Our perception of the physical world we inhabit is a creation of the brain. The brain uses electrochemical nerve impulses that are sent to it by sensory receptors to construct its perspective of the world. Sensory receptors transduce or change different forms of energy like sounds, warmth, smells, colors, textures or tastes into the energy of nerve impulses and transmit them to the brain. The different modalities or forms of sensory perception result from the differences in neural pathways and synaptic connections. The brain interprets these impulses and these are the origin of our sensations.

Our senses allow us to perceive a limited range of energies. Our visual abilities only include the visual spectrum and do not include the ultraviolet or infrared spectra. The perception of cold is entirely a sensation that is created by the nervous system, since in nature there are only different degrees of temperature. Nevertheless, the ability to perceive cold is a useful capacity for survival and our senses allow us to effectively interact with out environment.

Sensory receptors are classified according to their structure and functionality. Structurally, sensory receptors might contain free dendritic endings, as in the case of receptors that sense pain and temperature, or encased in nonneural structures, like those that respond to pressure. Sensory receptors are also classified according to the type of stimulus that transduce. For example, chemoreceptors sense chemical stimuli in the environment or blood. These would include taste buds, olfactory epithelium and the aortic or carotid bodies. Photoreceptors, which include the cones and rods of the eye, respond to light. Thermoreceptors respond to cold and heat, and mechanoreceptors are stimulated by mechanical deformation of the receptor membrane. Nociceptors, or pain receptors, have a higher threshold for activation than do the other cutaneous receptors. This means that a more intense stimulus is required for their activation and that the firing rate of the receptor increases with stimulus intensity.

Receptors can also be classified according to the type of signal they deliver to the brain. Proprioceptors provide a sense of bodily position and allow fine control of muscle movements. Cutaneous receptors include touch and pressure receptors, heat and cold receptors, and pain receptors. Those receptors that mediate hearing, sight and equilibrium are known as special senses.

Another difference among sensory receptors is the ability of some receptors to issue a burst of activity when first stimulated, but quickly decrease their firing rate upon subsequent stimulation. In other words these receptors adapt to the stimulus. Receptors with this pattern of stimulation are known as phasic receptors. These receptors alert us to changes in sensory stimuli, and are part of the reason that we tend to cease paying attention to constant stimuli. The bathwater, for example, feels hotter when we first enter it. This phenomenon is known as sensory adaptation. Other receptors issue a constant rate of firing as long as the stimulus is maintained and these are known as tonic receptors. As an example, pain receptors continue firing in the face of continued stimuli and do not adapt.

The least amount of energy required to stimulate a receptor is called the adequate stimulus. A variety of stimuli might activate a sensory neuron, but for each sensory nerve the sensation generated is the same. A blow to the eye might create a flash of light. This is an unorthodox way of stimulating the photoreceptors of the eye, but the sensation that they generate, light, is the same.

The dendritic nerve endings of different sensory neurons mediate the cutaneous sensations of touch, pressure, heat, cold, and pain. The receptors for heat, cold and pain are simply naked endings of sensory neurons. The sensation of touch is mediated by expanded dendritic endings called Ruffini endings and Merkel’s discs. The sensations of touch and pressure are mediated by dendrites that are encapsulated within various structures, like Pacinian corpuscles, Meissner’s corpuscles and Krause’s end bulbs. Pacinian corpuscles contain dendritic endings that are encased in thirty to fifty layers of onion-like layers of connective tissue. These layers absorb some of the pressure when a stimulus is maintained and this also helps maintain the phasic response of this receptor.

There are far more free dendritic endings that respond to cold than respond to warm. The receptors for cold are located in the upper region of the dermis, just below the epidermis. Cold receptors are inhibited by warming, and are stimulated by cooling. Located deeper in the dermis are warmth receptors, which are stimulated by warmth and inhibited by cooling. Nociceptors are free sensory dendritic nerve endings and are either myelinated or unmyelinated. The initial sharp sensation of pain, as in the case of a pinprick, is transmitted by myelinated axons, whereas the dull, persistent ache is transmitted by slower conducting, unmyelinated axons, which use substance P and glutamate as their neurotransmitters.

Hot temperatures produce sensations of pain through the actions of a protein channel in dendritic membranes called the capsaicin receptor. This receptor is an ion channel and a receptor for the compound capsaicin. Capsaicin is also found in chili peppers, and eating them can cause the sensation of heat and pain. The opening of capsaicin receptors, in response to capsaicin from chili peppers or very high temperatures, allows the entry of calcium and sodium, which cause depolarization of the sensory neuron and an impulse to the CNS that is perceived as heat and pain.

Sensations from cutaneous receptors and proprioceptors are included in the somatesthetic senses. Sensory information from proprioceptors and pressure receptors are carried by large, myelinated nerve fibers that ascend in the dorsal columns of the spinal cord on the same or ipsilateral side. These fibers do not synapse until they reach the medulla oblongata of the brain stem. Therefore, fibers that carry these sensations from the feet are remarkably long. After the fibers synapse in the medulla with other second-order neurons, information to the latter neurons crosses over to the contralateral side as it ascends via a fiber tract called the medial lemniscus, to the thalamus. Third-order sensory neurons in the thalamus that receive this input project to the postcentral gyrus.

The sensations of heat, cold and pain are carried into the spinal cord by thin, unmyelinated sensory neurons. Within the spinal cord, these neurons synapse with second-order neurons that decussate to the contralateral side and ascend into the brain by means of the lateral spinothalamic tract. Fibers that mediate touch and pressure ascend in the anterior spinothalamic tract. Fibers of both the lateral and anterior spinothalamic tracts synapse with third-order neurons in the thalamus, which in turn project to the postcentral gyrus. The somatesthetic information is always carried to the postcentral gyrus by third-order neurons.

If a caliper is used to touch the skin, usually two different touch sensations are registered. However, as the points of the calipers are brought closer together, the subject will typically feel only one point. The minimum distance between the caliper points at which the subject still feels two touch sensations, is called the two-point touch threshold. At distances closer than the two-point touch threshold, only one sensation will be felt, even though two points are touching the subject. This distance represents the size of the field that is serviced by a single touch neuron. This field is called the receptive field and the size of the receptive field completely depends on the density of various sensory touch neurons. The two-point threshold differs for each part of the body. The big toe has a two-point touch threshold of 10 millimeters, while the first finger has a 2-millimeter two-point touch threshold. Braille dots are spaced 2.5 millimeters apart, which is just above the threshold for the fingertips.

When a blunt object touches the skin, several receptive fields are stimulated, but some more than others are. The neurons in the center of the point that was touched are most heavily stimulated while those at the periphery are the least stimulated. What we tend to feel is a sensation whose boundaries are well defined, and this is due to lateral inhibition. Those sensory neurons most strongly stimulated by the touch of the blunt object send signals to the central nervous system that inhibits some of the weaker signals, and this sharpens the signal and emerges from the brain.

The receptors for senses of taste and smell respond to molecules that are dissolved in fluid. These receptors are, therefore, chemoreceptors. Combinations of different receptors and their stimulation produce a vast array of tastes and smells. Taste, or gustation, and smell, or olfaction, respond to dissolved chemicals or gases. Also the sense of olfaction greatly influences the sense of taste.

Taste buds are modified epithelial cells that are located primarily on the surface of the tongue. They possess long microvilli that extend from the tips of the cells, through a pore in the surface of the taste bud. Although taste buds are not neurons, they can become depolarized when appropriately stimulated and release chemical transmitters that stimulate associated sensory neurons. The taste buds are bathed in saliva, and this means that the molecules that are presented to them are almost always dissolved. Taste buds located in the posterior third of the tongue are innervated by the glossopharyngeal nerve (IX) and the anterior two-thirds are innervated by the facial nerve (VII).

There are four basic modalities to the sense of taste: sour, sweet, salty and bitter. The receptors for these at the tip of the tongue (sweet), sides of the tongue (sour), back of the tongue (bitter) and concentrated at the sides (salty). The salty sensation is due to the passage of sodium ions through channels in the apical membranes of specific taste buds, which produces an action potential in the taste bud cell. The anion that is associated with sodium also seems to affect the saltiness of the food. Sour sensations are produced in the same way, but the now protons pass through membrane channels and this also causes the release of neurotransmitters. Since almost all sour foods are highly acidic, this mechanism makes sense. Most sweet molecules are sugars of some sort. Other organic molecules taste bitter, and this might be indication that the molecule is toxic, although not all toxins are bitter. Both sweet and bitter sensations are mediated by receptors that are coupled to G-proteins, and the particular G-protein involved in taste is called gustducin. The binding of the molecule to a receptor on the surface of the taste bud causes the activation of the G protein and this activates a second messenger system, which causes a depolarization. In the case of sweet and bitter the CNS distinguished between the two sensations.

In the superior portion of the nasal cavity, millions of bipolar sensory neurons lie within a pseudostratified epithelium. These olfactory receptor neurons replace themselves every 1-2 months, and each one has an unmyelinated axon that projects into the olfactory bulb where it synapses with a second-order neuron. The dendrites of these neurons are extends into the nasal cavity and is decorated with cilia at its apical end. The olfactory sensations are not sent to the thalamus like other sensations, but is sent directly to the cerebral cortex. The olfactory lobe is part of the limbic system and this explains why particular olfactory sensations can evoke charged memories.

The molecular basis of olfaction is complex. In some cases, ordorant molecules bind receptors that act through G-proteins to increase cAMP within the cell. There appear to be a large number of receptor molecules that are encoded by a gene family, and this might explain how the wide variety of molecules is detected by the olfactory system. Even so, a great deal about olfactory sensation in poorly understood.

The vestibular apparatus provides orientation with respect to gravity. The vestibular apparatus is connected to a structure called the cochlea, which is involved in hearing. Three different parts compose the vestibular apparatus. These are the otolith organs, which consist of the utricle and the saccule, and the semicircular canals. The sensory structures of the cochlea and the vestibular apparatus are located within the membranous labyrinth, which is a tubular structure filled with a fluid called endolymph. Endolymph is similar in composition to extracellular fluid. The membranous labyrinth is located within a cavity in the skull called the osseous labyrinth, and within the osseous labyrinth is a fluid called perilymph, which is similar in composition to cerebrospinal fluid. Perilymph is located between the membranous labyrinth and the bone.

The utricle and saccule provide information about linear acceleration, that is, changes in velocity when traveling horizontally or vertically. The semicircular canals provide sense of rotational or angular acceleration, which are oriented in three planes like the faces of a cube. This helps us maintain balance when turning the head, spinning or tumbling.

The receptors for equilibrium are modified epithelial cells called hair cells, which contain 20-50 hairlike extensions. All of these hairlike extensions, but one, are known as stereocilia. Stereocilia are processes containing filaments of protein surrounded by the cell membrane. One larger extension is known as a kinocilium and it has the structure of a true cilium. When the stereocilia are bent in the direction of the kinocilium, the membrane of the hair cell is depressed and becomes depolarized. Depolarization of the hair cell causes the release of a synaptic transmitter that stimulates the dendrites of the vestibulocochlear nerve (VIII). When the stereocilia are bent in the direction opposite that of the kinocilium, the hair cell becomes hyperpolarized and releases less synaptic transmitter.

The otolith organs, the utricle and the saccule, each contain a patch of modified epithelial cells called the macula that consists of hair cells and supporting cells. The hair cells project into the endolymph-filled membranous labyrinth and the hairs of the hair cells are embedded in a gelatinous otolith membrane. On top of the otolith membrane are small calcium carbonate crystals called otoliths, and these stones increase the mass of the otolith membrane. The higher inertia of the membrane is necessary for its function. During forward acceleration, the otolith membrane lags behind the hair cells, which pushes the hair cells backward. This causes the formation of an action potential that is interpreted by the brain as acceleration. The otolith organs also detect upward acceleration in an elevator.

The semicircular canals project in three different planes at nearly right angles to each other. Each canal contains an inner extension of the membranous labyrinth called a semicircular duct, and at the base of each duct is an enlarged swelling called the ampulla. An elevated area of the ampulla, called the crista ampullaris contains the sensory hair cells. These hair cells are embedded in a matrix called the cupula, which has a higher density than the surrounding endolymph. The cupula can be pushed one way or another by the movements of the endolymph. The endolymph of the semicircular canals serves a function that is analogous to that of the otolithic membrane — it provides inertia so that the sensory processes will be bent in a direction opposite to that if the angular acceleration.

The stimulation of an action potential activates sensory neurons of the vestibulocochlear nerve. These fibers transmit impulses to the cerebellum and to the vestibular nuclei of the medulla oblongata. The vestibular nuclei, in turn, send fibers to the oculomotor center of the brain stem and to the spinal cord. The oculomotor center controls eye movements, and neurons in the head stimulate movements of the head, neck and limbs.

When a person begins to spin, the inertia of the endolymph within the semicircular canal causes the cupula to bend in the opposite direction. As the spin continues, the inertia of the endolymph is overcome and the cupula straightens. At this time, the endolymph and the cupula are moving in the same direction and at the same speed. If the movement is suddenly stopped, the greater inertia of the endolymph causes it to keep moving in the previous direction of spin and to bend the cupula in that direction.

Bending of the cupula after movement has stopped affects muscular control of the eyes and body through the neural pathways previously described. The eyes slowly drift in the direction of the previous spin, and then are rapidly jerked back to the midline position, thus producing involuntary oscillations. These movements are called vestibular nystagmus. People experiencing this effect may feel that they are spinning, or that the room is spinning. The loss of equilibrium that results in called vertigo, and in susceptible individuals, the autonomic nervous system can become involved, thus causing dizziness, pallor, sweating and nausea. These are the symptoms of motion sickness.