Intro to Neuro Chapter 2

What is the Sensorimotor system, and why is it important?

A network of sensory, motor, and CNS components integrates sensory input with motor output. It uses information such as touch, balance, and vision to plan, execute, and control movements and interact with the environment.

Sensory neurons

Sensory (afferent) neurons respond to stimuli and carry information toward the CNS these are Excitatory. Sensory signals enter through dorsal roots, and the Sensory neuron cell bodies are in dorsal root ganglia.

Motor neurons

Motor (efferent) neurons contact muscles or glands and carry motor instructions outward. Excitatory. ; Motor signals leave through ventral roots.

Relay interneurons

integrate and pass signals between neurons, mostly in the CNS. Inhibitory.

Which brain regions are involved in the Sensorimotor system

Cortical regions plan and execute movement and process tactile, visual, and auditory inputs. The cerebellum, basal ganglia, thalamus, brainstem, and spinal cord also participate.

Somatosensation

The somatosensory system detects and processes touch, pain, and temperature through different sensory nerve fibers and skin receptors

Types of receptors on the skin

Mechanoreceptors detect touch, vibration, pressure, and stretch. Thermoreceptors detect temperature changes; nociceptors respond to pain; pruriceptors trigger itch. The latter three use free nerve endings.

Mechanoreceptors detect

touch, vibration, pressure, and stretch

Thermoreceptors detect

temperature changes

nociceptors respond

to pain

pruriceptors trigger

itch

Which receptors use free nerve endings?

Thermoreceptors, Nocicreceptors, Pruriceptors

Touch receptors and what they respond to

Merkel receptors detect fine texture; Meissner corpuscles and hair follicle receptors detect light touch; Pacinian corpuscles detect deep pressure and vibration; Ruffini endings detect skin stretch; free nerve endings detect crude touch. Receptor type and density determine fine-detail discrimination and touch localization.

Merkel receptors detect

fine texture

Meissner corpuscles detect

light touch

hair follicle receptors detect

light touch

Pacinian corpuscles detect

deep pressure and vibration

Ruffini endings detect

skin stretch

free nerve endings detect

crude touch

Sensory neuron cell bodies are in

the dorsal root ganglia.

Pain and temperature and how they use free nerve endings

Thermoreceptors are specialized free nerve endings that detect temperature;

Nociceptors detect pain.

Transient Receptor Potential (TRP) channels

TRP channels are ion channels on free nerve endings that function as temperature sensors. The slides associate TRPM8 with cool temperature and C fibers, and TRPV2 with high, noxious heat and A-delta fibers. The activation examples include mint/menthol and capsaicin from peppers.

Somatosensory transmission

Skin stimuli generate graded receptor potentials. Reaching threshold triggers an all-or-none action potential. Stronger stimuli increase firing frequency, recruit more neurons, and activate neurons with different intensity ranges (range fractionation). Duration is represented by activity over time: phasic receptors adapt rapidly, while tonic receptors adapt slowly.

Somatosensory pathways to the brain (Dorsal column, Spinothalamic tract)

The dorsal column pathway carries touch and vibration and crosses at the medulla.

The spinothalamic tract carries pain and temperature and crosses upon entering the spinal cord. Both pass through the thalamus and end in the primary somatosensory cortex.

The primary somatosensory cortex and its characteristics

S1 is in the postcentral gyrus and receives information from the opposite (contralateral) side of the body. Different body regions map to different parts of S1. More sensitive regions occupy larger cortical areas; this body map is the sensory homunculus.

The somatosensory cortex’s ability to reorganize

After hand amputation, neighboring body representations expand into the cortical area that previously represented the hand.

Somatosensory disorders (Congenital insensitivity to pain, Chronic pain, Hypersensitivity to touch, etc.)

Congenital insensitivity to pain is associated with loss-of-function sodium-channel mutations in pain fibers in dorsal root ganglia; gain-of-function mutations can produce severe burning pain. Chronic pain examples include nociceptive pain from tissue damage, neuropathic pain from nerve damage, and nociplastic pain from altered pain processing. Touch hypersensitivity produces stimulus avoidance, such as distress with hair washing or certain textures. Hyposensitivity produces stimulus seeking, such as craving touch or pinching/biting oneself.

Congenital insensitivity to pain

associated with loss-of-function sodium-channel mutations in pain fibers in dorsal root ganglia; gain-of-function mutations can produce severe burning pain.

Congenital insensitivity to pain is associated with

loss-of-function sodium-channel mutations in pain fibers in dorsal root ganglia.

Touch hypersensitivity produces

stimulus avoidance, such as distress with hair washing or certain textures.

Hyposensitivity produces

stimulus seeking, such as craving touch or pinching/biting oneself.

gain-of-function mutations can produce

severe burning pain.

Chronic pain examples include ______ pain from tissue damage, ______ pain from nerve damage, and ______ pain from altered pain processing.

nociceptive, neuropathic, nociplastic

Components of the neuromuscular system and their characteristics (Brain, Spinal cord, and Skeletal system and muscles)

The cortex plans, initiates, and executes motor commands.

Basal ganglia and cerebellum modulate actions.

The brainstem integrates commands and sends them to the spinal cord.

The spinal cord carries brain signals to skeletal muscles and can respond directly to sensory inputs in reflexes.

The skeleton and muscles power movement.

The brain regions involved in motor control

Prefrontal cortex decides whether/when to move; posterior parietal cortex integrates sensory information for planning.

Premotor cortex plans using external sensory information; supplementary motor area plans learned, complex sequences; M1 initiates and executes commands.

Basal ganglia (caudate, putamen, globus pallidus, substantia nigra, and subthalamic nucleus) regulate initiation/ending, amplitude, direction, smoothness, and learned movements.

The cerebellum supports error correction and motor learning through inhibitory Purkinje-cell output. The brainstem relays integrated commands to the spinal cord.

The steps of executing a motor plan

1. Determine the current state of the body.

2. Decide whether to move.

3. Select a movement plan.

4. Load the plan.

5. Execute the plan.

6. Use feedback to assess progress and whether the plan needs to change.

Motor control pathways (Pyramidal tracts)

Pyramidal pathways originate in primary motor cortex, pass through the medullary pyramids, and control voluntary movement. They include corticospinal and corticobulbar tracts.

Motor control pathways (Extrapyramidal tracts)

Extrapyramidal pathways originate in the brainstem and do not pass through the pyramids: rubrospinal supports fine movement; reticulospinal supports muscle tone and automatic breathing; vestibulospinal supports balance/posture; tectospinal supports head-eye-body coordination and saccades.

Corticospinal tract vs. Corticobulbar tract

Corticospinal: cortex → spinal cord/spinal nerves → muscles, for voluntary skeletal movement.

Corticobulbar: cortex → brainstem/cranial nerves → muscles, for voluntary face, head, and neck movement.

Upper motor neurons vs. Lower motor neurons

Upper motor neurons originate in cortex, descend to brainstem or spinal cord, synapse on lower motor neurons, and use glutamate.

Lower motor neurons originate in brainstem or spinal cord ventral horn, project directly to muscles or glands, and use acetylcholine.

Their subtypes are alpha, gamma, and beta.

How skeletal muscles facilitate movement

Skeletal muscles move bones and consist of bundles of muscle fibers.

Each fiber is innervated by one motor neuron; one motor neuron branches to many fibers.

Fewer fibers per neuron permit precise movements; more fibers permit powerful movements.

At the neuromuscular junction, acetylcholine causes muscle-membrane depolarization and an action potential.

This triggers calcium release so protein filaments slide and the muscle contracts.

How sensory feedback guides muscle actions (Muscle spindles, Golgi tendon organs)

Muscle spindles detect muscle length/stretch; Golgi tendon organs detect tension.

Sensory neurons send feedback to the brain, which compares actual and intended movement and adjusts contraction or relaxation.

Excessive tension can trigger protective reflex action, such as dropping an overly heavy box.

Cortical homunculus (Motor vs. Somatosensory)

The motor homunculus maps body regions in the precentral gyrus; the sensory homunculus maps them in the postcentral gyrus.

Motor representation emphasizes regions requiring fine control, while sensory representation emphasizes regions with greater sensitivity.

The motor cortex’s ability to reorganize

This part of the brain can reorganize with experience. Professional musicians have larger ____ cortexes and larger finger representations than non-musicians.

Pain withdrawal reflex

polysynaptic: pain receptors activate a sensory neuron, spinal interneurons activate flexors and relax extensors, and the brain receives pain information afterward.

The patellar reflex

monosynaptic in its main pathway: a tendon tap stretches quadriceps, muscle spindles activate sensory neurons, and these directly activate spinal motor neurons to contract quadriceps. A sensory branch activates an inhibitory interneuron to relax hamstrings.

ALS

motor-neuron degeneration causes weakness, twitching/stiffness, loss of motor control, swallowing and respiratory problems.

Motor-cortex injury

opposite-side weakness, impaired fine movements, clonus, spasticity, and speech problems.

Parkinson’s disease

loss of substantia nigra dopamine cells causes tremor, bradykinesia, shuffling gait, and postural instability

Cerebellar ataxia

poor coordination, unsteady walking, tremor, speech problems, and nystagmus

The spinal-cord injury slide lists flaccid paralysis and loss of reflexes, sensation, and muscle strength below the injury.

Myasthenia gravis

antibodies against ACh receptors cause weakness, drooping eyelids, blurred/double vision, and swallowing, breathing, and speech difficulties.

Outer ear

the pinna captures sound and the ear canal guides it to the eardrum

Middle ear function

the eardrum vibrates; malleus, incus, and stapes concentrate/amplify vibrations onto the oval window; the Eustachian tube equalizes air pressure. Tensor tympani and stapedius dampen loud sounds.

Inner ear

the fluid-filled cochlea and hair cells convert vibrations to electrical signals; CN VIII carries them to the brain. Vestibular structures detect head movement for balance.

How sound waves are converted to electrical signals in the inner ear

Oval-window vibration moves cochlear fluid, bending hair-cell stereocilia. Deflection that pulls tip links opens mechanically gated channels: K+ enters, depolarization opens voltage-gated Ca2+ channels, and Ca2+ entry triggers glutamate release onto auditory sensory neurons. Deflection in the opposite direction closes channels and hyperpolarizes the cell. Spiral ganglion neurons carry signals through CN VIII.

The vestibular system in the inner ear and its function and structure (Semicircular canals, utricle, and saccule)

Three fluid-filled semicircular canals lie in three planes of head movement.

Each ampulla contains receptors for rotation/angular acceleration.

The utricle and saccule are two bulbs with receptors that signal acceleration and deceleration.

Fluid movement bends stereocilia, activating CN VIII; signals go to brainstem vestibular nuclei or directly to cerebellum.

The vestibulo-ocular reflex moves eyes opposite head movement to stabilize the image.

Auditory pathways to the brain (Cranial nerve, Brainstem, Thalamus, Cortex)

Auditory nerve (CN VIII) → cochlear nucleus in pons → superior olivary nucleus in pons → inferior colliculus in midbrain → medial geniculate nucleus of thalamus → auditory cortex in temporal lobe.

Brainstem processing analyzes basic frequency/intensity; superior olive receives input from both ears; thalamus relays signals to cortex for interpretation.

The location, structure, and function of the Auditory cortex.

Auditory cortex is in the temporal lobe.

Primary auditory cortex (A1/core) processes basic sound detection; secondary auditory cortex processes complex sounds, including speech, music, and spatial location.

Neurons have preferred frequencies/tuning curves and are organized tonotopically, so different cortical regions process different frequencies.

Place coding vs. Temporal coding

Place coding identifies pitch from the cochlear location of maximum activity: low frequencies peak near the apex and high frequencies near the base. Temporal coding uses firing timing: neurons phase-lock to lower-frequency waves. At higher frequencies, individual neurons skip cycles but fire at a consistent phase, producing a population volley pattern.

How the brain locates sound (Intensity differences, Timing differences)

The brain compares sound intensity and arrival time between the two ears. Brainstem neurons perform binaural comparisons; the superior olive is the main localization area. Auditory cortex combines these cues to represent sound location.

How does the brain analyze complex sound (Ventral stream)

The ventral “what” stream projects to anterior temporal regions and supports sound identity, speech recognition, and meaning.
Structured acoustic patterns, attention, and prior knowledge help distinguish speech from noise.

How does the brain analyze complex sound (Dorsal stream)

The dorsal “where/how” stream projects toward posterior temporal and parietal regions and supports localization, spatial processing, and sensorimotor integration.
Structured acoustic patterns, attention, and prior knowledge help distinguish speech from noise.

The 3 categories of hearing loss and characteristics of each

Conductive loss: outer/middle-ear disorders prevent sound from reaching the cochlea; otitis media can cause fluid buildup and temporary muffled hearing.

Sensorineural loss: cochlear hair-cell or auditory-nerve damage, including congenital, noise-induced, and age-related loss; tinnitus causes persistent ringing.

Central loss: damage to ascending brain pathways, brainstem, or cortex. Pure word deafness disrupts spoken-language comprehension while preserving nonverbal sound recognition; auditory agnosia prevents recognition of verbal or nonverbal sounds despite normal pure-tone hearing

Anatomy of the tongue (Papillae, Taste buds, Facial nerve, etc.)

Fungiform papillae occur near the tip/sides, circumvallate papillae form a V near the back, foliate papillae form posterior side folds.

Filiform papillae have no taste buds.

The tongue has 2,000–8,000 taste buds, each with 50–150 receptor cells.

Microvilli contact tastants; receptor cells synapse with gustatory sensory neurons and are replaced every 1–2 weeks.

CN VII carries taste from the anterior two-thirds; CN IX carries it from the posterior third.

The 5 basic tastes the tongue can detect

Sour, bitter, salty, sweet, and umami. All tongue areas can detect all five, although differing receptor-cell abundance makes some areas more sensitive to particular tastes.

Transduction of taste

Salty and sour tastants act on ion channels, depolarize taste receptor cells, and lead to serotonin (5-HT) release.

Sweet, bitter, and umami act on G-protein-coupled receptors and lead to depolarization and ATP release.

Neurotransmitter release activates gustatory sensory neurons.

Pathways of the human gustatory system (The gustatory cortex)

Taste receptor cells → CN VII, IX, X → solitary nucleus in medulla → ventral posteromedial thalamic nucleus → gustatory cortex in anterior insula. Gustatory cortex combines taste with smell and internal hunger/satiety signals, and projects to amygdala and hypothalamus to link taste with emotion, memory, and metabolic regulation.

Purposes of Olfaction

Olfaction identifies the identity, concentration, and quality of chemical odors. It guides food/mate searches, helps avoid predators and danger, influences reproductive/endocrine functions and mother-child interactions, and provides pleasure.

Anatomy of the nose

Olfactory receptor neurons in the olfactory epithelium detect odors with receptors on dendritic cilia.

Their axons form CN I and pass through holes in the cribriform plate to the olfactory bulb. Mitral cells are the bulb’s main output neurons;

the olfactory tract carries their information onward.

Most receptor neurons express one receptor type and are replaced every 1–2 months from basal stem cells.

Odorants and the transduction of odor

Odorants are chemical ligands for odor receptors;

multiple odorants combine to produce a scent.

Odorant binding activates a GPCR → Golf → adenylyl cyclase III → cAMP. cAMP opens Na+/Ca2+ channels; ion entry depolarizes the neuron. Ca2+ also opens Cl− channels, and Cl− exits to increase depolarization. Reaching threshold triggers action potentials and eventual glutamate release onto mitral cells.

Pathways of the human olfactory system

Olfactory receptor neurons → CN I → mitral cells in olfactory bulb → olfactory tract → piriform (primary olfactory) cortex → higher regions including orbitofrontal cortex, amygdala, hippocampus, hypothalamus, thalamus, and anterior cingulate cortex.

Odorant perception

Receptor neurons vary in which odorants activate them and in response strength.

Axons expressing the same receptor type converge at glomeruli onto mitral cells.

Combinations of activated and inactive glomeruli distinguish scents; increasing odorants activates more glomeruli.

Pleasant odors strongly activate orbitofrontal and anterior cingulate cortices; unpleasant odors strongly activate anterior cingulate cortex.

Genetic differences changing an individual’s sense of smell and taste

OR6A2 variation affects detection of aldehydes in cilantro and can make cilantro taste soapy.

OR2M7 variation affects detection of methanethiol, associated with the sulfur odor of urine after eating asparagus.

Ageusia

complete loss of taste; texture and temperature remain detectable. Listed causes include viral illness, sinus infection, cranial-nerve injury, medications, nutritional deficiencies, diabetes, hypothyroidism, and oral/gum problems

Anosmia

complete or partial loss of smell. Conductive causes include nasal blockage, infection, allergies, and polyps; sensorineural causes include head trauma, neurodegenerative disease, toxins, genetics, and aging.

Phantosmia

phantom odors and can involve abnormal peripheral or central neural activity

Light

electromagnetic radiation visible to the eyes. It travels as electric and magnetic waves described by wavelength, frequency, and amplitude. Shorter wavelengths have higher frequency/energy; amplitude represents intensity or brightness.

The electromagnetic spectrum

includes all electromagnetic radiation, ordered by wavelength and frequency. Visible light is a small part of it. Longer wavelengths have lower frequency/energy; shorter wavelengths have higher frequency/energy

How does light travel

In a vacuum, light rays travel in straight lines. Interaction with matter can cause reflection, absorption, or refraction. Refraction bends light rays to form images in the eye.

Anatomy of the eye

The outer protective layer includes sclera and cornea;

the middle vascular layer supplies nutrients and controls light entry/color; the inner neural layer is retina. Vitreous humor is a clear gel that maintains shape and contains debris-removing phagocytes. Aqueous humor is watery and supplies cornea/lens nutrients.

The pupil admits light, iris regulates pupil size, lens focuses light, ciliary muscles change lens shape, retina converts light into signals, and optic nerve (CN II) carries them to the brain.

How do eyes capture and focus light

Cornea and lens refract light to a focal point on retina. Ciliary muscles change lens shape to accommodate near/far objects; pupils constrict in bright light and dilate in darkness. Retinal images are upside down and curved, but the brain interprets them upright. Myopia focuses light before retina; hyperopia behind it; presbyopia results from lens stiffening.

The retina and its characteristics and structure

• contains light-sensitive CNS tissue at the back of the eye.

  • Its photoreceptors convert light to electrical signals.

• The Fovea is the central pit with highest acuity and dense cones;

• The macula is the central region of high acuity.

• Optic disc is where optic-nerve axons exit; it has no photoreceptors and creates the blind spot.

The 5 types of “neurons” in the retina

Photoreceptors detect light. Bipolar cells relay signals from photoreceptors to ganglion cells.

Horizontal cells regulate photoreceptor/bipolar inputs and contribute to lateral inhibition.

Amacrine cells regulate ganglion cells through contacts with bipolar and ganglion cells.

Retinal ganglion cells are the output neurons whose axons form CN II.

The slides contrast graded potentials in the other cell types with action potentials in ganglion cells.

Rods

about 120 million, concentrated peripherally; rhodopsin; highly light-sensitive; dim-light vision, no color, low acuity.

Cones

about 6 million, concentrated in fovea; iodopsin; bright-light vision, color, high acuity. S, M, and L cones respond to short/blue, medium/green, and long/red wavelengths. Photopigments lie in outer segments; inner segments contain mitochondria; photoreceptors release glutamate onto bipolar cells.

Color blindness

Missing or damaged cone cells impair color detection.

Protanopia affects long/red wavelengths;

deuteranopia affects medium/green wavelengths;

tritanopia affects short/blue wavelengths and produces rare blue-yellow color blindness.

The slides illustrate screening with the Ishihara test.

Phototransduction (In the dark, exposure to light)

In darkness, cGMP keeps Na+/Ca2+ channels open, maintaining depolarization (about −40 mV) and glutamate release. Light activates photopigment signaling that lowers cGMP and closes these channels. The photoreceptor hyperpolarizes and releases less glutamate.

Bipolar cells vs. Retinal ganglion cells

Bipolar cells relay photoreceptor signals to retinal ganglion cells using graded potentials. Ganglion cells generate action potentials, form the optic nerve, and send retinal output toward the thalamus. Convergence of multiple photoreceptors onto downstream cells combines their information.

On-center vs. Off-center bipolar cells

ON-center bipolar cells are inhibited by photoreceptor glutamate in darkness and become depolarized when light reduces glutamate. OFF-center bipolar cells are excited by glutamate through AMPA receptors in darkness and become less active when light reduces glutamate.

On-center vs. Off-center ganglion cells

ON-center ganglion cells increase firing for light in the receptive-field center and are inhibited by light in the surround. OFF-center cells show the opposite pattern. Center-surround organization and lateral inhibition emphasize contrast and edges.

Where visual information is processed

Visual information is processed in the visual cortex of the occipital lobe.

Visual pathways to the brain (Visual signals, Thalamus, Cortex

Retinal ganglion axons form optic nerves → optic chiasm → optic tracts → lateral geniculate nuclei of thalamus → optic radiations → visual cortex. Nasal retinal fibers cross at the chiasm; temporal retinal fibers remain on the same side. Each hemisphere processes the opposite visual field.

The Lateral geniculate nucleus and its function and structure

LGN relays retinal input to visual cortex.

Its six layers include ventral magnocellular layers 1–2 (large neurons) and dorsal parvocellular layers 3–6 (small neurons).

M-type retinal ganglion cells supply M layers; P-type supply P layers. Ipsilateral eye input reaches layers 2, 3, 5; contralateral input reaches 1, 4, 6.

M layers project to cortical layer 4Cα and process speed/direction; P layers project to 4Cβ and process detailed shape, size, and color.

Primary visual cortex (V1) vs. Secondary visual cortex (V2-5)

V1 is the first major cortical visual-processing area and processes edges, lines, orientation, and location.

Secondary visual cortex (V2–V5) combines features into shapes, faces, and objects and processes complex motion and color.

2 major types of neurons in the primary visual cortex

Simple cells and complex cells

classified by their receptive-field properties.

Simple cells vs. Complex cells

Simple cells respond best to a bar with a particular orientation at a particular location.

Complex cells respond to a preferred orientation across different positions and detect movement direction.

Simple cells receive LGN input; complex cells receive input from simple cortical cells.

The organization of the primary visual cortex

Ocular-dominance columns prefer input from one eye. Orientation columns prefer a particular line orientation.

Blobs respond strongly to particular colors.

Neurons encountered perpendicular to the cortical surface share similar receptive-field/orientation properties.

This organization supports parallel processing of visual features.

The function of V2 in the Secondary Visual cortex

V2 combines edges/lines into shapes, patterns, and contours.

The function of V3 in the Secondary Visual cortex

processes overall shape/form.