CHAPTER 12: NERVOUS SYSTEM NERVOUS SYSTEM DIVISIONS NERVOUS NERVE IMPULSE TISSUE NERVOUS SYSTEM FUNCTIONS HISTOLOGY I. Introduction:

A. The nervous system (NS), along with the endocrine system, helps control and integrate all body activities.

B. Three basic functions are served by the nervous system: 1. Sensing changes (sensory) 2. Interpreting those changes (integrative) 3. Reacting to those changes (motor)

C. Neurology: It is the branch of medical science that deals with the normal functioning and disorders of the nervous system.

II. Nervous System Divisions: [Fig 12.2, p 388] A. The central nervous system (CNS) consists of the brain and

the spinal cord. B. The peripheral nervous system (PNS) consists of cranial

and spinal nerves; it has sensory (afferent) and motor (efferent) components.

1. The sensory system includes a variety of different

receptors as well as sensory neurons. 2. The motor system conducts nerve impulses from the CNS

to muscles and glands. C. The PNS is subdivided into somatic (voluntary), autonomic

(involuntary), and enteric nervous systems.

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1. The somatic nervous system (SNS) consists of neurons that conduct impulses from cutaneous and special sense receptors to the CNS, and motor neurons that conduct impulses from the CNS to the skeletal muscle tissue.

2. The autonomic nervous system (ANS) contains sensory neurons from visceral organs and motor neurons that convey impulses from the CNS to the smooth muscle tissue, cardiac muscle tissue, and glands. The ANS has two subdivisions, viz., sympathetic nervous system and parasympathetic nervous system.

3. The ENS (enteric nervous system) is the “brain of the gut” and its operation is involuntary. Once thought to be part of the ANS, it consists of approximately 100 million neurons in enteric plexuses that extend the entire length of the GI tract. Many of these neurons of these plexuses function independently of the ANS and CNS to some extent, though they communicate with the CNS via sympathetic and parasympathetic neurons. Sensory neurons of the ENS monitor chemical changes within the GI tract and the stretching of its walls, whereas the enteric motor neurons govern contraction of GI tract smooth muscle, secretion of the GI tract organs (e.g., acid secretion by the stomach and activity of the enteroendocrine cells).

III. Histology of Nervous Tissue: A. Neuroglia (meaning “nerve glue”):

1. Neuroglial or glial cells are specialized tissue cells that support neurons, attach neurons to blood vessels, produce the myelin sheath around axons, carry out phagocytosis, and form cerebrospinal fluid (CSF).

2. Neuroglial cells include: (Table 12.1, pp. 392-393)

a. Astrocytes are star-shaped with many processes; participate in the metabolism of neurotransmitters, maintain proper K+ balance (for generation of nerve

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impulse), participate in brain development, help form blood-brain barrier (provide a link between neurons and blood vessels).

b. Oligodendrocytes (oligo = a few): These are most common glial cells; smaller than astrocytes and contain few processes; form a supporting network by twining around neurons of the CNS; produce myelin sheath around axons of neurons of CNS (each oligodendrocyte wraps myelin sheath around several axons).

c. Microglia: Small phagocytic neuroglia with few processes derived from monocytes; protects the CNS from disease by engulfing invading microbes and clearing away debris from dead cells.

d. Ependymal cells: These are epithelial cells – cuboidal to columnar and many are ciliated; line the fluid-filled ventricles of the brain and central canal of the spinal cord; form cerebrospinal fluid (CSF) and assist its circulation.

CSF: Clear and colorless fluid (80-150 ml or 3-5 oz); contains glucose, proteins, lactic acid, urea, Na+, K+, Ca2+, Mg2+, Cl−, HCO3

−; some WBCs. Functions:

1. Mechanical protection (shock-absorbing medium)

2. Chemical protection (for accurate neural signaling)

3. Circulation (medium for exchange between blood and neural tissue)

e. Neurolemmocytes (Schwann cells): These cells are found in the PNS; flattened cells arranged around axons of neurons in the PNS; each cell produces part of the myelin sheath around a single axon of a PNS neuron.

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f. Satellite cells: These are flattened cells arranged around the cell bodies of neurons in ganglia (collections of neuronal cell bodies in the PNS); support neurons in ganglia of PNS.

3. Two types of neuroglia produce myelin sheath: oligodendrocytes myelinate axons in the CNS, while neurolemmocytes (Schwann cells) myelinate axons in the PNS; at intervals along an axon, the myelin sheath has gaps called neurofibral nodes or nodes of Ranvier – each neurolemmocyte wraps the axon segment between two nodes.

B. Neurons: [Figures 12.3-12.4, pp.389-391] 1. Most neurons (nerve cells) consist of a cell body or soma,

many dendrites, and usually a single axon. a. Soma (perikaryon or cell body) contains a nucleus

(with a nucleolus) surrounded by cytoplasm that includes typical organelles such as lysosomes, mitochondria, RER (Nissl bodies), and a Golgi complex. Many neurons contain cytoplasmic inclusions such as lipofuscin pigment (occurs as clumps of yellowish brown pigments) – probably an end product of lysosomal activity.

b. The dendrites conduct impulses from receptors or other neurons to the cell body.

c. The axon conducts nerve impulses from the neuron to the dendrites or cell body of another neuron or to an effector organ of the body (muscle or gland).

d. A nerve fiber is a general term for any neuronal process – dendrite or axon (usually an axon and its sheaths); the processes of neurons are arranged into bundles called nerves in the PNS and tracts in the CNS. Nerve cell bodies in the PNS form clusters called ganglia.

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2. Axonal Transport: It is natural mechanism of intracellular transport in neurons (axoplasm = cytoplasm in the axon). Certain pathogens (e.g., herpes and rabies viruses and tetanus bacterium’s toxin) use this transport to reach other parts of the nervous system. • Slow axonal transport: It conveys axoplasm in one

direction only – from the cell body toward the axon terminals (1-5 mm/day).

• Fast axonal transport: It conveys axoplasm in both directions at a speed of 200-400 mm/day and uses proteins that function as “motors” (to move materials) along the surfaces of microtubules.

3. On the basis of the number of processes extending from the cell body, neurons are classified as multipolar, bipolar, and unipolar (Fig. 12.4, p 391).

4. On the basis of the direction in which they transmit nerve impulses, neurons are classified as: i. afferent or sensory neurons (conducting impulses

from receptors to the CNS), ii. association or connecting neurons or

interneurons (conducting impulses to other neurons, including motor neurons, and

iii. efferent or motor neurons (conducting impulses to effectors, muscles, or glands).

C. Gray and White Matter: (Fig. 12.7, p 395) 1. White matter is composed of aggregations of myelinated

processes whereas gray matter contains nerve cell bodies, dendrites, and axon terminals, or bundles of unmyelinated axons and neuroglia.

2. In the spinal cord, gray matter forms an H-shaped inner core surrounded by white matter; in the brain a thin outer shell of gray matter covers the cerebral hemispheres.

3. A nucleus is a mass of nerve cell bodies and dendrites inside the CNS.

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IV. NEURO PHYSIOLOGY:

A. Ion Channels: (Fig. 12.8, p 396; Fig. 12.12, p 401) Broadly there are two types, viz., leakage (nongated) and gated channels. 1. Leakage channels are always open. 2. Gated channels open and close in response to some sorts

of stimuli. • Four types of gated channels are (i) voltage-gated, (ii)

chemically gated, (iii) mechanically gated, and (iv) light-gated.

• Voltage-gated channels in nerve and muscle plasma membrane give these cells excitability (irritability).

• The presence of chemically, mechanically, or light-gated channels in a membrane permits the approximate stimulus to cause a graded potential.

• A graded potential is a small deviation from the resting membrane potential that is caused by an appropriate stimulus (Fig. 12.10, p 398).

B. Resting Membrane Potential (Fig. 12.9, p 397; Fig. 12.11, p 399): It is the voltage difference between the inside and the outside of a cell membrane when the cell is not responding to a stimulus. In many neurons and muscle fibers it is –70 mV to –90 mV, with the inside of the cell negative relative to the outside. 1. The membrane of a non-conducting neuron is positive

outside and negative inside owing to the distribution of different ions across the membrane and the relative permeability of the membrane toward Na+ and K+.

2. The typical value of RMP (resting membrane potential) is –70 mV, and at this value the membrane is said to be polarized.

3. The sodium-potassium pumps compensate for slow leakage of Na+ into the cell by pumping it back out.

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C. Graded Potentials: 1. Produced by opening and closing of chemically gated

channels in response to neurotransmitters. 2. Flow of ions through a particular channel may cause

either hyperpolarization or depolarization relative to the resting membrane potential, depending on the charge of the ions and the direction of flow.

D. Action Potential (Impulse): (Fig.12.11, p 399; Fig.12.12, p 401)

1. During action potential (impulse), voltage-gated Na+ and K+ channels open in sequence. This results first in depolarization, the loss and reversal of membrane polarization (from –70 mV to 0 to +30 mV) and then in repolarization, the recovery of RMP (from +30 mV to 0 to –70 mV).

2. During refractory period, another action potential (impulse) cannot be generated at all (absolute refractory period) or can be triggered by a suprathreshold stimulus (relative refractory period).

3. An action potential conducts or propagates (travels) from point to point along the membrane; the traveling action potential is a nerve impulse.

4. Local anesthetics prevent opening of voltage-gated Na+ channels, so nerve impulse cannot pass the obstructed region.

5. According to all-or-none principle, if a stimulus is strong enough to generate an AP (action potential), the impulse travels at a constant and maximum strength for the existing conditions; a stronger stimulus will not cause a larger impulse.

6. In saltatory conduction, nerve impulse jumps from neurofibral node (node of Ranvier) to node.

7. The propagation speed of a nerve impulse is not related to stimulus strength:

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a. Larger-diameter fibers conduct impulses faster than those with smaller diameters.

b. Myelinated fibers conduct impulses faster than unmyelinated fibers.

c. Nerve fibers conduct impulses faster when warmed and slower when cooled.

E. Transmission at Synapses: 1. A synapse is the functional junction between one neuron

and another or between a neuron and an effector such as a muscle or a gland.

2. Electrical Synapse: • At an electrical synapse, electric current spreads directly

from one cell to another through gap junctions; electrical synapses are faster than chemical synapses and they can synchronize the activity of a group of neurons or muscle fibers. It can set up two-way transmission of impulses.

3. Chemical Synapse: • At a chemical synapse, there is only one-way

information transfer from a presynaptic neuron to a postsynaptic one.

4. Neurotransmitters at chemical synapses bring about either an excitatory or inhibitory graded potential. • An excitatory neurotransmitter is one that can

depolarize or make the postsynaptic neuron’s membrane less negative, bringing the membrane potential closer to threshold. • A depolarizing postsynaptic potential (PSP) is called

an excitatory postsynaptic potential (EPSP). • Although a single EPSP normally does not initiate a

nerve impulse, the postsynaptic neuron does become more excitable; it is already partially depolarized and thus more likely to reach threshold when the next EPSP occurs. This effect is called summation.

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• An inhibitory neurotransmitter hyperpolarizes the membrane of the postsynaptic neuron, making the inside more negative and generation of a nerve impulse (AP) more difficult. A hyperpolarizing PSP is inhibitory and is called IPSP (inhibitory postsynaptic potential).

• Removal of neurotransmitter from the synaptic cleft is essential for normal synaptic function, which is achieved in 3 ways: diffusion, enzymatic degradation (e.g., Acetylcholinesterase acts on ACh), and uptake into cells (neurons and glia).

• If several presynaptic end bulbs release their neurotransmitter at about the same time, the combined effect may generate a nerve impulse due to summation; the summation may be spatial or temporal. The postsynaptic neuron is an integrator; it receives and integrates signals, and then responds. [Fig. 12.15, p 407]

• [See Table 12.3, p 408 for summary of neuronal structure and function!] STRUCTURE FUNCTIONS Dendrites Receive stimuli through activation

of chemically or mechanically gated ion channels; in sensory neurons, produce generator or receptor potentials; in motor and association neurons, produce EPSPs and IPSPs.

Cell body Receives stimuli and produce EPSPs and IPSPs through activation of chemically or mechanically gated channels.

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Junction of axon hillock & initial segment of axon Trigger zone in many neurons;

integrates EPSPs and IPSPs, and if sum is a depolarization that reaches threshold, initiates AP (nerve impulse).

Axon Propagates nerve impulses from initial segment (or from dendrites of sensory neurons) to axon terminals in a self-reinforcing manner; impulse amplitude does not change as it propagates along the axon.

Axon terminals & synaptic end bulbs Inflow of Ca2+ caused by depolarizing

phase of nerve impulse triggers neurotransmitter release by exocytosis of synaptic vesicles.

F. Neurotransmitters: • Both excitatory and inhibitory neurotransmitters are present in

the CNS and PNS; the same neurotransmitter may be excitatory in some locations and inhibitory in others.

• Important neurotransmitters include acetylcholine, glutamate, gamma aminobutyric acid (GABA), glycine, norepinephrine, and dopamine. Even simple gases can function as neurotransmitters, such as NO (nitric oxide), CO (carbon monoxide). Certain disorders like, Parkinson’s disease, Alzheimer’s disease, anxiety, and schizophrenia are caused by problems relating to neurotransmitters.

• Neurotransmitters can be divided into two classes: small-molecule neurotransmitters and neuropeptides.

• Small-molecule neurotransmitters include ACh, amino acids,

biogenic amines, ATP and other purines, and gases.

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• Neuropeptides include neurotransmitters formed of 30-40 amino acids linked by peptide bonds.

F. Alteration of Impulse Conduction & Synaptic

Transmission: • A neuron’s chemical and physical environment influences

both impulse conduction and synaptic transmission. • Chemical synaptic transmission may be stimulated or

blocked by affecting neurotransmitter synthesis, release, removal, or the receptor site.

• Alkalosis, acidosis, mechanical pressure, hypnotics, tranquilizers, anesthetics, caffeine, nicotine, botulinum toxin, benzedrine, curare, etc. may all modify impulse conduction and/or synaptic transmission.

G. Neuronal Circuits: [Fig. 12.16, p 411] [Learn from pp 410-

411] • Neurons in the CNS are organized into definite patterns

called neuronal pools. Each pool differs from all others and has its own role in regulating homeostasis. A neuronal pool may contain thousands or even millions of neurons.

• Neuronal pools are organized into circuits that include simple series (a presynaptic neuron stimulates only a single neuron), diverging, converging, reverberating (oscillatory), and parallel after-discharge circuits.

H. Disorders: Homeostatic Imbalances

• Multiple Sclerosis (MS): • MS is an autoimmune disease that results in the

progressive destruction of myelin sheaths in neurons in the CNS.

• Myelin sheaths deteriorate to scleroses, which are hardened scars or plaques, in multiple regions.

• This is a progressive debilitating disease.

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• Epilepsy: • The second most common neurological disorder after

stroke is epilepsy that affects 1% of population. It is characterized by short, recurrent, periodic attacks of motor, sensory, or psychological malfunction called epileptic seizures.

• These seizures are initiated by abnormal synchronous electrical discharges from millions of neurons in the brain, perhaps resulting from abnormal reverberating circuits.

• Epileptic seizures can be eliminated or alleviated by drugs that depress neuronal excitability.

CHAPTER 15: SENSORY, MOTOR, AND INTEGRATIVE SYSTEMS RECEPTORS SENSATION PAIN DISORDERS LEARNING

SENSORY, MOTOR, AND INTEGRATIVE

SYSTEMS SLEEP WAKEFULNESS MEMORY

I. INTRODUCTION The components of the brain interact to receive sensory input, integrate and store the information, and transmit motor responses. To accomplish the primary functions of the nervous system there are neural pathways to transmit impulses from the receptors to the circuitry of the brain, which manipulates the circuitry to form directives that are transmitted via neural pathways to effectors as response.

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II. SENSATION: A. Sensation is conscious or unconscious awareness of

external or internal stimuli. Perception is the conscious awareness and interpretations of sensations.

B. Modality: • Modality is the property by which one sensation is

distinguished from the other. [Examples include temperature, pain, pressure, balance and position, and special senses.]

• Generally a given sensory neuron carries only one modality.

• The classes of sensory modalities are general senses and special senses. • The general senses include somatic and visceral

senses, which provide information about conditions within internal organs.

• The special senses include the modalities of smell, taste, vision, hearing, and equilibrium.

C. Components of Sensation:

For a sensation to arise, four events must occur. These are stimulation, transduction, conduction, and translation. • Stimulation: A stimulus is a change in the environment

that can activate sensory neurons and must occur within the receptive field of the sensory neuron.

• Transduction: A sensory receptor or sense organ must respond to the stimulus and transduce or convert it to a generator potential.

• Impulse generation and conduction: First order sensory (afferent) neurons propagate impulses into the CNS.

• Integration and translation: A region in the CNS must receive and integrate the sensory nerve impulses and translate them into sensation.

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D. Sensory Receptors (Fig. 15.1, p 500; Table 15.1, p 501; Fig. 15.2, p 503)

1. Classification of Receptors: a. On the basis of complexity:

i. Simple (associated with general senses) ii. Complex (associated with special senses)

b. On the basis of location: i. Exteroceptors: Receptors adapted for the reception of

stimuli from outside the body. ii. Interoceptors (Visceroceptors): Receptors located in

blood vessels and viscera that provide information about the body’s internal environment.

iii. Proprioceptors: Receptors that are located in muscles, tendons, or joints that provide information about the body position and movements.

c. On the basis of stimulus type: i. Mechanoreceptors: Receptors that are sensitive to

mechanical pressure such as touch, sound, or exerted by muscle contraction.

ii. Thermoreceptors: Receptors sensitive to temperature changes.

iii. Nociceptors: Free (naked) nerve endings that detect painful stimuli.

iv. Photoreceptors: Receptors that detect light shining on the retina of the eye.

v. Chemoreceptors: Receptors that detect the presence of chemicals.

2. Adaptation of Sensory Receptors:

Adaptation is a characteristic of many sensations, i.e., a change in sensitivity, and usually a decrease in sensitivity to a long-lasting stimulus. The receptors that are involved are important in signaling information regarding the steady states of the body.

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III. Somatic Sensations A. Cutaneous sensations include tactile sensations (touch,

pressure, vibration), thermoreceptive sensations (cold and heat), and pain. The receptors of these sensations are located in the skin, in connective tissue under the skin, in mucous membranes and at the ends of GI tract. Nerve impulses, generated by cutaneous receptors, pass along the somatic afferent neurons located in the spinal and cranial nerves, through the thalamus to the somatosensory area of the parietal lobe of the cerebral cortex.

a. Touch sensations: Crude touch refers to the ability to

perceive that something has simply touched the skin. Discriminative touch refers to the ability to recognize exactly what point of the body is touched. Receptors for touch include: [Fig.15.2, p 503] i. Meissner’s corpuscles and hair root plexuses – rapidly

adapting receptors; ii. Merkel discs (type I cutaneous mechanoreceptors) and

end organs of Ruffini (type II cutaneous mechanoreceptors) – slowly adapting receptors.

b. Pressure sensations generally result from stimulation of

tactile receptors in deeper tissues. [Pressure is a sustained sensation that is felt over a larger area than touch.] [Fig.15.2, p 503] i. Type II cutaneous mechanoreceptors (Ruffini

corpuscles) and lamellated (Pacinian) corpuscles are pressure receptors.

ii. Lamellated corpuscles adapt rapidly.

c. Vibration sensations result from rapidly receptive sensory signals from tactile receptors, e.g., corpuscles of touch and lamellated corpuscles, which detect low frequency and high-frequency vibrations respectively.

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d. Itch and tickle receptors are free nerve endings.

e. Thermoreceptors are free nerve endings; separate thermoreceptors respond to hot and cold stimuli.

f. Pain sensations: Pain is a vital sensation because it provides us with information about noxious tissue-damaging stimuli and thus often enables us to protect ourselves from greater damage. i. Pain receptors (nociceptors) are free nerve endings of

nerves that are located in nearly every body tissue; adaptation is slight if it occurs at all. [Fig.15.2, p 503]

ii. Classification of Pain: Classified as one of two types, based on speed of onset, quality of sensation, and duration.

• Acute (fast) pain occurs very rapidly, usually within 0.1 sec after a stimulus is applied and not felt in deeper tissue of the body. This type is also known as sharp, fast, and pricking pain (e.g., pain felt from needle puncture or knife cut to the skin). Impulses from acute pain conduct along large diameter, myelinated A-fibers.

• Chronic (slow) pain begins after a second or more and gradually increases over a period of several seconds or minutes. This type of pain may be excruciating. It is also known as burning, aching, throbbing, and slow pain. It can occur in the skin and deeper tissues or in internal organs, also pain associated with toothache. Impulses from chronic pain conduct along smaller diameter unmyelinated C-fibers.

• Pain arises from the stimulation of receptors in the skin called superficial somatic pain, whereas stimulation of receptors in skeletal muscles, joints, tendons, and fascia causes deep somatic pain.

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• Visceral pain results from stimulation of receptors in the visceral organs.

• Referred pain: Pain that is felt at a site remote from the place of origin. In general, the area to which the pain is referred and the visceral organs involved are served by the same segment of the spinal cord, as for example, sensory fibers from the heart and skin over the heart and along the medial aspect of the left arm enter spinal cord segments T1-T5. Thus a pain of a heart attack is typically felt in the skin over the heart and along the left arm.

• Phantom pain (Phantom limb sensation) is the sensation of pain in a limb that is amputated. The brain interprets nerve impulses arising in the proximal portion of the sensory nerves as coming from the nonexistent (phantom) limb.

B. Proprioceptive Sensations: a. Receptors located in skeletal muscles, tendons, in and

around joints and in internal ear convey nerve impulses related to muscle tone, movement of body parts, and body position. This awareness of the activities of muscle, tendons, and joints and of balance or equilibrium is provided by proprioceptive or kinesthetic sense.

b. The receptors include muscle spindles, tendon organs, and joint kinesthetic receptors (Fig. 15.4, p 506).

[See Table 15.1, p 501 for Classification of Sensory Receptors and Table 15.2, p 507 for Summary of Receptors for Somatic Sensations!]

IV. Integration of Sensory Input and Motor Output: A. Sensory input keeps the CNS informed of changes in the

environment.

B. Incoming sensory information is integrated at many stations along the CNS, at both conscious and subconscious levels.

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C. A motor response to make a muscle contract or a gland secrete can be initiated at any of these stations or levels. 1. As the location of the sensory-motor linkage climbs to

higher levels in the CNS, additional contributions are introduced that enrich the growing inventory of motor responses.

2. When the input reaches the highest center, the process of sensory-motor integration occurs. This involves not only the utilization of information contained within that center, but also the information impinging on that center that is delivered from other centers within the CNS.

V. Integrative Functions: A. Memory: It is the ability to recall thought and is generally

classified into two kinds based on how long the memory persists: short-term and long-term memory. A memory trace in the brain is called an engram (a change in the brain that represents the experience). 1. Short-term memory lasts only seconds or hours and is

the ability to recall bits of information. It is related to electrical and chemical events.

2. Long-term memory lasts from days to years and is related to anatomical and biochemical changes at synapses.

B. Sleep and wakefulness are integrative functions that are controlled by reticular activating system (RAS). [Fig.15.10, p 518]

[RAS: A portion of the reticular formation that has many ascending connections with the cerebral cortex. When this area of the brain stem is active, nerve impulses pass to the thalamus and widespread areas of cerebral cortex, resulting in generalized alertness or arousal from sleep.] [Reticular Formation: A network of small groups of neuronal cell bodies scattered among bundles of axons (mixed gray and white matter) beginning in the medulla oblongata and extending superiorly through the central part of the brain.]

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1. The RAS can maintain a general state of wakefulness (consciousness) and also initiate the increased cortical activity seen in arousal from deep sleep. a. A number of factors can noticeably alter the state of

consciousness, e.g., amphetamines, alcohol, and other drugs, meditation, anesthetics, and a diseased or damaged CNS.

b. Coma is the final stage of brain failure that is characterized by total unresponsiveness to all external stimuli.

2. During sleep (a state of altered consciousness from which an individual can be aroused by different stimuli), activity in the RAS is very low.

[Fig 15.11, p 519] a. Normal sleep consists of two types: non-rapid eye

movement sleep (NREM) and rapid eye movement sleep (REM) i. NREM or slow wave sleep consists of four stages,

each of which gradually merges into the next. Each stage has been identified by EEG recordings. • Stage 1: Transition stage between wakefulness

and sleep; normally lasts from one minute to seven minutes; α-waves diminish and θ-waves appear on the EEG.

• Stage 2: First stage of true sleep; a little harder to awaken the person; fragments of dreams may be experienced; eyes may roll slowly from side to side. EEG shows sleep spindles (occur at 12-14 Hz – cycles/sec).

• Stage 3: Period of moderately deep sleep; person is very relaxed, body temperature begins to fall, blood pressure decreases; difficult to awaken the person. EEG shows a mixture of sleep spindles and δ-waves. This stage occurs about 20 minutes after falling asleep.

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• Stage 4: Deep sleep occurs; the person is very relaxed and responds slowly if awakened. When bed-wetting and sleepwalking occur, they do so during this stage; δ-waves dominate the EEG.

ii. REM sleep: Most dreaming occurs during this period.

[In a typical 7-8 hour sleep period, a person goes from stage 1 to 4 of NREM; then the person ascends to stages 3 and 2 and then to REM sleep within 50-90 minutes; the cycle normally repeats throughout the sleep period.]

b. The neurotransmitters that affect sleep are serotonin and norepinephrine (NE).

VI. Disorder: Homeostatic Imbalances: A. Spinal Cord Injury. B. Cerebral Palsy: Loss of muscle control due to problems

during development that impact the motor control of brain; conditions are nonprogressive, but permanent.

C. Parkinson’s Disease: Progressive degeneration of CNS neurons of the basal nuclei region due to unknown causes that decrease dopamine neurotransmitter production; this condition produces motor coordination problems of involuntary tremor and/or rigidity. Motor performance can be described as bradykinesia (slow) and hypokinesia (limited). Limited treatment is provided with L-dopa, a precursor to dopamine, or through ACh inhibition.

CHAPTER 17: THE AUTONOMIC NERVOUS SYSTEM I. Introduction

A. The ANS regulates the activity of smooth muscle, cardiac muscle, and certain glands.

B. Operation of the ANS to maintain homeostasis depends on a continual inflow of sensory (afferent) input, from receptors in organs, and efferent (motor) output to the same effector organs.

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1. Structurally, the ANS includes autonomic sensory neurons, integrating centers in the CNS, and autonomic motor neurons. [Fig.17.1, p 567]

2. Functionally, the ANS usually operates without conscious control.

C. The autonomic nervous system is regulated by centers in the brain, mainly the hypothalamus and medulla oblongata, which receives from the limbic system and other regions of the cerebrum.

D. Limbic system: A portion of the forebrain, termed also visceral brain, concerned with various aspects of emotion and behavior.

II. Comparison of SNS and ANS: A. Sensory neurons of somatic nervous system receive input

from special senses, general somatic senses, and proprioceptors; sensory neurons of the ANS receive input from the special senses, general visceral senses, and interoceptors.

B. Somatic nervous system operates under conscious control; ANS operates without conscious control.

C. Axons of motor neurons of the SNS extend from the CNS synapse directly to an effector and release ACh; autonomic pathways consist of sets of 2 neurons: 1. Axon of the first motor neuron of the ANS extends from

the CNS and synapses in a ganglion with the second neuron.

2. The second neuron synapses to an effector. Preganglionic fibers release ACh and postganglionic fibers release ACh or NE (norepinephrine).

D. SNS effectors are skeletal muscles; ANS effectors include cardiac and smooth muscles and glands.

E. SNS response to neurotransmitters is excitation; ANS

response to neurotransmitters is excitation or inhibition. [See Table 17.1, p 5567 for Summary of ANS &SNS]

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III. Anatomy of Autonomic Motor Pathway: A. Overview

1. Preganglionic neurons are myelinated; postganglionic neurons are unmyelinated.

2. The first of two autonomic motor neurons is called a preganglionic neuron. a. Cell body lies in the CNS. b. Myelinated axon, called a preganglionic fiber, passes

out of the CNS as part of a cranial or spinal nerve, later separating from the nerve and extending to an autonomic ganglion, where it synapses with the postganglionic neuron.

3. Postganglionic neuron: It is the second neuron in the autonomic motor pathway, which lies entirely outside the CNS. a. Its cell bodies and dendrites are located in an

autonomic ganglion, where it makes synapses with one or more preganglionic fibers.

b. The axon of the postganglionic fiber is unmyelinated and terminates in a visceral effector.

4. The cell bodies of sympathetic preganglionic neurons are in the lateral gray horn of the 12 thoracic and first 2 or 3 lumbar segments. Cell bodies of parasympathetic preganglionic neurons are located in the cranial nerve nuclei (III, VII, IX, and X) in the brain stem and lateral gray horns of the second through fourth sacral segments of the cord.

5. Autonomic ganglia are classified as sympathetic trunk (vertebral chain) ganglia (on both sides of spinal column), prevertebral (collateral) ganglia (anterior to the spinal column, and terminal (intramural) ganglia (near or inside visceral effectors). [Sympathetic division includes sympathetic trunk ganglia and prevertebral ganglia, whereas the parasympathetic division includes terminal ganglia.]

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6. In addition to autonomic ganglia, the ANS contains autonomic plexuses.

[Fig 17.2, p 569; Fig 17.3, p 570] B. Sympathetic and Parasympathetic Divisions:

1. Sympathetic preganglionic neurons synapse with postganglionic neurons in ganglia of the sympathetic trunk or prevertebral ganglia.

2. Parasympathetic preganglionic neurons synapse with postganglionic neurons in terminal ganglia.

IV. ANS Neurotransmitters and Receptors: [Fig.17.6, p 575] A. Cholinergic Neurons and Cholinergic Receptors;

1. Cholinergic neurons release ACh and include all sympathetic and parasympathetic preganglionic neurons and all parasympathetic and sympathetic postganglionic neurons that innervate most sweat glands.

2. Cholinergic receptors are integral membrane proteins in the postsynaptic membrane. The two types of cholinergic receptors are nicotinic and muscarinic. a. Activation of nicotinic receptors causes excitation of

the postsynaptic cell. b. Activation of muscarinic receptors causes either

excitation or inhibition depending on the cell that bears the receptors.

B. Adrenergic Neurons and Adrenergic Receptors: 1. The adrenergic neurons release NE (norepinephrine) and

include most of the sympathetic postganglionic neurons. 2. The main types of adrenergic receptors are α and β

receptors. These receptors are further divided into subtypes.

3. Depending on the subtype, activation of the receptors can result in either excitation or inhibition.

4. Effects triggered by adrenergic neurons generally are longer lasting than those cholinergic neurons.

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C. Receptor Agonists and Antagonists:

1. An agonist is a substance that binds to and activates a receptor, mimicking the effect of a natural neurotransmitter or hormone.

2. An antagonist is a substance that binds to and blocks a receptor, preventing a natural neurotransmitter or hormone from exerting its effect.

3. Different drugs can serve as agonists or antagonists to selectively activate or block ANS receptors.

V. Physiological Effects of the ANS:

A. Most body structures receive dual innervation, that is, fibers from both sympathetic and parasympathetic divisions. Usually one division causes excitation and the other causes inhibition.

B. The sympathetic responses prepare the body for emergency situations (“fight-or-flight” activities).

1. The effects of sympathetic stimulation are longer lasting

and more widespread than those of parasympathetic stimulation.

2. Raynaud’s disease is due to excessive sympathetic stimulation of arterioles within the fingers and toes resulting in diminished blood flow to the digits.

C. The parasympathetic responses support body functions that

conserve and restore body energy during times of rest and recovery (“rest-and-digest” activities). 1. Parasympathetic responses stimulate salivation,

lacrimation, urination, digestion, and defecation (SLUDD).

2. Parasympathetic responses decrease heart rate, airway diameter, and pupil diameter.

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VI. Integration and Control of Autonomic Functions

A. Autonomic Reflexes: 1. A visceral autonomic reflex adjusts the activity of a

visceral effector, often unconsciously. 2. A visceral autonomic reflex arc consists of a receptor,

sensory neuron, association neuron, autonomic motor neuron, and visceral effector.

B. Control by Higher Centers:

1. The hypothalamus controls and integrates the autonomic nervous system; it is connected to both the sympathetic and parasympathetic divisions.

2. Control of the ANS by the cerebral cortex occurs

primarily during emotional stress.

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