NERVOUS SYSTEM. Basic functions. Monitor changes Sensory input
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1 NERVOUS SYSTEM
2 The Nervous System
3 Basic functions Monitor changes Sensory input NERVOUS SYSTEM Inside & outside body Integrate input Process, analyze, interpret response Store information (memory) Initiate response Motor output Fig
4 Organizational Overview Two primary divisions Central nervous system (CNS) Peripheral nervous system (PNS) 4
5 Organizational Overview Peripheral nervous system (PNS) Afferent (sensory) division Impulses from body CNS Somatic afferents From skin, muscles, joints Visceral afferents From visceral organs 5
6 Organizational Overview Peripheral nervous system (PNS) Afferent (sensory) division Efferent (motor) division Impulses from CNS body 6
7 Organizational Overview Peripheral nervous system (PNS) Afferent (sensory) division Efferent (motor) division Somatic nervous system CNS skeletal muscle, joints Autonomic nervous system Sympathetic division Mobilize body in response to stress Fight or flight (4-E s) Parasympathetic division Maintenance, energy conservation measures Rest & digest (3-D s) 7
8 The parasympathetic nervous system is a subdivision of all of these EXCEPT: A) Central nervous system B) Peripheral nervous system C) Efferent nervous system D) Autonomic nervous system 8
9 Neuron General structure Histology Receptive, conductive, secretory components Cell body Processes Dendrites Axon Axon terminus General characteristics Fig
10 Supportive cells Histology CNS Glial cells Astrocytes Microglia Ependymal cells Oligodendrocytes PNS Satellite cells Schwann cells 10
11 Functional Classes of Neurons Motor neurons Impulses sent away from CNS Multipolar Sensory neurons Impulses sent from receptors toward CNS Unipolar, bipolar, multipolar Interneurons (association neurons) Send impulses between neurons Largest group of neurons Multipolar 11
12 A neuron which receives information from a neuron and passes information to another neuron is a(n) A) Sensory neuron B) Motor neuron C) Interneuron D) May be any of the above 12
13 Generation of Nerve Impulses Membrane potential Voltage across the surface of a membrane Diffusion potential is the result of a concentration gradient across a membrane Nernst potential Figs. 5-2,3 13
14 Generation of Nerve Impulses Membrane potential Voltage across the surface of a membrane Nernst potential EMF = ±61 log ( [ion] inside / [ion] outside ) EMF = electromotive force Figs. 5-2,3 14
15 What is the EMF when there is a 10:1 ratio of K + inside:outside the cell? A) 10 V B) -10 mv C) 61 V D) -61 mv 15
16 Membrane Potential Primary ions involved in establishing charge differential Na + K + Fig
17 Membrane Potential Ion movement driven by electrochemical gradients Diffusion in response to ion concentration Diffusion in response to charge differential 17
18 Membrane Potential 18
19 Membrane Potential Establishing resting potential Leak channels Passive process Randomly flicker open/closed states between ~100x more permeable to K + than Na + more K + leaks out Resting potential depends more on K + gradient than Na + gradient Na + /K + ion pump Active process Pump more Na + out (3:2 ratio) Fig
20 Resting membrane potential depends mostly on the potassium (K + ) concentration gradient because A) It is the largest gradient B) The plasma membrane has the most permeability to K + at rest C) K + ions are larger than Na + ions, so they move faster D) All of the above 20
21 Membrane Potential Controlled depolarization of the resting membrane creates an electrical signal Involves voltage-gated ion channels Open/close in response to changes in voltage Generates nerve impulses (action potentials) Allows rapid long-distance communication Fig
22 Generation of an Action Potential Figs. 5-6,9 22
23 Like the ideal toilet Action Potentials Push the handle Threshold stimulus Depolarize membrane Drain the bowl All or nothing Action potential Refill the tank Refractory period Return to resting potential 23
24 Generation of an Action Potential Resting potential Voltage gated Na + & K + channels closed Leak channels active Fig
25 Generation of an Action Potential Stimulus / Depolarization Na + gates begin to open Na + influx Fig
26 Generation of an Action Potential Stimulus / Depolarization Reach threshold voltage Activation of voltage-gated Na + channels (mass Na + influx) Leads to complete depolarization of membrane Generates action potential: all-or-nothing Fig
27 Generation of an Action Potential Repolarization Na + gates inactivated K + gates open Fig
28 Generation of an Action Potential Afterpotential (undershoot) K + gates slow to close Membrane is refractory to new stimuli Fig
29 Generation of an Action Potential Return to resting potential K + & Na + voltage gated channels closed Ion distribution restored by Na + /K + ion pump Membrane can respond to another stimulus Fig
30 During an action potential, the voltage of the membrane changes because A) The concentration gradient for K + changes B) The concentration gradient for Na + changes C) The permeability of the membrane to Na + changes D) All of the above 30
31 Given typical K + and Na + concentration gradients at rest, what is the concentration of Na + inside the cell during depolarization? A) 14 meq/l B) 142 meq/l C) 140 meq/l D) 4 meq/l 31
32 Propagation of the Action Potential Voltage change spreads in all directions from action potential Activates nearby gates and continues impulse Continues along entire length of membrane Depolarization wave followed by repolarization wave So how can this occur unidirectionally along an axon? Fig
33 Propagation of the Action Potential Voltage change spreads in all directions from action potential Activates nearby gates and continues impulse Continues along entire length of membrane Depolarization wave followed by repolarization wave So how can this occur unidirectionally along an axon? 33
34 Saltatory Conduction Involves myelin sheath along axon Ion gates concentrated at Nodes of Ranvier Fig
35 Benefits Saltatory Conduction Increases transmission rate ~50x (~100 m/s) Depolarization occurs at regular gaps instead of every point along the membrane Ion need reduced by 100x Less energy to repolarize membrane Na + /K + ion pump Repolarization occurs faster Fewer ions need to be replaced 35
36 Myelination Myelin lipoprotein within a plasma membrane Schwann cells Single cells wrap around axon Schwann cell partially wraps around multiple axons of adjacent neurons Fig
37 Myelination Myelin lipoprotein within a plasma membrane Schwann cells Oligodendrocytes Single cells extend projections to wrap around axons of multiple neurons 37
38 Multiple sclerosis Myelination Demyelination of neurons Autoimmune reaction Decreases nerve transmission rate Vision problems, muscle control, speech problems, incontinence Periods of Remission Axon not initially damaged New ion channels develop to restore transmissibility (temporary) 38
39 Myelination increases speed of transmission by A) Making current flow faster through the voltage-gated channels B) Reducing the number of action potentials required to propagate a signal down the axon C) Preventing leakage of ions 39
40 Transmission of Nerve Impulses The chemical synapse Space (gap) between axon terminus and effector cell Electrical stimulus is converted to chemical message to transfer stimulus Ca 2+ required for neurotransmitter release Activates proteins at release sites to promote fusion / exocytosis of secretory vesicles synapse Fig
41 Transmission of Nerve Impulses The chemical synapse Fig
42 Chemical Synapses Two categories based on how they affect membrane potential Excitatory postsynaptic potentials (EPSP s) Open Na + channels (influx) Inhibit K + & Cl - channels Begin to depolarize membrane May lead to action potentials Fig
43 Chemical Synapses Two categories based on how they affect membrane potential Excitatory postsynaptic potentials (EPSP s) Inhibitory postsynaptic potentials (IPSP s) Open K + (outflow) and Cl - (inflow) channels Hyperpolarizes membrane Inhibits ability to generate action potentials Fig
44 Chemical Synapses Outcome of EPSP / IPSP stimulation results from the summation of the signals Single EPSP or IPSP insufficient to induce or inhibit action potential Both EPSP/IPSP typically present dominant signal dictates outcome Integrated at axon hillock Fig
45 Spatial summation Chemical Synapses Fig
46 Temporal summation Chemical Synapses 46
47 EPSPs are typically generated as a result of A) Opening potassium channels B) Opening sodium channels C) Closing potassium channels D) Closing sodium channels 47
48 Neurotransmitters Group 1: Small molecule, rapidly acting transmitters General mode of action Alter ion channel conductance OR Stimulate receptor-activated enzyme systems Synthesis Synthesized in cytosol of presynaptic terminal Stored / exocytosed in secretory vesicles See Table
49 Neurotransmitters Acetylcholine (ACh) Location Many CNS neurons All neuromuscular junctions Preganglionic neurons of ANS Postganglionic neurons of Parasympathetic NS; few Sympathetic NS 49
50 Neurotransmitters 50
51 Neurotransmitters Acetylcholine (ACh) Action Typically excitatory Some inhibitory effects in Parasympathetic NS Drug interactions Release blocked by botulinum toxin Effects prolonged by nerve gas, organophosphates Inactivate acetylcholinesterase Many snake venoms block postsynaptic receptors Enhanced by nicotine (binds nach receptors) 51
52 Neurotransmitters Biogenic amines Dopamine Location Secreted by neurons of midbrain (substantia nigra) Action feel good Usually inhibitory Target of recreational drugs Release enhanced by amphetamines Uptake blocked by cocaine 52
53 Neurotransmitters Biogenic amines Norepinephrine Location Many CNS neurons (mood, increasing wakefulness) Most postganglionic neurons of SNS Action Excitatory or inhibitory depending on target Synaptic removal blocked by cocaine & other antidepressants 53
54 Neurotransmitters Biogenic amines Serotonin Location Secreted by neurons of brain stem Action Pain inhibitor, mood enhancer (inhibitory effects), sleep Re-uptake blocked by Prozac (SSRI) Relief of depression / anxiety 54
55 Neurotransmitters Amino acids & derivatives Glutamate Action Fast excitatory synapses of brain Fast-pain fibers in spinal cord Role in stroke (enhances damage) Damaged brain cells (O 2 deprivation) release mass amounts of glutamate Overexcites neighboring cells Leads to generation of free radicals (destroy cells) 55
56 Neurotransmitters Nitric oxide (NO) Location Nerve terminals in brain related to long-term behavior & memory Action Synthesized as needed (not stored) Readily diffuses through membranes Doesn t significantly directly alter membrane potential Modifies intracellular metabolic activity of post synaptic neuron to affect neuronal excitability 56
57 Which of these NTs acts only in an excitatory fashion? A) Acetylcholine (ACh) B) Norepinephrine (NEpi) C) Dopamine D) Glutamate 57
58 Neurotransmitters Group 2 : Neuropeptides (slow-acting transmitters or growth factors) Hormones or releasing/inhibitory factors Affect neuron receptors / synapses (# s & sizes) Characteristics More potent than fast acting transmitters Smaller quantities released Actions more prolonged Synthesis Synthesized in neuron cell body, packaged by Golgi and transported down axon to termini Then stored / exocytosed in secretory vesicles See Table
59 Clearance of the Synapse Enzymatic degradation E.g., ACh Split in synapse by cholinesterase (ACh choline + acetate) Choline transported back into presynaptic terminal More Ach synthesized (acetyl-coa + choline ACh) Re-uptake E.g., dopamine Diffusion 59
60 NPY is a neurotransmitter involved in appetite regulation. Would you guess that it is fastacting (Group 1) or slow-acting (Group 2)? A) Fast Group 1 B) Slow Group 2 60
61 Characteristics of Synaptic Transmission Fatigue Protection against excess neuronal activity Causes Exhaustion of transmitter stores Inactivation of postsynaptic membrane receptors Abnormal ion concentrations Effect of ph Alkalosis increases excitability May lead to seizure Acidosis decreases excitability May lead to coma 61
62 Characteristics of Synaptic Transmission Effect of hypoxia O 2 deprivation can lead to cessation of excitability Effects of anesthetics Increase membrane threshold Lipid-based forms may alter threshold by integrating into membrane 62
63 The lack of awareness of certain stable stimuli, such as clothes touching your skin, or a stable environmental temperature, may be partially due to A) The effect of ph on the NT release B) The effect of hypoxia on NT receptor action C) Synaptic fatigue due to reduced NT receptor activation D) All of the above 63
64 Classes of Sensory Receptors 5 classes based on type of stimulus detected Mechanoreceptors Deformation of membrane receptors opens ion channels Thermoreceptors Change in temp alters membrane permeability See Table
65 Classes of Sensory Receptors 5 classes based on type of stimulus detected Chemoreceptors Chemical binding opens ion channels Electromagnetic receptors Light alters conformation of membrane proteins Nociceptors E.g., pain See Table
66 Baroreceptors are a type of A) Mechanoreceptor B) Thermoreceptor C) Chemoreceptor D) Electromagnetic receptor E) Nociceptor F) None of the above it s its own class 66
67 Sensory Receptor Specialization Receptive component Highly specialized to detect specific stimuli Fig
68 Detection & Transmission of Stimuli How are sensory impulses regulated to differentiate stimuli of varied intensities? Stimulate multiple receptors Varied responses from individual receptors Development & rate of action potentials are dependent on the intensity of the stimulus at the receptor This allows a single receptor to respond to a range of stimuli with a range of responses Weak extreme Based on receptor potential 68
69 Receptor Potential The change in electrical potential of the receptor Action potentials result when this rises above the threshold Fig
70 Detection & Transmission of Stimuli Increasing receptor potentials increase the frequency of action potentials Fig
71 Detection & Transmission of Stimuli Receptor potential (amplitude) relates to stimulus strength Allows receptors to transmit a range of responses Weak stimulus = receptor potential = low frequency of action potentials Strong stimulus = receptor potential = high frequency of action potentials Fig
72 Signal Transmission in Nerve Tracts Based on principles of summation Spatial summation Fig
73 Signal Transmission in Nerve Tracts Based on principles of summation Spatial summation Temporal summation Fig
74 Adaptation Receptors can adapt to repetitive stimuli Frequency of action potentials begins to decrease with continuous stimuli Fig
75 True or false: Stronger stimuli make the receptor generate bigger action potentials. A) True B) False 75
76 Adaptation Adaptation may be partial or complete Rate and degree varies with receptor type Fast adapting receptors Send impulses to notify brain of changes in stimulus strength E.g., Pacinian corpuscle (mechanoreceptor) Slow adapting receptors Keep brain constantly apprised of body status May never completely adapt Continue to send signals to brain, although not at maximum rate E.g., nociceptors, chemoreceptors 76
77 Adaptation Example: Pacinian Corpuscles Sensory mechanism Pressure forces redistribution of fluids within corpuscle Mechanical gated ion channels open Generates initial stimulus If maintained, fluids equalize throughout corpuscle Gates close Stimulus ceases (adaptation to extinction) If pressure released, fluids redistributed again Gates open Stimulus generated 77
78 Adaptation Methods for adaptation may involve Readjustments to the structure of the receptor E.g., Pacinian corpuscle fluid redistribution Accommodation Inactivation of Na + channels in nerve fiber 78
79 True or false: Adaptation of receptors means that receptors will continue to send a signal as long as the stimulus is present. A) True B) False 79
80 Signal Processing & Transmission Neuronal pools Functional groups of neurons that integrate and relay information Fig
81 Neuronal pools Neuronal Pools Discharge zone (center of field) Provide primary stimulatory / inhibitory potentials Fig
82 Neuronal pools Neuronal Pools Facilitated zones (periphery of field) Provide sub-threshold stimuli but may facilitate input from other neurons Fig
83 Diverging circuits Circuit Patterns Presynaptic fiber(s) influence multiple post synaptic neurons Amplified divergence (single tract) Divergence occurs along same tract E.g., neurons in motor cortex & muscle control Fig
84 Diverging circuits Circuit Patterns Presynaptic fiber(s) influence multiple post synaptic neurons Amplified divergence (single tract) Multiple tract divergence Signal diverges along multiple nerve tracts E.g., spinal reflex Fig
85 Converging circuits Circuit Patterns Presynaptic fiber(s) converge to influence a single post synaptic neuron Single source convergence Fig
86 Converging circuits Circuit Patterns Presynaptic fiber(s) converge to excite a single post synaptic neuron Multiple source convergence Input may come from several different areas Results in spatial summation Fig
87 Inhibitory circuits Circuit Patterns Involve both EPSP s and IPSP s E.g., antagonistic muscle groups E.g., spinal reflexes Fig
88 Circuit Patterns Reverberating (oscillating) circuits Provide positive feedback to amplify or maintain a signal (after discharge) Often involve axon collaterals Some reverberate continuously E.g., respiratory centers (medulla, pons) Intrinsic excitability (unstable membrane potentials always on) EPSP s output IPSP s output Fig
89 Reverberating Circuits Fig
90 A neuronal circuit which begins with one neuron, then spreads to many other neurons is a circuit. A) Diverging B) Converging C) Reverberating D) Oscillating 90
91 Circuit Patterns Control over neuronal circuits Inhibitory feedback circuits Stimuli from circuit terminus sent back to inhibit input or intermediary neurons Common in sensory pathways 91
92 Circuit Patterns Control over neuronal circuits Synaptic fatigue Prolonged / intense periods of excitation weaken synaptic transmission Short term adjustments constraints on neurotransmitter production / release / uptake Long term adjustments downgrade receptors due to over activity, upgrade receptors with under activity 92
93 Signal Output Synaptic fatigue Fig , 15 93
94 Synaptic Fatigue Fig
95 The role of synaptic fatigue in regulation of neuronal circuits is to A) Inhibit signals which have been on for some time already B) Potentiate (enhance) signals which have been on for some time already C) Recharge neurons so they can send additional signals D) All of the above 95
96 THE CENTRAL NERVOUS SYSTEM Structural and functional overview of the brain 96
97 THE CNS Structural and functional overview of the spinal cord 97
98 Afferent nerve tracts Dorsal column-medial lemniscal pathway Crossover in medulla Critical tactile input Nerve Pathways Fig
99 Afferent nerve tracts Anteriolateral pathway Crossover in spinal cord (immediate) Pain, temp, mechanoreceptors Nerve Pathways Fig
100 Motor & Somatosensory Areas of Cerebral Cortex See Fig. 47-5,6,7, 55-1,2,3 10
101 Efferent nerve tracts Direct pathway Nerve Pathways Pyramidal tracts (corticospinal tracts) Crossover in inferior medulla or spinal cord Fig
102 Efferent nerve tracts Nerve Pathways Indirect pathway Branching in basal ganglia, cerebellum, etc. Fig
103 Somatosensory-Motor Pathways Fig
104 Spinal Reflexes Response to stimuli without cortical involvement Typically involve extreme or potentially damaging stimuli E.g., flexor-crossed extensor reflex Diverging circuit (multiple tract) with reciprocal inhibition Fig
105 THE PERIPHERAL NERVOUS SYSTEM: EFFERENT PATHWAYS Central nervous system Peripheral nervous system Afferent (sensory) nervous system Efferent (motor) nervous system Somatic nervous system Autonomic nervous system (ANS) Sympathetic nervous system (SNS) Parasympathetic nervous system 105
106 Somatic Nervous System Neuron cell bodies Myelination Neurotransmitter Effect Target CNS Heavy ACh Stimulatory Skeletal muscle 106
107 Which of these NTs is used in the somatic nervous system? A) Acetylcholine (ACh) B) Norepinephrine (NEpi) C) Dopamine D) Glutamate E) All of the above 107
108 Autonomic Nervous System Sympathetic division Preganglionic neurons Cell body Axon length Myelination Neurotransmitter Effect Target CNS Typically short Light ACh Stimulatory A) neurons in ganglion, B) adrenal medulla A B 108
109 Autonomic Nervous System Sympathetic division Postganglionic neurons Cell body Axon length Myelination Neurotransmitter Effect Target Ganglia Long Nonmyelinated 1 norepinephrine Target dependent Smooth muscle, glands, heart, misc. organs A B 109
110 Autonomic Nervous System Sympathetic division Adrenal medulla (as postganglionic neuron ) Cell body Axon length Myelination Neurotransmitter Effect Target A Medulla (modified neurons) n/a n/a Epinephrine & NorEpi Target dependent (prolonged) Smooth muscle, glands, heart, misc. organs B 110
111 Sympathetic Spinal Nerves Exit from thoracic & upper lumbar regions (T 1 -L 2 ) Synapses Sympathetic chain ganglia (paravertebral ganglia) Prevertebral ganglia Celiac Hypogastric Fig
112 True or false: All postganglionic neurons use the same neurotransmitter. A) True B) False 112
113 The adrenal medulla is analogous to which of the following structures? A) Preganglionic sympathetic neuron B) Postganglionic sympathetic neuron C) Preganglionic parasympathetic neuron D) Postganglionic parasympathetic neuron 113
114 Autonomic Nervous System Parasympathetic division Preganglionic neurons Cell body Axon length Myelination Neurotransmitter Effect Target CNS Typically long Light ACh Stimulatory Ganglion / effector 114
115 Autonomic Nervous System Parasympathetic division Postganglionic neurons Cell body Axon length Myelination Neurotransmitter Effect Target Ganglion / on effector Shorter None ACh Target dependent Smooth muscle, glands, heart, misc. organs 115
116 Parasympathetic Nerves Exit from cranial and sacral regions Synapse near/on effector organ Fig
117 Emerges from medulla oblongata Only cranial nerve to extend beyond head/neck Mixed nerve Efferents primarily parasympathetic Vagus Nerve (X) Fig
118 The Vagus nerve uses which neurotransmitter? A) Acetylcholine B) Epinephrine C) Norepinephrine D) Glutamate 118
119 Neurotransmitter Synthesis: Acetylcholine choline + Acetyl-CoA Acetylcholine Synthesized in axon terminals by choline acetyltransferase Stored in secretory vesicles Degraded in synaptic cleft (acetylcholinesterase) Acetate + choline Choline uptake by axon terminals 119
120 Neurotransmitter Synthesis: Norepinephrine Synthesis begins in cytoplasm of axon terminals but is completed within secretory vesicles Tyrosine DOPA DOPA Dopamine (transported into secretory vesicles) Dopamine Norepinephrine 120
121 Neurotransmitter Synthesis: Epinephrine Synthesis begins in cytoplasm of axon terminals but is completed within secretory vesicles Occurs in adrenal medulla via methylation Norepinephrine Epinephrine 121
122 Neurotransmitters & Receptors of ANS Cholinergic fibers & receptors Release & bind ACh ( parasympathetic transmitter ) 122
123 Neurotransmitters & Receptors of ANS Cholinergic fibers & receptors Release & bind ACh ( parasympathetic transmitter ) Adrenergic fibers & receptors Release & bind norepinephrine ( sympathetic transmitter ) 123
124 Adrenergic fibers release which of the following neurotransmitters? A) Acetylcholine B) Epinephrine C) Norepinephrine D) Glutamate 124
125 Cholinergic Fibers & Receptors Cholinergic fibers All ANS preganglionic fibers All parasympathetic postganglionic fibers 125
126 Cholinergic Fibers & Receptors 2 categories of cholinergic receptors Nicotinic receptors (nachrs) Direct ion channels Effects always stimulatory Found on Skeletal muscle All ANS preganglionic neurons Hormone-producing cells of the adrenal medulla 126
127 Cholinergic Fibers & Receptors 2 categories of receptors Muscarinic receptors (machrs) G-protein coupled receptors Effects depends on effector Found on: All parasympathetic target organs E.g., heart, lungs, digestive organs Some sympathetic target organs (where ACh involved) E.g., eccrine sweat glands, some blood vessels of skeletal muscle 127
128 Fibers Adrenergic Fibers & Receptors (Nearly) All sympathetic postganglionic fibers See Table
129 Adrenergic Fibers & Receptors 2 primary categories of receptors: ( 1, 2 ), ( 1, 2, 3 ) Organs responding to norepinephrine or epinephrine contain both types Norepinephrine binds stronger than Epinephrine binds both, nearly equally Effect Dependent on type & number of receptors on effector organ Receptor classes not necessarily associated with direct stimulation or inhibition See Table
130 Muscarinic receptors work by which of the following mechanisms? A) Depolarizing membrane directly via opening ion channels B) Depolarizing membrane indirectly via intracellular signaling mechanisms C) Hyperpolarizing membrane directly via closing ion channels D) All of the above 130
131 Autonomic Pharmacology Sympathomimetic drugs Epinephrine Phenylephrine alpha Isoproterenol beta Albuterol beta 2 Drugs that block adrenergic activity Alpha blockers phenoxybenzamine Beta blockers - propanolol Parasympathomimetic drugs Pilocarpine, methacholine Antimuscarinic drugs -??? 131
132 If you only had these four drugs to choose from, which of these drugs would you likely administer to reduce a rapid heart rate? A) Alpha receptor blocker - phenoxybenzamine B) Beta receptor blocker - propranolol C) Parasympathomimetic - pilocarpine D) Antimuscarinic - atropine 132
133 Primary Effects of ANS Stimulation Organ Symp. Stimulus Parasymp. Stimulus Eye (iris) dilation of pupil constriction of pupil Salivary/gastric glands inhibits secretions stimulates secretions Sweat glands stimulates sweating none / palms Arrector pili contraction none Heart increases rate / force decreases rate / force Blood vessels vasoconstriction little / none Lungs bronchiole dilation bronchiole constriction Digestive organs decreased gland activity, increased secretion & muscle constriction motility, sphincters relax Liver stimulates glucose release slight glycogen synthesis Pancreas inhibits secretions stimulates secretions Adrenal medulla stimulates secretions none Kidney decreased urine output none Metabolism increased rate none Mental function increased alertness none See Table
134 Patterns of ANS Stimulation Mass vs. discrete discharge Sympathetic division Displays mass discharge effects E.g., stress response Arterial pressure Blood flow to skeletal muscle / strength Blood flow to GI / renal organs Cellular metabolism / glycolysis / blood [glusose] Mental activity Blood coagulation Can show discrete control E.g., heat regulation in skin Parasympathetic division Typically discrete 134
135 Role of the Adrenal Medulla in the ANS Response Stimulated simultaneously with sympathetic mass discharge Produces sustained effect (5-10x) Longer time required to clear hormone from blood than synapse May compensate for destruction / interference of sympathetic fibers Allows stimulation of targets not innervated by sympathetic fibers E.g., general cellular metabolism 135
136 What is the benefit of discrete discharge as compared to mass discharge? A) Faster response B) Longer-lasting response C) More specific response D) All of the above 136
137 Sympathetic & Parasympathetic Tone Both systems continually active at some basal level (tone) Both neural and adrenal Tone allows both systems to either or activity of a particular organ Fine-tuned regulation E.g., vasodilation / vasoconstriction Tone provides normal degree of constriction (~1/2 diameter) sympathetic stim. vasoconstriction sympathetic stim. vasodilation 137
138 Sympathetic & Parasympathetic Tone Effect of denervation on tone Immediate loss of tone Intrinsic tone develops over time Up-regulation of receptors to increase sensitivity Fig
139 Brain stem Arterial pressure Heart rate Respiratory rate Hypothalamus Control over most brain stem function Autonomic Control Fig
140 Autonomic Reflexes Cardiovascular reflexes Response to change in arterial blood pressure Gastrointestinal reflexes Salivation, increased motility in response to smell Emptying of rectum Urinary reflexes Emptying of the urinary bladder 140
141 Which is these is not a mechanism which can alter sympathetic tone? A) Medullary signals B) Hypothalamic regulation C) Emotional input to hypothalamus D) Conscious effort 141
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