The peripheral nervous system is the part of the nervous system outside the brain and spinal cord. It is responsible for collecting most of the sensory information relayed to the central nervous system (CNS). It is also responsible for the transmission of motor signals to skeletal and smooth muscles. As discussed in Chapter 8, the peripheral nervous system involves sensory and motor components (Fig. 8.2). The autonomic nervous system (ANS) is a part of this motor component. Parts of a neuron were described in Chapter 8. A nerve, in contrast, is a collection of axons from many different neurons located in the peripheral nervous system. Nerves vary in size and are surrounded by multiple connective tissue layers (Fig. 10.1). The dense epineurium consisting of a network of collagen fibers is the outermost layer. The perineurium is the next innermost layer. It partitions the nerve into a series of fascicles each containing a bundle of axons. The innermost layer is the endoneurium, the connective tissue surrounding each individual axon. Arteries and veins enter through the epineurium and branch within the perineurium. Capillaries penetrate the endoneurium where they nourish axons, Schwann cells, and fibroblasts within the connective tissue. Consequently, a nerve is more than just an axon. Because the peripheral nervous system has both sensory and motor components, nerves are classified based on function. Nerves directing impulses toward the CNS are called sensory or afferent nerves, while those carrying impulses away from the CNS are called motor or efferent nerves. A memory aid is that efferent nerves carry impulses toward an effector. A nerve that carries both sensory and motor impulses is a mixed nerve. Peripheral nerves can function within the autonomic (visceral) nervous system or somatic nervous system. Consequently, they can be further classified as visceral afferent, visceral efferent, somatic afferent, or somatic efferent. Nerves leaving the CNS are called either spinal nerves or cranial nerves. Cranial nerves were discussed in Chapter 8. A pair of spinal nerves exit at each spinal segment. Each spinal nerve has a dorsal and ventral root that enters and exits the spinal cord, respectively (Fig. 10.2). Thus, the dorsal roots contain afferent fibers while the ventral roots contain efferent fibers composed of motor neurons from both the somatic nervous system and ANS. Near the spinal cord, the two roots merge forming a spinal nerve. These are mixed nerves because they contain both afferent and efferent fibers. Each dorsal root has an enlargement, called the dorsal root ganglion, situated near the spinal cord, which contains the cell bodies of the neurons passing through the dorsal root. The dorsal and ventral roots pass through the intervertebral foramen located between adjacent vertebrae while the dorsal root ganglion lies between the pedicles of adjacent vertebrae. Spinal nerves exit at every vertebra. The first spinal nerve exits superior to the first cervical vertebra while an additional spinal nerve exits inferior to each vertebra. Therefore, cervical spinal nerves are named for the vertebrae immediately following where they exit. Because there are seven cervical vertebrae, there are eight cervical cranial nerves (C1–C8). All other cranial nerves are named for the vertebra immediately preceding where they exit (i.e., T1, T2, etc.). After leaving the spinal cord, the dorsal and ventral roots merge forming a spinal nerve. Shortly thereafter, the spinal nerve branches into the dorsal and ventral ramus. The ventral ramus carries fibers to the skeletal muscles of the body wall and limbs, as well as postganglionic fibers to smooth muscles, glands, body walls, and limbs. The dorsal ramus carries similar fibers to the back. Fig. 10.1 Peripheral nerve. A peripheral nerve consists of many bundles of axons, each called a fascicle. There are three connective tissue layers surrounding various parts of the nerve. The epineurium is the outermost layer, wrapping around the entire nerve. The perineurium surrounds each fascicle, while the endoneurium surrounds each axon. Fig. 10.2 Spinal nerves. (A) The sensory neurons from the periphery enter the spinal cord through the dorsal root, and their cell bodies are in the dorsal root ganglion. These fibers synapse in the dorsal gray horn of the central gray area of the spinal cord. The sensory visceral (autonomic) fibers may or may not pass through the sympathetic chain. (B) The motor fibers exit the spinal cord via the ventral root. The visceral motor fibers may enter the sympathetic chain via the white ramus. Like other cells, neurons do die. It is believed that neurotrophic factors are responsible for keeping neurons alive. The presence of these factors suppresses latent biochemical pathways present in all cells linked to cell death. Cells can die by a process called apoptosis, or programmed cell death, which involves four steps. The cell shrinks, the chromatin condenses, the cell fragments into apoptotic bodies, and the cellular remnants are phagocytized by macrophages or other such cells. Using sympathetic neurons as a model, a proposed mechanism for apoptosis is as follows. The loss of neurotrophic factors such as nerve growth factor (NGF) decreases the activity of the MAP kinase and phosphatidylinositol 3‐kinase pathways, resulting in an increase in reactive oxygen species. This leads to an increase in c‐jun N‐terminal kinases and phosphorylation of c‐jun protein. As well as increased expression of genes including c‐jun, cyclin D1, and c‐fos but a decrease in overall RNA and protein synthesis. There is a decrease in Bcl‐2 family proteins. Bcl‐2 family proteins are expressed on the outer surface of mitochondria and are bound to a molecule of Apaf‐1. When damaged, the Bcl‐2 family protein releases Apaf‐1, which activates caspases (Cysteine Aspartate Specific Proteases). Caspases are a family of over a dozen proteins that cleave cellular proteins at aspartate residues (Fig. 10.3). Cells can also die from trauma or necrotic cell death, a process called necrosis that is distinguishable from apoptosis. Traumatic death is characterized by an initial swelling of the cell, modest condensation of the chromatin, and then rapid lysis of cellular membranes without endogenous programmed cell death. Necrotic cells elicit an inflammatory response that recruits macrophages to eliminate the cellular debris. In contrast, during apoptosis, individual cells are generally phagocytized prior to releasing their contents (Box 10.1). Ganglia are collections of neuron cell bodies located in the peripheral nervous system. Recall that within the CNS, a collection of cell bodies is called a nucleus. The ganglia for afferent (sensory) neurons are in the dorsal root ganglia discussed above. Somatic motor neurons do not have ganglia because these motor neuron cell bodies are in the dorsal horn of the spinal cord. However, autonomic motor neurons are associated with ganglia because there are two consecutive nerve fibers associated with each autonomic motor pathway. These autonomic ganglia will be discussed as related to the ANS. Fig. 10.3 Apoptosis. In a healthy cell, Bcl‐2 is found on the outer mitochondria membrane and is bound to Apaf‐1. Internal damage to the cell, such as the presence of reactive oxygen species, or lack of neurotrophic factors, such as nerve growth factor (NGF), causes Bcl‐2 to release Apaf‐1. A related protein called Bax also penetrates the mitochondrial membranes, causing the leakage of cytochrome C into the cytoplasm. Released Apaf‐1 and cytochrome C bind to inactive caspase. The resulting complex containing cytochrome C, Apaf‐1, caspase 9, and ATP is called the apoptosome. Once activated, caspase 9 activates other caspases, leading to the digestion of structural proteins in the cytoplasm and degradation of chromosomal DNA and phagocytosis of the cell. Sensations are the awareness of a stimulus whereas perception requires the interpretation of the sensation and is dependent on the CNS. All senses involve three steps: (1) a physical stimulus, (2) transformation of the stimulus into a nerve impulse, and (3) a response to the sensation in the form of a perception or conscious experience of sensation. Furthermore, all sensory systems give four types of information about the stimuli including modality, location, intensity, and timing, which collectively yield sensation (Table 10.1). The various modalities of sense include vision, hearing, touch, taste, smell, the vestibular sense of balance, and the somatic senses including nociception (pain), temperature, itch, and proprioception (posture and movement of body parts). The term general senses include temperature, pain, touch, pressure, vibration, and proprioception while special senses include olfaction (smell), vision (sight), gustation (taste), equilibrium (balance), and audition (hearing). General sensory receptors are located throughout the body while receptors for special senses are in specialized structures or organs. General senses are discussed below while special senses are covered in Chapter 11. There are five classes of sensory receptors: mechanical, chemical, nociceptors (nocere = to injure), thermal, and electromagnetic. Mechanoreceptors can detect touch, proprioceptive sensation (muscle stretch or contraction), joint position, hearing, and sense of balance. Chemoreceptors function in the sense of itch, taste, and smell. Nociceptors detect pain. Thermoreceptors can sense either hot or cold, while photoreceptors sense electromagnetic energy. Table 10.1 Sensory receptors and modalities. These receptors can be further classified by location as exteroceptors, interoceptors, or proprioceptors (from the Latin word proprius, meaning “belong to one’s own self”). Mechanoreceptors detect distortions in their cell membranes such as bending and stretching. There are three classes of mechanoreceptors: Named after the German and Italian histologists who discovered them, the two principal mechanoreceptors located in the superficial skin layers are Merkel’s discs and Meissner’s corpuscles. The Merkel disc receptor is a slowly adapting receptor consisting of a small epithelial cell surrounding a nerve terminal. They are involved in the sense of touch and pressure. Meissner’s corpuscles are rapidly adapting, and consist of a globular, fluid‐filled structure enclosing a stack of flattened epithelial cells around which the sensory nerve is entwined. The two mechanoreceptors found in the deep subcutaneous layers are the Pacinian corpuscle (Fig. 10.4) and the Ruffini ending. Although larger than the receptors found in the superficial layers, these receptors are less numerous. The Pacinian corpuscle, physiologically like Meissner’s corpuscle, is a large receptor measuring as long as 2 mm and nearly 1 mm in diameter. The Pacinian corpuscle, also called a large lamellated corpuscle, is fast‐adapting and responds to rapid indentation of the skin but not steady pressure. Because the capsule surrounding this receptor is attached to the skin, this receptor can sense low frequency vibration occurring several centimeters away. These receptors are activated by touching a tuning fork (200–300 Hz) to the skin or bony structure. Fig. 10.4 Receptive field. Meissner’s corpuscles have a smaller receptive field compared with the more deeply located Pacinian corpuscles. Ruffini endings, slightly smaller than Pacinian corpuscles, slowly adapt. They consist of a capsule surrounding a core of collagen fibers that are continuous with fibers in the surrounding dermis. Dendrites from the sensory neuron are intertwined with the collagen fibers in the capsule. They link the subcutaneous tissue with folds in the skin at the joints and nails. Thus, they sense stretches from the skin bending in these regions. Vibration is the detection of sinusoidal oscillations of objects in contact with the skin. The various tactile receptors differ in their sensitivity to vibration. Merkel discs are most responsive to lower frequency oscillations (5–15 Hz). Meissner’s corpuscles are sensitive to midrange oscillations (20–50 Hz) and Pacinian corpuscles to high frequencies (60–400 Hz). The lowest stimulus intensity to which a receptor produces an action potential is called the receptor’s tuning threshold. The intensity of the vibration is coded by the number of sensory nerve fibers that are firing rather than the frequency of action potentials within a fiber. The size of the receptive fields for the various touch receptors differs (Fig. 10.4). Meissner’s corpuscles and Merkel discs, located in the superficial skin layers, have small receptive fields. A single dorsal root ganglion cell innervates 10–25 of these receptors and produces a receptive field of 2–10 mm in diameter. Therefore, these receptors are responsible for fine‐discriminating touch that detects small spatial differences. These receptors are important in a two‐point discrimination test. When performed on people, the skin is simultaneously touched by two pointed objects, and the person is asked whether they can detect two objects or a single object. As the two points are moved closer together, the person will eventually be unable to discriminate between two objects. In contrast, each Pacinian corpuscle and Ruffini ending, located in deeper skin layers, is innervated by a single nerve fiber, but their receptive field is larger because these receptors can detect changes from mechanical displacement over a greater distance. Because of their large receptive fields, these receptors are involved in coarse resolution of touch. The combination of the adaptation rate and size of the receptive field leads to variations in how the tactile receptors respond to stimuli (Fig. 10.5). In addition to differences in receptive fields of the various tactile receptors, there are also differences in the number of these receptors located throughout the body. The smallest receptive fields, that is, most receptors, are in the tips of the paws and whiskers of cats; for example, or the face and lips of humans. Consisting of free nerve endings, baroreceptors sense the change in the wall of distensible organs including blood vessels, and a portion of the respiratory, digestive, and urinary tract. When the pressure in the walls of these organs increases, the walls are stretched causing a deformation in the sensory nerves. As the pressure in these organs decreases, the elastic fibers cause the walls to return to their original structure. Fig. 10.5 Response of tactile receptors to stretch. The various tactile receptors change their firing rate qualitatively and quantitatively in response to stretch. Whereas Meissner’s and Pacinian corpuscles respond quickly but also adapt quickly, Merkel’s discs and Ruffini’s endings adapt more slowly. Baroreceptors monitor blood pressure in the major vessels, particularly in the carotid artery at the carotid sinus, and the aortic arch of the aorta. Increases in blood pressure at these sites initiate the baroreceptor reflex, in which an increased firing rate is relayed to the CNS, and appropriate adjustments in heart rate and blood pressure are initiated. Baroreceptors in the lungs send information regarding lung inflation to the respiratory rhythmicity centers in the brain stem to regulate breathing. Similarly, baroreceptors in the colon and urinary bladder function in defecation and micturition, respectively. There are also baroreceptors along the gastrointestinal tract (GIT) that are involved in peristalsis. Proprioceptors monitor the position of joints, and the tension in tendons, ligaments, and muscles. These receptors do not adapt, and continuously send information to the CNS. There are three groups of proprioceptors: Axons of skin sensory receptors are designated, in order of decreasing size, as Aα, Aβ, Aδ, and C, which correspond to axons innervating muscles and tendons called groups I, II, III, and IV, respectively. Aα, Aβ, and Aδ are myelinated; C fibers are unmyelinated. Sensory nerves from the skin do not have Aα fibers. Mechanoreceptors send their messages via Aβ. These fibers enter the dorsal horn of the central gray area of the spinal cord and branch. One branch synapses on second‐order sensory neurons deep in the dorsal horn and is involved in reflexes. The other branch ascends to the brain in the dorsal column‐medial lemniscal pathway (Fig. 10.6). This branch enters the ipsilateral dorsal column of the spinal cord. Composed of primary sensory axons and second‐order axons from neurons in the central gray area of the spinal cord, these fibers ascend to the dorsal column nuclei at the junction of the spinal cord and medulla where they synapse. The fibers leaving the dorsal column nuclei decussate (cross to the other side) and ascend in the medial lemniscus that courses through the medulla, pons, and midbrain and synapses in the ventral posterior nucleus of the thalamus. Pain is mediated by nociceptors. These receptors respond to stimuli that can damage tissue. Some nociceptors respond directly to stimuli while others respond indirectly to chemicals released by damaged tissue. Some of these include histamine, K+, and proteases released from injured cells, bradykinin, substance P, acidity, ATP, prostaglandins, serotonin, and acetylcholine (ACh). Fig. 10.6 Dorsal column‐medial lemniscal pathway. Mechanoreceptor signals enter the spinal cord through the dorsal root where they either synapse on secondary fibers in the gray area or ascend in the dorsal column. Nerve fibers ascending in the dorsal column, synapse in the dorsal column nuclei (nucleus gracilis and cuneatus). Fibers from these nuclei immediately decussate and ascend to the ventral posterior nucleus of the thalamus via the medial lemniscus. From there, fibers ascend to the primary somatosensory cortex. Chemical mediators are released in response to various stimuli. Bradykinin appears when peptidases released from injured cells cleave the extracellular protein kininogen to form bradykinin. Bradykinin acts directly on nociceptors it also increases the local synthesis and secretion of prostaglandins. Tissue acidity can increase when, for example, a galloping horse begins anaerobic metabolism producing lactic acid that leads to an increase in extracellular H+ ions. Histamine is released when mast cells found in the connective tissue are stimulated, such as during a bee sting. Prostaglandin E2 is a metabolite of arachidonic acid and is generated by the enzyme cyclooxygenase released from damaged cells. Aspirin and other nonsteroidal anti‐inflammatory analgesics work by blocking cyclooxygenase and inhibiting the synthesis of prostaglandins. There are three classes of nociceptors. Mechanical and thermal nociceptors are sensitive to mechanical and thermal stimuli, respectively, whereas polymodal nociceptors respond to traumatized tissue rather than physical properties. Mechanical nociceptors respond to a strong tactile or sharp penetrating stimulus. Their firing rate increases with the relative destructiveness of the mechanical stimuli. Thermal nociceptors respond to extremes in temperature. One group responds to noxious heat above 45°C; the second group responds to noxious cold below 5°C. The polymodal nociceptors respond not only to painful mechanical stimuli such as a strong pinch or puncture but also to noxious heat and cold or irritating chemicals. Stimulation of these receptors evokes slow, burning pain. These are the primary receptors in tooth pulp. Pain signals are carried by lightly myelinated Aδ and unmyelinated C fibers. These fibers have different conduction velocities; therefore, pain information can produce two different kinds of pain perceptions (Fig. 10.7). Initial pain is a fast, sharp pain mediated by Aδ fibers; it is followed by secondary pain that is a duller, but a longer lasting mediated by C fibers. Once stimulated, branches of the nociceptor neurons can secrete substance P and calcitonin gene‐related peptide (CGRP), which are peptide neurotransmitters, from the peripheral terminals of collaterals of the primary nociceptive neurons. These two peptides can cause vasodilation as well as the release of histamine from mast cells. Heat, redness, swelling, and pain are the cardinal signs of inflammation. Substance P can cause all these symptoms. The heat and redness are caused by vasodilation, swelling is caused by the leakage of proteins and cells from these blood vessels into the interstitial space, and the pain can result from the induced release of histamine that stimulates nociceptors. The Aδ and C fibers enter the spinal cord through the dorsal root and synapse in the substantia gelatinosa of the central gray area. The neurotransmitters released at this site are thought to be glutamate and substance P. The glutamate, released from Aδ and C fibers, acts at AMPA‐type glutamate receptors and evokes fast synaptic potentials in dorsal horn neurons. Substance P is released from C fibers and evokes slow excitatory postsynaptic potentials (EPSPs). Glutamate and substance P act together to transmit pain signals and, with substance P enhance and prolong the actions of glutamate. The impulse is then carried by secondary fibers that immediately decussate and then ascend to the brain via the spinothalamic tract (Fig. 10.8). Many times, shortly after an injury, the site becomes extremely painful and especially sensitive to touch. This is called hyperalgesia and is the body’s way of protecting this site from further injury. Primary hyperalgesia is associated with the damaged tissue; however, the surrounding area can also become supersensitive, a process called secondary hyperalgesia. Hyperalgesia is due to the action of various compounds released during injury that make the nociceptors more sensitive. Fig. 10.7 Nociception. Damage to the skin can cause the release of certain substances, including ATP, prostaglandins, and bradykinin. These substances can stimulate the nociceptors. Collaterals of the receptors can release substance P and calcitonin gene‐related peptide (CGRP) that can stimulate mast cells to release histamine. Histamine can stimulate nociceptors as well as cause vasodilation. Hence, the redness is associated with inflammation. The pain signals are carried by Aδ and C fibers through the dorsal root to the substantia gelatinosa of the central gray area of the spinal cord. Here the fibers release glutamate and/or substance P, which signals secondary fibers. The secondary fibers cross to the contralateral side and synapse on neurons that carry the impulse to the brain via the spinothalamic tract. Fig. 10.8 The spinothalamic pathway. Pain and temperature information is carried to the brain via the spinothalamic pathway. Sensory fibers enter the spinal cord by way of the dorsal root and synapse in the central gray area of the spinal cord. They synapse on fibers that decussate and then ascend through the spinothalamic tract to the intralaminar and ventral posterior nuclei of the thalamus, where they synapse on fibers that then course to the primary somatosensory cortex. Nociceptors from the viscera also enter the spinal cord by the same route as those from cutaneous nociceptors. These signals can get mixed within the spinal cord because the afferent fibers from the viscera and somatic area converge on the same projection neurons in the dorsal horn of the spinal cord (Fig. 10.9). This leads to the phenomenon of referred pain in which visceral pain is perceived as a cutaneous sensation. Such is the case with angina in which ischemia in the heart leads to pain in the upper chest and down the left arm. Thermoreceptors alter their firing rate because of changes in temperature. Unlike mechanoreceptors that are silent in the absence of stimuli, thermoreceptors maintain a low, tonic firing rate (2–5 spikes/sec) at normal body temperature. There are separate cold and warm receptors, which can be shown by differential mapping on the skin. These free nerve endings are in the dermis of the skin, skeletal muscles, liver, and hypothalamus. Warm receptors begin firing around 30°C, increasing their firing rate up to 45°C, after which their firing rate decreases (Fig. 10.10). Above 50°C warm receptors stop firing. Instead, the animal senses heat pain rather than warmth due to the firing of thermal nociceptors fire. Cold receptors actively fire at temperatures ranging from 35°C down to 10°C. Below this temperature, cold becomes an anesthetic. For unknown reasons, some cold receptors increase their firing rate above 45°C. Fig. 10.9 Referred pain. Referred pain occurs when visceral nociception is perceived as a cutaneous sensation. The classic example of this is angina, in which the heart receives insufficient oxygen, resulting in pain from this region. However, the body perceives the pain as coming from the upper chest or left arm because cutaneous sensations from this region synapse in the spinal cord near the same region, and the brain is unable to distinguish between the two. Fig. 10.10 Thermoreceptors. Thermoreceptors change their firing rate in response to changes in skin or organ temperature. At normal body temperatures (36–38°C), both cold and warm receptors are discharged. As skin temperature decreases below 30°C, warm receptors discontinue firing, whereas cold receptors increase their firing rate, which is maximal at 25°C. Warm receptors fire maximally at 45°C. Thermoreceptors are very sensitive to differences in temperature between an object being touched and skin temperature. They respond vigorously to these abrupt changes in temperature and then adapt their firing rate. This can be demonstrated by placing your hand in a beaker of cold water. Notice that with time, the sensations of cold decrease. Then, take your hand and plunge it into a beaker of warm water. Notice that the water will feel hot due to the sudden change in temperature. Cold receptors connect to Aδ and C fibers, whereas warm receptors connect only with C fibers. These fibers synapse in the substantia gelatinosa of the dorsal horn in the spinal cord. The secondary fibers then decussate and ascend in the contralateral spinothalamic tract along with the pain signals. Pain and temperature information from the face and head reaches the thalamus via the trigeminal pathway (Fig. 10.11). Fibers in the trigeminal nerve synapse on second‐order neurons in the spinal trigeminal nucleus in the brainstem. These fibers decussate and ascend to the thalamus in the trigeminal lemniscus. The pain and temperature pathways are summarized in Figure 10.12. Chemoreceptors are responsible for detecting changes in concentrations of specific chemicals or compounds. These receptors are also responsible for the special senses of taste, or gustation, and smell, or olfaction. Taste and olfaction, which are considered special senses whose signals are relayed to the primary sensory cortex, will be discussed separately below. The chemoreceptors whose signals do not travel to the primary sensory cortex will be discussed here. They are responsible for sensing irritating substances on the skin, nutrients within the GIT or brain, and carbon dioxide or oxygen levels in our blood. Fig. 10.11 Trigeminal pathway. Pain and temperature information from the face send information via the trigeminal nerve (cranial nerve V). This information is carried to the trigeminal nucleus and synapses on second‐order neurons that decussate and ascend to the thalamus where they synapse on neurons and then ascend to the primary somatosensory cortex. Fig. 10.12 Pain and temperature pathways. The two major ascending pathways that carry pain and temperature information include the dorsal column‐medial lemniscal pathway and the spinothalamic pathway. Note that the dorsal column medial lemniscal pathway enters the spinal cord through the dorsal root and ascends to the medulla where it synapses on second‐order neurons that cross over to the contralateral side and then ascend to the cerebral cortex. In the spinothalamic tract, nerves enter the spinal cord via the dorsal root and synapse on second‐order nerves in the central gray area. These second‐order neurons cross over to the contralateral side before ascending to the thalamus where they synapse on neurons that then project to the cerebral cortex. There are chemoreceptors in the respiratory centers of the brain that sense changes in H+ and CO2 concentrations. There are also chemoreceptors in the carotid bodies located near the origin of the internal carotid arteries and in the aortic bodies found between the major branches of the aortic arch. These receptors respond to changes in blood pH, CO2, and oxygen concentrations. Signals for the carotid and aortic bodies travel to the respiratory centers through the glossopharyngeal (cranial nerve IX) and vagus (cranial nerve X). Sensory receptors are morphologically specialized structures that respond to specific stimuli. When stimulated, these receptors transform the stimulus into an electrical signal called a receptor potential, which is a graded potential causing either depolarization or hyperpolarization of the cell. The amplitude and duration of the receptor potential are related to the magnitude and length of time of the stimulus. If the receptor potential is large enough to reach the threshold, it is termed a generator potential and causes an action potential to form in the sensory neuron. The process of converting the stimuli into a receptor potential is called stimulus transduction. The various types of sensory receptors have different mechanisms for transducing the stimulus into a receptor potential. In mechanoreceptors, when there is a conformational change in the tissue in which the receptor resides, it causes a change in the plasma membrane of the mechanoreceptor, thus causing a physical change in the cation channels located in the sensory neuron membrane (Fig. 10.13). This physical change results in the opening of stretch‐sensitive channels that increase ion conductance. This leads to depolarization of the neuron and generation of a receptor potential. This mechanism is very similar to the production of an EPSP. The amplitude of the receptor potential is proportional to the intensity of the stimulus. Greater conformational change in the tissue will result in a greater number of channel openings on the mechanoreceptor. When the stimulus is removed, the ion channels close. Fig. 10.13 Mechanoreceptor depolarization. Mechanoreceptors respond to the physical deformation of the plasma membrane. In this example, a Meissner’s corpuscle, located in the skin, is deformed when the skin is pressed. This produces a physical change in the corpuscle membrane, which causes an opening of an ion channel on the plasma membrane. As cations move inward, a receptor potential is generated in the corpuscle. Receptors involved in general senses are either free or encapsulated dendritic endings. Free nerve endings are widely distributed but are especially abundant in epithelial and connective tissue. They are nonmyelinated and end in a knoblike swelling, sensitive to touch and pressure. There appear to be no structural differences between those that detect touch and pressure from those that detect temperature and pain. While these are the only sensory receptors on the surface of the eye, there are specialized tactile receptors located throughout the body surface that are probably more important. A summary of the various sensory receptors is shown in Table 10.2. Table 10.2 Sensory receptors: structure and function.
10
The Peripheral and Autonomic Nervous System
Nerves and Ganglia
Nerves
Classification of Nerves
Spinal Nerves
Degeneration and Regeneration of Nerves
Ganglia
Sensory Receptors
Classes of Sensory Receptors
Sensory System
Modality
Stimulus
Receptor Class
Receptor Cell Type
Auditory
Hearing
Sound
Mechanoreceptors
Hair cells (cochlea)
Visual
Vision
Light
Photoreceptors
Rods and cones
Vestibular
Balance
Gravity
Mechanoreceptors
Hair cells (vestibular labyrinth)
Somatosensory
Somatic Senses:
Touch
Proprioception
Temperature
Pain
Pressure
Displacement
Thermal
Chemical, thermal, or mechanical
Mechanoreceptors
Mechanoreceptors
Thermoreceptors
Chemoreceptors, thermoreceptors, or mechanoreceptors
III, IV, VI, VII, X, and cervical nerves
Gustatory
Taste
Chemical
Chemoreceptors
Taste buds
Olfactory
Smell
Chemical
Chemoreceptors
Olfactory sensory neurons
General Senses
Mechanoreceptors
Tactile Receptors
Baroreceptors
Proprioceptors
Dorsal Column‐Medial Lemniscal Pathway (Mechanoreceptor Pathway)
Nociceptors
Pain Pathway
Thermoreceptors
Thermoreceptor Pathway
Chemoreceptors
Detection of Sensory Stimuli
Type
Illustration
Function
Adapting
Location
Unencapsulated
Free dendritic nerve endings
Nociceptors, thermoreceptors, mechanoreceptors
Slowly adapting
Most body tissues; dense concentration in connective tissues, including ligaments, tendons, dermis, joint capsules, periostea; epithlia (epidermis, cornea, mucosa, glands)
Merkel discs: modified free dendritic endings
Mechanoreceptors (fine touch)
Slowly adapting
Basal layer of epidermis of skin
Root hair plexuses
Mechanoreceptors
Rapid
In and around hair follicles
Encapsulated
Meissner’s corpuscles
Mechanoreceptors (light pressure, discriminative touch, low‐frequency vibration)
Rapidly adapting
Dermal papillae of hairless skin, especially nipples, external genitalia, fingertips, soles of feet, eyelids
Krause’s end bulbs
Pacinian corpuscles (laminated corpuscles)
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