Premed · Premed · General Biology 2
Lecture 22: Sensory and Motor Systems
General Biology II — Organismal, Evolution & Ecology
Learning Objectives
By the end of this lecture, students will be able to:
- Explain how sensory receptors transduce stimuli into neural signals
- Classify sensory receptors by stimulus type and describe key examples
- Describe the structure and function of the vertebrate eye and ear
- Explain the mechanisms of taste and smell (chemoreception)
- Describe the organization of the vertebrate skeletal muscle and the sliding filament model of contraction
- Explain excitation-contraction coupling at the neuromuscular junction
- Distinguish between the types of skeletal muscle fibers and their functional roles
Lecture Content
I. Principles of Sensory Reception
Sensory receptors are specialized cells or neurons that detect stimuli from the environment and convert them into electrical signals. This process, called sensory transduction, transforms stimulus energy into a change in membrane potential known as a receptor potential. Receptor potentials are graded -- their amplitude is proportional to the intensity of the stimulus -- and if a receptor potential is strong enough to reach threshold, it triggers action potentials in the associated sensory neuron for transmission to the CNS.
Sensory adaptation is the phenomenon in which a receptor's responsiveness decreases during exposure to a sustained, constant stimulus. Tonic receptors adapt slowly and continue firing throughout a prolonged stimulus, making them well suited for monitoring ongoing conditions such as pain and body position (proprioception). Phasic receptors adapt rapidly and respond primarily to changes in stimulus intensity, as many touch receptors in the skin do.
Sensory receptors are classified by the type of stimulus they detect. Mechanoreceptors respond to physical forces such as pressure, touch, stretch, vibration, sound, and changes in position. Chemoreceptors detect specific chemicals, mediating taste, smell, and the monitoring of blood oxygen, carbon dioxide, and pH. Electromagnetic receptors detect light (photoreceptors) and, in some fish, electrical fields. Thermoreceptors sense temperature changes. Nociceptors respond to tissue damage, extreme temperatures, and harmful chemicals, producing the sensation of pain.
II. Mechanoreception — Touch and Hearing
A. Touch and Pressure
The skin contains multiple types of mechanoreceptors distributed at different depths. Merkel cells (discs) detect sustained pressure and fine texture and are slowly adapting. Meissner's corpuscles, located in the dermal papillae, detect light touch and texture discrimination and are rapidly adapting. Pacinian corpuscles, found in the deeper dermis and viscera, detect deep pressure and vibration and adapt rapidly. Ruffini endings sense skin stretch and joint position and adapt slowly. Proprioceptors provide the body with information about its own position and movement: muscle spindles detect changes in muscle length, Golgi tendon organs detect muscle tension, and joint receptors monitor joint angle and movement.
B. Hearing and the Ear
The vertebrate ear converts sound waves -- pressure waves traveling through air -- into neural signals through a series of mechanical and electrochemical steps. The outer ear collects sound with the pinna (auricle), channels it through the auditory canal, and sets the tympanic membrane (eardrum) vibrating. The middle ear contains three tiny ossicles -- the malleus, incus, and stapes -- that amplify these vibrations approximately 22-fold. The stapes transmits the amplified vibrations to the oval window of the cochlea, while the Eustachian tube equalizes pressure between the middle ear and the atmosphere.
The inner ear houses the cochlea, a fluid-filled, coiled structure divided into three chambers: the scala vestibuli, scala media (cochlear duct), and scala tympani. Within the scala media, the organ of Corti sits on the basilar membrane and contains the sensory hair cells, mechanoreceptors with bundles of stereocilia projecting from their apical surfaces. When sound vibrations pass through the oval window into the perilymph, they set the basilar membrane in motion, deflecting the stereocilia against the overlying tectorial membrane. This deflection opens mechanically gated ion channels, allowing K+ influx that depolarizes the hair cells, triggering neurotransmitter release and generating signals in the cochlear nerve that travel to the brain. The cochlea is organized tonotopically: the base, where the basilar membrane is stiff and narrow, responds to high-frequency sounds, while the apex, where it is flexible and wide, responds to low frequencies.
C. Vestibular System (Equilibrium)
Located adjacent to the cochlea in the inner ear, the vestibular system monitors balance and spatial orientation. Three semicircular canals, oriented in perpendicular planes, detect rotational acceleration. When the head rotates, the endolymph within the canals shifts and deflects hair cells embedded in a gelatinous structure called the cupula within each canal's ampulla. The otolith organs -- the utricle and saccule -- detect linear acceleration and the position of the head relative to gravity. Otoliths, tiny crystals of calcium carbonate resting on a gelatinous membrane over the hair cells, shift with gravity and linear motion, bending the stereocilia and altering neural signals.
<image>A detailed cross-sectional anatomy of the human ear showing all three regions. The outer ear includes the pinna and auditory canal leading to the tympanic membrane. The middle ear contains the three ossicles (malleus attached to the tympanic membrane, incus in the middle, stapes pressing against the oval window) and the Eustachian tube. The inner ear shows the cochlea (uncoiled in an inset to reveal the three chambers: scala vestibuli, scala media, and scala tympani, with the organ of Corti on the basilar membrane). A magnified inset of the organ of Corti shows inner and outer hair cells with stereocilia touching the tectorial membrane, supporting cells on the basilar membrane, and afferent nerve fibers at the base of the hair cells. Adjacent to the cochlea, the vestibular apparatus is shown with three semicircular canals, the ampulla with cupula and hair cells, and the utricle and saccule with otolith membrane and hair cells.</image>
III. Photoreception — Vision
The vertebrate eye is a remarkable optical instrument. The cornea, a transparent outer layer, provides the initial refraction (bending) of incoming light. Behind it, the aqueous humor fills the anterior chamber. The iris, a colored muscular ring, adjusts the diameter of the pupil to regulate how much light enters the eye. The lens, a flexible transparent structure, fine-tunes the focus through a process called accommodation: when the ciliary muscles contract, the lens becomes rounder for near focus; when they relax, it flattens for distant focus. The vitreous humor, a gel-like substance, fills the posterior chamber and maintains the eye's shape. The retina, lining the back of the eye, contains the photoreceptor cells and layers of neural processing. The fovea, at the center of the retina, has the highest density of cone photoreceptors and provides the sharpest vision. The optic disc, where the optic nerve exits the eye, lacks photoreceptors entirely and constitutes the blind spot.
Two classes of photoreceptors serve different visual functions. Rods -- approximately 120 million per retina, concentrated in the peripheral retina -- are exquisitely sensitive and function in dim light (scotopic vision) but do not discriminate color. Cones -- approximately 6 million per retina, concentrated in the fovea -- mediate color vision and high visual acuity in bright light (photopic vision) and come in three types sensitive to short (blue), medium (green), and long (red) wavelengths.
Phototransduction in rod cells illustrates the elegance of sensory conversion. Rods contain stacks of membrane discs in their outer segments loaded with the photopigment rhodopsin, a complex of the protein opsin and the light-absorbing molecule retinal (a derivative of vitamin A). In darkness, intracellular cGMP levels are high, holding cGMP-gated Na+ channels open so that Na+ flows steadily into the cell (the dark current), keeping the rod depolarized and releasing glutamate continuously. When light strikes rhodopsin, retinal changes from its 11-cis to all-trans conformation, activating opsin, which in turn activates the G protein transducin, which activates phosphodiesterase. Phosphodiesterase breaks down cGMP, causing the Na+ channels to close. The rod hyperpolarizes and reduces its glutamate release -- the signal that light has been detected. This cascade provides extraordinary amplification: a single photon can trigger the hydrolysis of thousands of cGMP molecules.
Visual processing begins in the retina itself. Photoreceptors synapse with bipolar cells, which in turn synapse with ganglion cells, whose axons form the optic nerve. Horizontal cells and amacrine cells provide lateral connections that enhance contrast and edge detection through lateral inhibition. From the retina, signals travel along the optic nerve to the optic chiasm (where fibers partially cross), then to the lateral geniculate nucleus of the thalamus, and finally to the primary visual cortex in the occipital lobe.
<image>A diagram of the vertebrate eye and retinal processing. The main panel shows a horizontal cross-section of the human eye with all major structures labeled: cornea, iris, pupil, lens with ciliary muscles and suspensory ligaments, anterior chamber with aqueous humor, posterior chamber with vitreous humor, retina, choroid, sclera, fovea, optic disc (blind spot), and optic nerve. Light rays are shown entering through the cornea and lens, converging on the retina. An enlarged inset of the retinal layers shows the arrangement of cells (from back to front): pigmented epithelium, photoreceptors (rods shown as elongated cells with disc-stacked outer segments, and cones shown as shorter tapered cells), bipolar cells, and ganglion cells with axons converging to form the optic nerve. Horizontal cells and amacrine cells are shown making lateral connections. A second inset details a single rod cell with its outer segment (membrane discs containing rhodopsin), inner segment (mitochondria), cell body, and synaptic terminal.</image>
IV. Chemoreception — Taste and Smell
A. Gustation (Taste)
Taste buds are clusters of 50-100 taste receptor cells located within papillae on the tongue surface. Humans perceive five basic taste modalities: sweet (sugars and some amino acids), sour (H+ ions from acids), salty (Na+ ions), bitter (a diverse array of compounds, many of them toxic), and umami (the savory taste of glutamate). The transduction mechanisms differ by modality. Salt and sour tastes involve the direct gating of ion channels by Na+ or H+ ions. Sweet, bitter, and umami tastes are mediated by G-protein-coupled receptors (GPCRs) that activate intracellular second messenger cascades, ultimately leading to neurotransmitter release. Taste information travels via cranial nerves VII (facial), IX (glossopharyngeal), and X (vagus) to the gustatory cortex.
B. Olfaction (Smell)
The olfactory epithelium, located in the upper nasal cavity, contains approximately 10-20 million olfactory receptor neurons. Each neuron expresses a single type of odorant receptor, drawn from a repertoire of roughly 400 receptor genes in humans (approximately 1,000 in mice). When odorant molecules dissolve in the nasal mucus and bind to GPCRs on the cilia of olfactory neurons, a signaling cascade is activated: the G protein Golf stimulates adenylyl cyclase, which produces cAMP, which opens cation channels, depolarizing the neuron and triggering an action potential. Axons of olfactory neurons pass through the cribriform plate of the ethmoid bone and synapse in the olfactory bulb at structures called glomeruli, from which signals travel to the olfactory cortex. Notably, olfaction is the only sense that projects directly to the cortex without an obligatory thalamic relay, though the thalamus is involved in conscious olfactory perception. The brain discriminates among thousands of odors through combinatorial coding, in which each odorant activates a unique combination of receptor types.
V. Skeletal Muscle Structure and the Sliding Filament Model
Skeletal muscle is organized in a precise hierarchy: whole muscles are composed of fascicles (bundles of fibers), each fascicle contains individual muscle fibers (cells), each fiber contains myofibrils, and each myofibril is a chain of sarcomeres -- the basic contractile units. A muscle fiber is a multinucleated syncytium formed by the fusion of myoblasts during development. Its plasma membrane, the sarcolemma, is invaginated by T-tubules (transverse tubules) that carry action potentials deep into the fiber. The sarcoplasmic reticulum (SR), a specialized form of smooth endoplasmic reticulum, stores and releases calcium ions.
The sarcomere -- the repeating unit between two Z-lines -- is the fundamental unit of contraction. Thin filaments (actin, decorated with the regulatory proteins tropomyosin and troponin) extend inward from each Z-line. Thick filaments (myosin, bearing globular heads with ATPase activity) occupy the center. Several bands and zones provide landmarks: the A band spans the full length of the thick filaments and does not change during contraction; the I band, containing thin filaments only, shortens during contraction; the H zone at the center of the A band, containing thick filaments only, also shortens; and the M-line at the midpoint anchors the thick filaments.
The sliding filament model explains muscle contraction: the thin filaments slide past the thick filaments, drawing the Z-lines closer together and shortening the sarcomere. The filaments themselves do not shorten -- they slide. This sliding is powered by the cross-bridge cycle of myosin heads. In step one, ATP binds to the myosin head, causing it to release from actin. In step two, ATP hydrolysis cocks the myosin head into a high-energy position, with ADP and inorganic phosphate (Pi) still bound. In step three, the myosin head binds to actin, forming a cross-bridge; Pi is released, triggering the power stroke in which the myosin head pivots and pulls the thin filament toward the M-line, after which ADP is released. The cycle repeats as long as ATP is available and calcium is present.
VI. Excitation-Contraction Coupling
The neuromuscular junction (NMJ) is the synapse between a motor neuron and a skeletal muscle fiber. When an action potential arrives at the motor neuron terminal, voltage-gated Ca2+ channels open and calcium enters, triggering the release of acetylcholine (ACh) into the synaptic cleft. ACh binds to nicotinic receptors -- ligand-gated Na+ channels -- on the motor end plate of the muscle fiber, producing an end-plate potential that depolarizes the sarcolemma to threshold and initiates an action potential. Acetylcholinesterase (AChE) in the cleft rapidly degrades ACh to terminate the signal.
Excitation-contraction coupling links the electrical signal to mechanical contraction. The action potential propagates along the sarcolemma and into the T-tubules. The voltage change in the T-tubules activates dihydropyridine receptors (DHP receptors), which are voltage sensors physically coupled to ryanodine receptors (RyR) on the sarcoplasmic reticulum. When the DHP receptors change conformation, they mechanically open the ryanodine receptors, releasing stored Ca2+ into the cytoplasm. Calcium binds to troponin C on the thin filament, inducing a conformational change that shifts tropomyosin away from the myosin-binding sites on actin, exposing them and allowing cross-bridge cycling to begin. Relaxation occurs when calcium is pumped back into the SR by the SERCA pump (Ca2+-ATPase), tropomyosin slides back to cover the binding sites, and contraction ceases.
<image>A multi-panel diagram of skeletal muscle organization and contraction. Panel A: Hierarchical structure from whole muscle to sarcomere — a muscle is shown with one fascicle pulled out, revealing individual muscle fibers (cells), then one fiber is expanded to show myofibrils within, and a single myofibril is expanded to show the banding pattern of sarcomeres. Panel B: A detailed sarcomere diagram showing two Z-lines at either end, thin filaments (actin) extending inward from each Z-line, thick filaments (myosin) in the center, the A band spanning the thick filaments, the I band at each end (thin filaments only), the H zone in the center (thick filaments only), and the M-line at the midpoint. A comparison of the sarcomere in relaxed versus contracted state shows that the I band and H zone shorten while the A band remains constant. Panel C: The cross-bridge cycle shown in four sequential steps — (1) ATP binding and myosin release from actin, (2) ATP hydrolysis and myosin head cocking, (3) cross-bridge formation and power stroke with Pi release, (4) ADP release and myosin tightly bound to actin awaiting new ATP. Arrows connect the steps in a circular cycle.</image>
VII. Muscle Fiber Types and Motor Units
Skeletal muscle fibers are classified into three types that differ in their metabolic and contractile properties. Slow-twitch (Type I) fibers rely on oxidative metabolism, are rich in mitochondria and myoglobin (giving them a red color), resist fatigue, and are recruited for sustained activities such as maintaining posture and endurance running. Fast-twitch oxidative-glycolytic (Type IIa) fibers have intermediate characteristics, with both aerobic and anaerobic capacity and moderate fatigue resistance. Fast-twitch glycolytic (Type IIx/IIb) fibers depend primarily on anaerobic glycolysis, fatigue quickly, but have the largest diameter and generate the most powerful contractions for short bursts of activity such as sprinting and weightlifting. While the proportion of fiber types is largely genetically determined, training can shift fibers toward more oxidative characteristics, particularly among Type IIa fibers.
A motor unit consists of a single motor neuron and all the muscle fibers it innervates. Small motor units, with only a few fibers per neuron, enable fine motor control in structures like the eye muscles and fingers. Large motor units, innervating hundreds of fibers, power the gross movements of muscles like the quadriceps. The nervous system increases muscle force through recruitment -- activating additional motor units according to the size principle, in which small motor units are recruited first and larger ones are added as greater force is needed. Muscle tension is also modulated by stimulus frequency: a single stimulus produces a twitch, rapid repeated stimuli produce summation as contractions build upon one another, and very high-frequency stimulation produces tetanus -- a sustained maximal contraction that progresses from incomplete to complete tetanus as stimulus frequency increases.
