemorrhaging or edema

– Atherosclerosis - narrowing of blood vessel by deposits

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VI. Autonomic Nervous System• 1. Peripheral Nervous system

– Somatic NS - – Autonomic NS - involuntary motor system that

connects to cardiac and smooth muscles and glands

• 2. Two divisions of the ANS– Parasympathetic NS– Sympathetic NS

• 3. Dual Innervations - both parasympathetic and sympathetic systems connect to the same effectors– Heart Intestine Salivary glands etc.– Why have two systems to same organs?

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Fig. 14.2

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Fig. 14.3

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• 4. Antagonist Functions of the 2 ANS divisions– One system excites and the other system

inhibits• Organ Parasympathetic Sympathetic• Heart

• Smooth • muscle• Of • Digestive• System

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Heart

(cardiac muscle)

Inhibits Heart Rate & Strength of beat

Increases HR & Strength of beat

Smooth Muscle of Digestive System

Stimulates Peristalsis - smooth rhythmic contraction of gut

Inhibits Peristalsis

Organ Parasympathetic Sympathetic

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• 5. Properties of Parasympathetic NS– a) 80% of all parasympathetic activity from brain is

associated with the Vagus Nerve (10th cranial nerve), all parasympathetic nerves originate from the top or bottom of the spinal cord

– b) main neurotransmitter released is Acetylcholine

– c) main functions: conserve or restore energy levels in the body

• Appetite related

• Digestion

• excretion

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120Figs. 14.4/6

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• 6. Properties of Sympathetic NS– a) no one single nerve, but nerves originate from the

middle of the spinal cord– b) main neurotransmitter released is Norepinephrine

plus these nerves also release hormones of the adrenal gland to prolong the actions of the sympathetics

– c) main function: utilize energy• Fight or Flight Syndrome• Stress Related - opposite of homeostasis

– d) too much stress causes imbalance between these two systems resulting in changes in blood pressure, ulcers, heart arrhythmias, etc.

– e) reduce stress in your life - don’t let Biology get to you!

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Fig. 14.9

Levels of ANS Control

Copyright © 2010 Pearson Education, Inc.

Figure 14.9 Levels of ANS control.

Cerebral cortex(frontal lobe)

Limbic system(emotional input)

Communication atsubconscious level

HypothalamusOverall integrationof ANS, the boss

Spinal cordUrination, defecation,

erection, and ejaculationreflexes

Brain stem(reticular formation, etc.)

Regulation of pupil size,respiration, heart, blood

pressure, swallowing, etc.

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THANKS FOR A GREAT SEMESTER