The Integumentary System and Sensory Physiology
The integumentary system is part of a sensory system rooted in the nervous system. Sensory receptors receive stimuli from the external environment, where neural pathways conduct information to the brain (1).
When a human body receives information from the external or the internal environment, it will process the information through sensory pathways (1).
This information is called sensory information. When an individual is aware of that sensation, they translate that sensation into perception. When someone feels pain, that sensation perceives as pain. Sensory pathways transduce this energy in the form of graded potentials (1).
Sensory Receptors
When the body takes in information from its environment, sensory receptors are at the ends of afferent neurons that initiate action potentials that travel to the central nervous system (1).
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The energy or chemical that the body takes from the environment is known as a stimulus. There is a type of stimulus called the adequate stimulus, which is simply a stimulus that responds at a low threshold (1).
Another type of stimulus can initiate mechanoreceptors, which respond to some pressure or stretch from the body. Mechanoreceptors respond to many kinds of information, including muscle tension, blood pressure, or sensory touch (1).
Thermoreceptors are responsible for temperature, while photoreceptors respond to wavelengths of light.
Chemoreceptors respond to specific chemicals in the receptor membrane. Nociceptors detect any pain or tissue damage to the body (1).
When a stimulus transforms into a response, this is known as sensory transduction. Sensory receptors open or close ion channels where the channels receive the information and reach a threshold that will ignite an action potential influx through the membrane potential (1).
When action potentials initiate, they can form into graded potentials, which combine multiple action potentials, forming a receptor potential. A receptor potential is simply the space that allows a graded potential to carry its potential to its target membrane (1).
For myelinated neurons, the node of Ranvier allows graded responses to travel further along the membrane. The magnitude of the receptor will always determine the frequency of action potentials but not necessarily the amplitude of those action potentials (1).
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Adaptation is when receptors have decreased sensitivity. Slowly adapting receptors are known as tonic receptors and maintain a sustained stimulus to initiate action potentials in the afferent neurons. Rapidly adapting receptors are called phasic receptors and generate action potentials quickly but, over time, cease to respond (1).
Primary Sensory Coding
Coding is converting stimulus energy into a signal that relays sensory information directly to the central nervous system. One single afferent neuron is known as a sensory unit. The receptor field is where the afferent neuron has stimulation. Modality is any stimulus regulated by heat, cold, sound, or pressure (1).
Summary
In summary, when there is a stimulus on the skin, the target is the receptive field. The receptive field is where there are multiple peripheral receptors. These peripheral receptors carry the stimulus along the afferent neuron and head into the central terminals and the central nervous system region (1).
Receptor potentials are simply the graded potentials and action potentials that carry along the afferent neuron. In this case, the sensory receptor would be the peripheral ends of the peripheral receptors that pick up the stimulus in the receptor field (1).
The Skin
The outer layer of skin is the epidermis. This layer is thinner than the inner layer, which is the dermis. The epidermis consists of keratinocytes, which are a fibrous protein, also known as keratin. The epidermis also contains melanocytes responsible for skin pigments concerning melanin, which gives skin color (1).
In the inner layer of skin, the dermis contains blood vessels, sweat glands, and hair follicles (1).
The skin layers include the epidermis with named sections as the stratum basale, spinosum, granulosum, lucidum, and corneum (1).
The skin is part of a system of hair, nails, sweat glands, and sebaceous glands. The skin is the largest body component and the human body’s largest organ (1).
There are seven functions of the skin.
The first is protection from microorganisms, dehydration, or ultraviolet light (2).
The second purpose of the skin is sensation—pain, temperature, touch, or pressure (2).
The third purpose of the skin is to allow muscle movement so that the body can contract and move (2).
The fourth purpose of skin is to allow for the endocrine system to function correctly (2).
The integumentary system’s fifth function concerns the excretion of water, urea, or ammonia (2).
The integumentary system’s six functions are to help alert the body of pathogens or foreign substances that could damage the body (2).
The integumentary system’s last function is to help the body regulate temperature, such as warming the body or cooling it (2).
Sweat Glands
Sweat glands are an essential part of the skin related to exocrine glands and apocrine glands. Exocrine glands secrete substances on the epithelial surface and produce sweat. In contrast, the apocrine glands are in the nipples, scrotum, labia minora, penis, and clitoris (2).
Eccrine glands are major sweat glands that secrete through a duct on the open pore of the skin. Sebaceous glands open directly on the skin’s surface and help the skin protect it from pathogens. The hypodermis’ subcutaneous tissue is a layer of adipose tissue that increases the skin’s mobility (2).
Mucocutaneous junctions are areas of the skin concerning the smooth muscle that becomes skeletal muscle. Breasts are superficial structures on the anterior thoracic wall and are in the subcutaneous tissue (2).
There are various blood supplies of the skin. Cutaneous circulation is crucial for thermoregulation, while direct cutaneous is known for venous vessels (2).
Musculocutaneous vessels pierce the muscles and fascia. Cutaneous blood vessels are located deep in the fascia concerning thermoregulation (2).
Stimulus Intensity
Stimulus intensity stems from something called recruitment. Recruitment is the calling of other neurons that carry a more substantial stimulus through the afferent neuron. This calling allows for more significant sensations and bursts of action potentials for the brain to translate (1).
When the body is attempting to locate a stimulus, several different pathways can occur. Labeled lines are anatomical pathways that provide specific regions to the central nervous system. When the skin attempts to sense the location of a stimulus, it is affected by the receptive field’s size or the number of sensory units in the area (1).
The body has a range of different sensory receptors in various places along the body. For example, lips and fingertips have much more sensory units in those locations that allow a person to sense material far more than places like the back or elbow. The somatosensory regions are more significant and have denser, more sensitive receptive fields than other body areas (1).
When two stimuli simultaneously trigger the receptive field, the stimulus that triggers a more significant effect or frequency of action potentials will be the one in which the stimulus is closer to the receptive field (1).
In other words, imagine stimulus A along the skin that was closer to a receptive field than stimulus B. There would be a higher frequency of action potentials in stimulus A relatives to stimulus B (1).
Lateral inhibition is an essential mechanism in which neurons at the edge of a stimulus follow inhibition to locate another stimulus (1).
For example, say that a person is blindfolded and unaware of a stimulus to the skin. If someone were to take a feather and lightly move the feather across different parts of their skin, the body would attempt to locate the feather’s specific location (1).
Lateral inhibition works to inhibit specific receptive fields around the stimulus’s location and increase receptive fields closer to the stimulus. This effect increases the brain’s ability to pinpoint the location of the sensory input.
Ascending Neural Pathways in Sensory Systems
There are pathways called ascending pathways that project up to the brain. When these pathways reach the central nervous system, they relay information to the interneurons (1).
Somatic receptors carry information from the skin, skeletal muscle, bones, tendons, and joints. Somatic receptors essentially relay information to the brain about external stimuli. The somatosensory cortex lies in the parietal lobe of the brain. This cortex relays visual information, auditory information, gustatory cortex information related to taste and smell pathways (1).
These specific pathways relay any sensory information related to touch, smell, hearing, taste, and vision (1).
There are also nonspecific pathways activated in the neck that sense when something or anything is happening. These are not specific and are simply concerning different stimulus types like pressure, heating, and cooling. These nonspecific pathways end in the brain stem and project to other thalamus regions (1).
Association Cortex and Perceptual Processing
Cortical association areas are centers that relay information to the brain about arousal, attention, memory, and language (1).
The brain houses the perception of emotions, personality, experience, and different sensory receptor mechanisms. One phenomenon called Phantom limb is when a limb such as a hand or foot is missing by accident or amputation (1).
Even though the physical organ is no longer attached to the body, the brain can still sense certain sensations that perceive touch and pressure as if the limb was still present (1).
Even though these limbs are missing, the brain and the central nervous system can still trigger and act independently of specific peripheral input. Medicine has shown that some drugs can alter pain perceptions and alleviate particular pain or trauma by targeting these pathways (1).
Somatic Sensation
When somatic receptors are activated, the messier corpuscle responds to sensations for touch, pressure, and the body’s positions (1).
The skin has five different levels of sensation. Meissner’s corpuscle senses mechanoreceptor for touch and pressure. Merkel’s corpuscle works by slowly adapting neurons for touch and pressure (1).
Free neuron endings sense slow adapting nociceptors, thermoreceptors, and mechanoreceptors (1).
Pacinian corpuscles sense rapidly adapting mechanoreceptors (1).
Lastly, Ruffini’s corpuscle senses slowly adapting mechanoreceptors on the skin concerning posture and movement of different muscle spindle stretch receptors (1).
In terms of temperature, transient receptor potential proteins are different channels that open when the temperature changes. There is an influx of calcium and sodium when these channels open and depolarize (1).
Channels of neuropeptides, transmitters, or cytokines will release damaged cells surrounding pain or itching (1).
Referred Pain and Hyperalgesia
Referred pain is a phenomenon when the nociceptive afferent neuron and interneurons predict incoming pain (1).
Hyperalgesia is painful stimuli that can last for hours after the stimulus is gone. This type of response is common with severe injuries. Inhibition of pain is called analgesia and is the suppression of pain (1).
These areas can be electrically stimulated by the central nervous system and reduce pain by inhibiting the pathways. This phenomenon is called stimulation-produced analgesia (1).
Many drugs can bind to pain pathways and relieve pain by activating opioid receptors (1).
Acupuncture is a therapy that inserts needles in specific skin locations and activates individual neurons in the spinal cord and midbrain that release opioids and other neurotransmitters for pain relief (1).
Transcutaneous electrical nerve stimulation is another form of stimulating electrodes on the skin’s surface to inhibit neurons in their pain pathways (1).
Itching
When someone feels an itch, the skin’s sensory receptors are activated, where histamine is released as a chemical mediator to initiate some itching response (1).
Eczema is a skin condition that triggers inflammatory responses in the skin due to initiating these nociceptor mechanisms (1).
Neural Pathways of the Somatosensory System
Neural Pathways of pain or touch, or sensation can be complicated. There are two major types of somatosensory pathways from the spinal cord to the brain. The pathways are the ascending anterolateral pathway and the dorsal column pathway (1).
The anterolateral pathway initiates or senses some stimulus that carries along the efferent neuron, crosses over to the opposite side of the spinal cord, and progresses to the thalamus.
The anterolateral pathway is specific for pain and sends temperature information to the brain’s gray matter (1).
On the other hand, the dorsal column pathway relays to white matter sections of the brain, and the sensory receptor neurons do not cross over and synapse on the opposite side of the spinal cord. This stimulus portrays on the same side of the body directly to the brain stem (1).
However, both pathways will cross to the opposite side once in the central nervous system (1).
Vision
Understanding vision requires an understanding of light and wavelengths. Wavelengths are the distance between two peaks of electromagnetic radiation (1).
The visible spectrum is a combination of different wavelengths stimulating the receptors of the eye. Frequency is the radiation wave that varies in terms of wavelength (1).
Eye Anatomy
Eye anatomy involves the outer layer known as the sclera. The sclera connects to a capsule around the eye known as the cornea (1).
The layer beneath the sclera is called the choroid. In front of the choroid layer is the iris, or the color that gives eye color (1).
The ciliary muscle has fibers known as suspensory ligaments. The pupil is a smooth muscle fiber that can constrict and dilate in diameter due to light reception (1).
The eye’s lens determines the shape and the focusing power that allows the eye to see clearly. The eye’s central layer is the retina and forms the eye’s posterior surface (1).
The neurons in the eyes are sensory cells called photoreceptors. The macula lutea is a region of the retina that is free of blood vessels (1).
The fovea centralis is within the macula and is specialized to high visual acuity. The optic disc contains photoreceptors connected to the optic nerve and lays extensively on the retina’s inner surface (1).
The eye’s anterior chamber is filled with aqueous humor, while the posterior chamber fills with jelly-like substances called vitreous humor (1).
Optics of the Eye
When light receives from the eye, the wave changes direction at an angle that bends individual light waves called refraction. Refraction is the mechanism that allows us to focus on an object onto the retina (1).
The object in the eye center is the fovea centralis, where the image is formed upside down and reversed right to left in the brain (1).
In other words, humans technically see upside down. The brain turns this image upright to see images in the correct view (1).
Our brain does an incredible job restoring perception in real-time as the image is taken and refracted onto the cornea and focused on the fovea centralis, which turns the image upside down (1).
Accommodation focuses on the retina’s visual images and allows for changes to be made in the lens to better see something in view (1).
The ciliary muscle stimulates by parasympathetic nerves and allows the lens to contract. When the ciliary muscle relaxes, it increases the zonular fibers’ tension, and the lens alters by contraction and relaxation of the ciliary muscle (1).
Contraction of the ciliary muscle focuses the eyes on near objects, and constriction of the pupil also appears when the ciliary muscle is contracting to sharpen the image (1).
Therefore the ciliary muscle contracts when the eye wants to focus on near objects and relaxes when the eye wants to focus on distant objects. As people age, the ciliary muscle loses its shape and ability to contract and relax. This condition is known as presbyopia and is a normal part of the aging process (1).
When a person is nearsighted or myopic, the eye cannot see distant objects; the cause of nearsightedness is the abnormal development of the eyeball and the elongation of the eyeball (1).
When the eye is too short for the lens, images in the distance can become reasonably straightforward. However, images that have near objects become difficult to see. This process is known as farsightedness or hyperopia when a person has low near vision (1).
Astigmatism is a condition when the lens or cornea does not have a smooth surface. Essentially, the eye does not focus properly on the retina and causes blurred vision at any distance near or far (1).
The iris of the eye does not contribute to the clarity that a person can see. However, stimulation of sympathetic nerves to the iris can enlarge the pupil by causing muscle fibers to contract (1).
In contrast, parasympathetic fibers’ stimulation can make the pupil smaller by causing the muscle fibers that surround the pupil to contract (1).
Bright light will cause a decrease in the pupil’s diameter, which reduces the amount of light entering the eye and restricts the light to the central part of the lens. Constriction of the pupil protects the retina from bright light (1).
However, in dim light, the pupil increases to enhance the amount of light so that the eyes can see in the dark (1).
Photoreceptors
Photoreceptors are a specific part of the eye that transduces the action potentials that allow us to see (1).
Photoreceptors have an outer segment membrane called a disc. The discs house the information that is needed to respond to light. Photoreceptors have an inner section containing mitochondria. The mitochondria connect the photoreceptor to other neurons in the retina (1).
There are two types of photoreceptors, which are called rods and cones. The cones are responsible for light-sensitive information, and the rods are responsible for dark sensory information (1).
Rods function in low light, while cones function in bright light. For example, when the sun is bright, cones will give as much color to a person’s surroundings as possible (1).
While in the dark, rods will collect as much information from the environment to give to the person. Muller cells are the most common form of glial cells in the body and relay these different retina information types (1).
Two layers of the eye, the choroid and the pigment epithelium at the back of the retina, absorb light rays that bypass the photoreceptors. These mechanisms prevent photons’ reflection on the rods and cones and avoid blurring images as a person tries to see (1).
Absorption of Light by Photoreceptors
The photoreceptors specifically contain photopigments, which are what absorbs light. Rhodopsin is a photopigment in the retina and consists of a protein called opsonin. Opsonin binds to a chromophore molecule (1).
The chromophore is a derivative of vitamin A. Each photopigment absorbs light differently. The cell absorbs light in specific wavelengths that can either display red cones or blue cones. The photoreceptors are responsible for trapping light and allowing humans to absorb light in a way that defines the clarity of color (1).
Sensory transduction in photoreceptors
The photoreceptor depolarizes at -35 mV in the dark and hyperpolarizes by -70 mV in light (1).
In the absence of light or darkness, the enzyme guanylyl cyclase converts GTP into cyclic GMP. The cAMP maintains around cation channels that allow an influx of sodium and calcium to persist. Therefore, cGMP is high in the dark, and the photoreceptor is in a depolarized state (1).
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When there is light, there is a cascade of events that lead to hyperpolarization of the membrane. This membrane allows the absorption of energy from photons and dissociates from opsonin, enabling a protein called transducin to activate cGMP phosphodiesterase (1).
This enzyme degrades cGMP and allows cation channels to close, and the loss of depolarizing effect allows the membrane to polarize for potassium (1).
In summary, in the dark, cGMP allows sodium and calcium to influx. This process is depolarization. In light, the eyes use a transducin protein to allow those channels to close and opens potassium channels instead of sodium and calcium channels (1).
Adaptation of Photoreceptors
When moving from a place that has light into a darkened room, photoreceptors undergo adaptation. The rods work to enhance vision in the dark. The rhodopsin in the rods is activated when going from light to dark. Vitamin A is a vitamin essential for good night vision because it provides the chromophore retinal for rhodopsin (1).
In contrast, light adaptation occurs when someone moves from a dark place into a bright place. Initially, the eye is susceptible to light as the rods are overwhelmed by the visual image (1).
It may take a few moments for the rhodopsin to activate for the rods to turn off and for the cones to become responsive, allowing the light to illuminate the individual’s vision (1).
Light signals convert into action potentials through the interaction of photoreceptors called bipolar cells and ganglion cells. These cells undergo graded responses because they lack voltage-gated ion channels (1).
Ganglion cells are the first cells in the pathway where action potentials initiate. Bipolar and ganglion cells can either turn on or off based on photoreceptor response (1).
Bipolar cells on the ON-pathway depolarize in the absence of input. Bipolar cells on the OFF-pathway hyperpolarize in the absence of input (1).
Glutamate cells on the ON-pathway are inhibitory, whereas glutamate receptors on the OFF-pathway are excitatory. Glutamate has bipolar cells binding to metabotropic receptors that cause a breakdown of cGMP. The reaction hyperpolarizes the bipolar cells (1).
In the absence of light, ganglion cells on the pathway lack stimulation to fire action potentials. The process will reverse when light strikes the photoreceptors (1).
Summary
The ON-pathway will have bipolar cells that will depolarize in the absence of input (1).
Bipolar cells on the OFF-pathway will hyperpolarize in the absence of input. Glutamate receptors on the ON-pathway are inhibitory, whereas glutamate on the OFF-pathway is excitatory (1).
The OFF-pathway bipolar cells have glutamate receptors that are non-selective for cation channels. Depolarization of these bipolar cells stimulates neurotransmission for the firing of action potentials (1).
Therefore, the OFF-pathway generates action potentials in the absence of light to inhibit action potentials. The ON and OFF pathways of the retina improve resolution by increasing the brain’s ability to receive contrast (1).
Horizontal cells and amacrine cells pass information between areas of the retina. This information allows the retina to process shapes and the direction of movement (1).
One thousand rod cells can converge on a single bipolar cell of the retina, whereas the fovea can only have a few cells synapse on the bipolar cell. This system allows the retina to process various signals that travel up to the brain and process information (1).
ON-Pathway
- Photoreceptor depolarizes in the dark.
- Light hyperpolarizes photoreceptor cells.
- There is a following decreased glutamate release on the bipolar cell.
- Reduced inhibition by glutamate receptors and bipolar cells depolarizes and releases more excitatory neurotransmitters.
- Ganglion cell depolarizes and generates more action potentials (1).
OFF-Pathway
- Photoreceptor depolarizes in the dark.
- Light hyperpolarizes photoreceptor cells.
- There follows decreased glutamate release on the bipolar cell.
- Reduced excitation by glutamate receptors. The bipolar cell will hyperpolarize and release less excitatory neurotransmitters.
- The ganglion cell hyperpolarizes and generates fewer action potentials (1).
Ganglion Cell Receptor Fields
Ganglion cell receptor fields are in a series of ON-and-OFF pathways that either will depolarize or hyperpolarize the cell. Lateral inhibition is also common in this area because the brain is essentially trying to pull out the most precise information to determine its environment (1).
The Output from Ganglion Cells
Two optic nerves meet at the base of the brain called the optic chiasm. The optic chiasm has optic tracts on the opposite side of the brain, providing input to the cerebral hemispheres from each eye. Monocular vision is from one eye, while binocular vision is from two eyes. Optic nerve fibers project to different brain areas, including the thalamus, and record further information like color, intensity, shape, and movement (1).
Images are perceived when the eye takes in movement and color and translates that information along the optic chiasm. The data can either process parallel to the brain or crossover from the right side to the left side to reach the visual cortex (1).
Melanopsin is a pigment that carries visual information to the nucleus called the suprachiasmatic nucleus (1).
This area monitors light intensity and regulates the process by contributing to humans’ sleep cycle from waking up in the morning and sleeping at night. The visual center also passes to the brainstem, and the cerebellum allows for eye and head movements and pupil size changes (1).
Color vision
Color vision begins with photopigments in the cone photoreceptor cells. These wavelengths are found in various degrees when there is a specific wavelength stimulus (1).
For example, a wavelength of 531 nanometers responds with green cones maximally. When a specific wavelength stimulates, the corresponding cones react according to that wavelength. This process gives human beings color (1).
Ganglion cells of a second type are opponent color cells because they have an excitatory input from cone receptors and inhibitory inputs from other receptors (1).
Our brain can determine color based on the frequency of action potentials, wavelength, and light intensity that strikes the retina. Rods may respond in dim light. Moreover, in bright light, cones respond forcefully (1).
Color Blindness
The most common form of color blindness is red or green color blindness. Color blindness can result from a recessive mutation in one or more genes coding the pigments (1).
Genes encode red and green pigments locate very close to each other, and genes encoding the blue chromophore locate much further (1).
The close association of red and green genes creates a greater likelihood of genetic recombination during meiosis and is why more men than women suffer from color blindness. Since men only have a single X chromosome, the single allele from the mother could result in color blindness even though the mother might have normal vision. It also means that 50% of the male offspring of that mother will expect to be color-blind (1).
Eye Movement
The macula lutea region provides the highest visual acuity by packing cones convergent with the bipolar and ganglion cells (1).
When focusing on an area, the fovea may cause the eyeball and the surrounding skeletal muscles of the eyeball to increase its movement (1).
The fast movements, termed saccades, are jerking movements that bring the eye from one point to another when searching for an image (1).
Slow eye movements are involved in tracking visual objects and obtain information about head movement from the vestibular system (1).
Diseases of the Eye
One disease of the eye is called a cataract. A cataract is a clouding of the lens due to proteins in the lens tissue. Cataracts are typical for the elderly population due to the lens becoming denser due to age. Cataracts also initiate from smoking, trauma, or certain medications (1).
Another eye disease is glaucoma. Glaucoma composes of retinal cells that encounter damage due to pressure within the eye. This pressure within the eye depends on the volume of the aqueous humor and the vitreous humor. When the aqueous humor forms quickly, it can result in increased pressure within the eye. Glaucoma is a form of irreversible blindness, but treatments with medications reduce the aqueous humor after laser surgery (1).
Another primary eye disease is macular degeneration. This form of the disease also increases with age and can be referred to as age-related macular degeneration. AMD’s causes may be hereditary. Scientists believe that the fovea becomes damaged and leads to a loss of sharpness and color vision. There is not much research to back up any effective treatment for this disease (1).
Audition
The ear records sound through the external, middle, and inner parts of the ear. This information travels along the brain’s pathways, where the brain encodes information and perceives the sound (1).
Sound energy transmits by a vibration of the molecules of air. When there are no molecules, there is no sound. Sound waves consist of compressions in which the molecules are very close together, and pressure increases (1).
When molecules bump against each other, they create a ripple effect over a specific distance area. The more sound waves that ripple, the louder the sound. The difference in the pressure determines the wave’s amplitude (1).
The human ear is a structure made to sense these volume variations over a particular range. Decibels are the threshold for the intensity of sound that a human can hear. The frequency of vibration records in Hz frequencies by which humans can listen to the sound’s vibrations (1).
Sound Transmissions in the Ear
The first step to hearing sound is through the external auditory canal. The external auditory canal is made of the outer ear or pinna and works to amplify and direct the sound (1).
The ear takes the sound waves as pressure signals to the tympanic membrane, called the eardrum. Air molecules will push against the membrane and cause it to vibrate at the same frequency as the sound wave. Therefore high noise or sound will cause higher pressure and higher vibrations within the ear (1).
The middle ear is an air-filled cavity that allows pressure from the external auditory canal to equal the external environment’s atmospheric pressure (1).
The eustachian tube connects the middle ear to the pharynx. This tube is typically closed, but muscle movements like yawning, swallowing, or sneezing will open the tube (1).
Even though pressure from the outside external canal can change, the middle ear’s pressure remains constant because of the eustachian tube. The next step in hearing is when the sound goes from the middle to the inner ear, a fluid-filled inner sack (1).
The liquid is more challenging to move than air and transmits in the inner ear as amplification. Three bones in the middle ear are the malleus, incus, and stapes. These bones act like pistons to vibrate the sound waves from the tympanic membrane to the oval window (1).
The tensor tympani muscle attaches to the malleus and contracts the muscle as sound hits the ear. Stapedius connects to the stapes and controls its mobility. These muscles protect the inner ear but only to a certain point. People need to wear ear protection in environments where loud sounds could occur for an extended time (1).
The Cochlea
The inner ear portion is called the cochlea and is a spiral-shaped fluid-filled space that allows sensory receptors from the auditory system to fill with fluid.
The cochlea divides by the cochlear duct and allows the endolymph to act as an extracellular fluid high in potassium concentrations and low in sodium concentrations. There is a fluid called perilymph on either side of the duct, similar to cerebrospinal fluid (1).
The scala vestibuli is above the cochlear duct and is the entrance of the oval window. The scala tympani is below the cochlear duct and connects the middle ear to the round window (1).
The basilar membrane forms the side of the cochlear duct next to the scala tympani. The basilar membrane is where the organ of Corti sits and contains the ear’s receptor cells or hair cells (1).
When the sound goes from the external auditory canal to the middle ear and finally into the inner ear, they move in and out of the tympanic membrane causing the sound to bow hairs from the stimuli (1).
The stimuli create a wave of pressure in the scala tympani. The waves pass around the cochlear duct, and the sound represents the vibrations of the basilar membrane receptor cells. These cells are on the organ of Corti and relay frequency through the ear. The basilar membrane records different frequencies with high pitches near the middle ear and low pitches towards the far end (1).
Hair cells
Hair cells are on the organ of Corti. These cells act as mechanoreceptors and have a stereocilia system with different rows of inner and outer hair cells (1).
These hair cells extend into the endolymph fluid and have different types of pressure waves. The tectorial membrane is where outer hair cells are embedded and sharpen frequency along the basilar membrane (1).
When the stereocilia bend toward the location of the sound or the fibrous connections, there is an opening of gated cation channels, resulting in an influx of potassium (1).
Potassium hyperpolarizes the cells and opens voltage-gated calcium channels when the hair cells bend in the opposite direction (1).
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The neurotransmitter that is released is glutamate, just like in the eye. The generation of action potentials joins to form the cochlear branch of the vestibulocochlear nerve (1).
One principle for the ear is that the greater the sound, the greater the frequency. When sound is loud, the irreplaceable hair cells die. Tinnitus is ringing in the ear where hair cells are damaged or lost due to external sound (1).
Neural Pathways of Hearing
Cochlear nerve fibers enter the brain stem and synapse with interneurons (1).
In other words, these inputs allow a person to determine the sound’s location. If the right ear hears the sound first, the brain can translate it from the right side. This information is translated along the brain stem in a polysynaptic pathway to the thalamus on the temporal lobe’s auditory cortex (1).
Descending auditory nerve pathways allow us to determine the precise location of the sound. Hearing aids amplify incoming sounds into the ear canal. Cochlear implants are electronic devices that, in some cases, can restore functional hearing. These implants stimulate the cochlear nerve by sending electrical currents transmitted along the cochlea’s auditory pathways (1).
The Vestibular System
The vestibular apparatus consists of semicircular canals called the utricle and saccule. The shape of the cupola, saccule, and semicircular canals make up the labyrinth(1).
Semicircular Canals
The semicircular canals are responsible for detecting acceleration and rotation of the head. The stereocilia extend across the semicircular canal at the ampulla (1).
When the head moves, the semicircular canal attaches to the hair cells and move along with them. The ampulla’s movement pushes against fluid, which causes the bending and release of neurotransmission from the hair cells (1).
As a person moves, these mechanoreceptors change the hair cell potential and neurotransmission release.
The neurotransmitter released can increase or decrease based on where the hair cells will be bent.
When the hair cell receptor releases neurotransmitters, the stereocilia will bend in a specific position. The bending will cause the receptor cell to depolarize. When stereocilia turn in the opposite direction, that cell hyperpolarizes (1).
The Utricle and Saccule
The utricle and saccule respond to linear acceleration. The hair cells in the utricle stand straight up when a person is standing up. They also respond to acceleration in the horizontal plane. In the saccule, hair cells project at right angles and respond to gravitational effects from either a lying or a standing position (1).
The stereocilia are cells in the structures that embed in otoliths. The otoliths are calcium carbonate crystals that are heavier than the surrounding fluid (1).
In response to gravity or linear acceleration, the otoliths pull the hair cells so that the stereocilia on the hair cells bend and the receptor cells result in stimulation (1).
Vestibular Information
Nystagmus is a jerky back and forth movement of the eyes that can occur to unusual stimuli. When a person is spinning in a chair and stops abruptly, the fluid in the semicircular canals is rotating while the person is still (1).
The person’s eyes will involuntarily move as though trying to track the objects spinning in the field of vision (1).
In reflex mechanisms related to posture and balance, the vestibular apparatus supports the head during sudden movement. The vestibular information can also process awareness due to the body’s acceleration in a particular space (1).
Cell stimulation is related to the vestibular apparatus within the brainstem via the vestibular branch of the vestibulocochlear nerve. It is transmitted to the thalamus and sent to the cerebral cortex (1).
These descending projections are also sent from the brainstem to the spinal cord to influence skeletal muscle postural reflex. Vestibular information can come from several different organs concerning the eyes, joints, tendons, and skin. Motion sickness is a common effect of the vestibular system when a person experiences unfamiliar linear and rotational acceleration patterns (1).
Gustation or Taste
Gustation relates to sense organs that are associated with taste buds. These taste buds find themselves in the mouth, throat, and tongue (1).
A structure on the tongue called the lingual papillae serves as several epithelial cells that act as receptors for various food chemicals. There are hair-like microvilli on the receptor cells that integrate proteins to transduce these chemicals into receptor potentials (1).
The basal cells, which are the bottom of taste buds, replace taste receptor cells when damaged (1).
Taste submodalities in different categories include sweet, sour, salty, bitter, and umami (1).
Each taste category has a signal transduction mechanism in which it depolarizes the cell and stimulates action potentials (1).
Sour is associated with the acid content of hydrogen ions blocking potassium channels in the sour receptors (1).
Sweet receptors have natural sugars like glucose and artificial sweetener molecules that bind these receptors to activate a G protein that blocks potassium channels and depolarizes the receptor channel (1).
Bitter flavors are associated with a G protein second messenger pathways that evoke a bitter taste (1).
Salt has a simple mechanism in which sodium ion channels enter the receptor cell membrane channels, depolarizing the cell (1).
Lastly, umami depolarizes via the G protein-coupled receptor mechanism that blocks potassium channels (1).
These neurons relay action potentials along the central nervous system’s pathways, where the brain relays and conducts the information related to a specific taste (1).
Chemoreceptor cells are typical in the mouth and the tongue, and various areas of the body. G protein-coupled receptors activate the cells (1).
This fact is important because when an individual tastes food with carbohydrates, the taste receptors can also initiate within the gastrointestinal system and act as reflex secretions of digestive enzymes in the gut due to the chemoreceptors activated in the mouth (1).
Olfaction
Smell initiates through the olfactory epithelium. This epithelium is in the upper part of the nasal cavity and has afferent neurons in mucus cilia responsible for afferent neuron sensory stimulation (1).
The axons of the neurons from the olfactory nerve detect another substance called an odorant. The odorant molecules diffuse into the air and get taken up to the nose through the olfactory epithelium region (1).
Once they are there, the epithelium’s mucus binds to the odorant receptors and activates a specific type of plasma membrane concerning the odor (1).
Like the taste buds, the odorants initiate a specific response in the plasma membrane receptors (1).
Information passes from the olfactory bulbs directly to the olfactory cortex (1).
The olfactory receptor cells‘ axons synapse in a pair of structures known as the olfactory bulbs. Odorant receptor cells activate only specific olfactory bulb neurons and allow the brain to determine which receptor has stimulated. The brain interprets the neural firing as a particular odor (1).
Different odors will elicit different electrical activity types even though there are not as many olfactory receptors as odorants (1).
Science shows that there are ten thousand different types of odorants and only 400 olfactory receptor types. These few olfactory types can discriminate between various odorants. In general, women have better senses of smell, and many things can decrease the sensitivity of smell, such as age, smoking, or disease (1).
Genetic defects also occur that prevent the ability to smell. Defects in the X chromosome as well as in chromosomes 8 and 20 could cause Kallman syndrome. This syndrome is a condition where olfactory bulbs fail to form, and the brain cannot transduce the information from the receptor (1).
This section summarizes sensory physiology involving vision, taste, touch, hearing, and smell.
Sources
Hill, Richard W., et al. Animal Physiology. Oxford University Press, 2018.
Vander, Arthur J., et al. Vander’s Human Physiology: The Mechanisms of Body Function. McGraw-Hill Education, 2019.