CNS S2 Flashcards
External ear anatomy
Pinna, ear canal, tympanic membrane
Inner ear anatomy/function of each
Cochlea (hearing), vestibular apparatus (equilibrium)
Frequency and hearing
Low-frequencies are low-pitched sounds, high-frequencies are high-pitched
What range of sounds do humans hear (Hz)
16-20,000 Hz (10 octaves)
Amplitude and hearing
Amplitude determines loudness; the larger the amplitude, the louder the sound
How do soundwaves produce sound
Canal > vibrates eardrum > vibrates malleus bones > incus moves stapes > oval window > cochlea > round window
Oval window anatomy
A membrane between the middle and inner ear (cochlea). Stapes pushes against the window
Ossicles
Smallest bones in the body and carry vibrations from the eardrum to the oval window
Organ of Corti
Inside the cochlear duct in the vestibular and tympanic duct. Has receptor cells for hearing
Organ of Corti receptor cells name
Hair cells (mechanoreceptors)
Hair cells
Epithelial cells with 50-100 stiff stereocilia which extend to the tectorial membrane
Hair cells mechanism
Cilia bend towards longest cilium, depolarizing neurons to release a neurotransmitter to activate primary sensory neurons. Axons from these form the auditory nerve
Basilar membrane
Narrow and stiff membrane near the round and oval windows. Helicotrema end (wider and flexible at one end)
Basilar membrane function
Responds to different frequencies. High-frequency waves displace membrane at oval window, low-frequency waves at other end
Auditory signal pathway
Auditory nerves > cochlear nuclei in medulla > midbrain > medial geniculate nucleus in thalamus > auditory cortex in temporal lobe
How is loudness coded
By firing frequency (louder sounds have faster firing)
Conductive hearing loss
Hearing can’t be transmitted through the external or middle ear
Sensorineural hearing loss
Damage to hair cells or elsewhere in the inner ear
Central hearing loss
Damage to the to the cortex or pathways from cochlea to cortex. Trouble with interpreting sounds, not detecting
Rinne test
Tuning fork held against mastoid bone and then beside ear to determine where it’s louder.
Rinne test results
If louder through bone, there is conductive loss since sound can be transmitted through the bone
Weber test
Tuning fork held against forehead and midline to see which ear is louder
Weber test results
Louder in good ear with sensorineural, louder in bad ear with conductive
Vestibular apparatus and equilibrium
Utricle and saccule contain hair cells that activate with head tilt. Semicircular canals contain fluid to detect head rotation
Equilibrium pathway
Vestibular hairs > primary sensory neurons in vesitbular nerve > cerebellum OR synapse in medulle OR thalamus > cortex
Somatic senses
Touch, temperature, proprioception (body position), nociception (pain/itch)
Free nerve ending receptors
Detect mechanical stimuli, temperature, chemicals
Merkel receptors
Mechanoreceptor nerve endings in contact with epithelial (Merkel) disks
Encapsulated receptors
Mesinner and Pacinian corpuscles. Sheathed in connective tissue
Merkel disks
At the bottom of the epidermis. Sensitive to deformation, signal contact. More tonic than phasic
Meissner Corpuscles
Top of dermis mainly in erogenous zones. Detect sideways shearing. Phasic
Pacinian Corpuscles
Deep in dermis. Sense tiny, quick, displacements. Phasic
Thermoreceptors
Free nerve endings with more cold than warm receptors. Phasic-tonic
Nociceptors
Free nerve endings that respond to noxious, harmful stimuli (ex, chemicals from damaged cells, heat)
Small fibre afferents
C and A-delta which come from free nerve endings. C fibres are unmyelinated (slow pain), A-delta’s are thicker/myelinated (fast pain)
Long fibre afferents
A-delta. Come from Merkel disks or encapsulated mechanoreceptors. Myelinated
Long fibre projection
upward upon reaching spinal cord, run ipsilaterally to the medulla tracts (dorsal columns) Synapse in medulla
Small fibre projection
Synapse directly/via interneurons and motor neurons or on dorsal-horn neurons who run in spinothalamic tracts
Large fibre main functions
Provide feedback to the brain, especially motor cortex to manipulate objects
Small fibre main functions
Evoke simple responses to specific stimuli. Don’t need immediate input from the brain
Thalamus to the cortex
spinal cord/head > ventroposterolateral nucleus of thalamus/ventroposteromedial nucleus > primary somtaosensory cotex
Nociceptors and TRP ion channels
Transient receptor potential (TRP channels) which are also found in thermoreceptors
TRPV1 channels
Vanilloid receptors which respond to damaging heat/chemicals including capsaicin in chili
TRPM8 channels
Respond to cold and menthol in mints
Nociceptive signals
Evoke responses from the CNS and reach the limbic and hypothalamus. Descending pathways in thalamus can block cells in spinal cord
Referred pain
Pain in internal organs that is felt on the body surface
Pain gated by A-beta activity
C fibres in dorsal horn contact secondary neurons which are inhibited by A-fibre activity
Acetylsalicylic acid
Asprin. Inhibits prostaglandins and inflammation, slowing transmission of pain
Opioids
Decrease neurotransmitter release from primary sensory neurons and postsynaptically inhibits secondary sensory neurons
Smell and taste similarities
Forms of chemoreception
Olfactory epithelium
Contains olfactory receptors at the top of the nasal cavity
Olfactory epithelium pigment
Richness of colour is correlated with olfactory sensitivity
Olfactory receptor cells
Contain a single dendrite that extends to the epithelium to form non motile cilia that catch odorant molecules
How many primary odors do we have
About 400 as we have about 400 kinds of receptor cells
Odorant molecule binding
Binds to a receptor, activating G proteins, increasing cAMP to open cation channels for depolarization
How many cells must react before smells are sensed
40 cells, or, 40 odorant molecules are required
Olfactory receptor cell properties
Pinocytotic, short-lived, send axons to the brain through holes in the cribriform plate, project to olfactory bulb
Olfactory bulb
An extension of the cerebrum and lies on the underside of the frontal lobes. Projects directly to olfactory cortex (frontal/temporal)
Limbic system
Linked to motivation and emotion. Made up of hippocampus, amygdala, cingulate gyrus. Bulb projects here
Vomeronasal organ (VNO)
Found in rodents to respond to sex pheromones. Disappears during fetal development in humans
Taste buds
Live 10 days, we have around 5000. Each contain 100 receptor cells (epithelial cells) and contact oral cavity through taste pore
5 kinds of taste receptor cells
Sweet/umami (sugar/glu), bitter (poison), salty/sour (Na+, H+ ions)
Type I taste receptors
Sense salt
Type II taste receptors
Sense sweet, bitter and umami (release ATP which act on type III)
Type III taste receptors
May sense sour (synapse with sensory neurons, activating them with serotonin)
Membrane proteins for taste receptor cells
Sweet, umami, bitter have G protein called gustducin for ATP release. Salt/sour is not G protein linked (uses ion channels)
Taste signal pathway
Receptor cells in taste buds excite cranial nerves VII, IX, X which synapse in the medulla and thalamus to the cortex
Simple reflexes
Sensory neurons synapse with motor neurons in the spinal cord (simplest form of motor control)
Reflexes
Innate and genetically determined. Efferent signals (sensory stimulus > motor response)
Monosynaptic pathway
Sesnory afferent neuron synapses directly to motor neurons in CNS to produce response
Polysynaptic pathway
Sensory neuron synapses with interneuron that synapses with motor neurons
Stretch reflex
Subconscious (ex, posture) that is triggered by passive muscle stretch from applied load/contraction, causing active contractive
Stretch reflex properties
Essential for posture, strongest in postural muscles, multisynaptic paths, suppressed during movement
Golgi tendon reflex
Contracted, relaxed. Afferents synapse on interneurons in the intermediate zone of spinal cord to inhibit motor neurons of the same muscle
Golgi tendon stimulus/response
triggered by active tension in muscle, causing relaxation through negative feedback
Flexion withdrawal reflex
Triggered by noxious inhurt of limb, causing flexion of proximal joints to the stimulus (slow, multisynaptic)
Reciprocal inhibition of reflexes
Activation of one motor nucleus is coupled to inhibition of antagonistic motor nuclei
Patellar tendon reflex
Patellar tendon tap causes quad stretch/contraction and hamstring contraction inhibition
Cross extension flex
Step on something sharp, causing flexion on leg where the pain is an extension on other (multisynaptic)
Extensor thrust reflex
Pressure on the sole of the foot causes activation of leg extensors (walking)
Babinski sign
Extensor thrust reflexes are influenced by the corticospinal tract.
Corticospinal tract damage
Reflex pattern is switched to flexion withdrawal
Vestibulo-spinal reflex
Downward deviation of head on one side activates otolith afferents for downhill limb extension on same size
Central pattern generators
Networks of interneurons in the spinal cord and brainstem that coordinate interaction of motor groups
Leg step cycle CPGs
2 CPGs for each leg; flexor burst generators, extensor burst generators
3 properties of the leg step cycle
1) Pacemaker neurons: diffuse excitation
2) Reciprocal inhibition: only one CPG on at a time
3) Phase-dependent reflexes
Flexor burst generator activation
Activates flexor motor neuron in the ventral horn causing flexion
Which phase has a fixed duration
Flexion phase (swing phase when the leg is in the air)
Extensor burst generator activation
Activates extensor motor neuron in ventral horn for leg extension
What causes locomotion speed
Stance phase duration (extension phase)
Phase-dependent reflexes in the stance phase
Reflexes that can be modulated based on phase.
1) Stretch reflex
2) Golgi tendon reflex
3) Extensor thrust reflex
E3 (stance phase) ends when ___
1) leg is not bearing weight
2) hip is extended
3) opposite leg is in stance
What causes arm motion during walking
CPGs in the cervical cord
Arm swing mechanism
Flexion phase is synchronous with contra-lateral flexion in leg (diagonal)
What links leg and arm CPGs
The propriospinal tracts (from one segment to another)
What coordinates upper body motion and step cycles
Postural CPGs in the reticular formation of pons and medulla
What maintains head angles when walking
Visual, vestibular and proprioceptive reflexes
Complex/volitional movement
Motor output that is planned and refined by the motor cortex, basal ganglia and cerebellum. Learned
Red nucleus
Found in the midbrain for sophisticated distal limb movements
Rubrospinal cell pathway
Red nucleus > corticospinal/rubrospinal tract > midline > intermediate zone on other side
Synergy
A group of muscles contracting together for a specific purpose
Reticulospinal tract synergies
Widespread and cover over half the body for support postures
Rubrospinal tract synergies
Highly localized in specific areas such as the face/distal limb
Motor cortex location
Precentral gyrus of the central sulcus
Somatotopic organization
Mapping of the body is upside down and isn’t proportionate
Motor nuclei/motor columns
Motor nuclei are represented in columns at many loci and each muscle column is in a different neighbourhood
Motor field
How one corticospinal axon synapses with a set of motor nuclei in more than 1 segment
Somatosensory input
Only sensory input with direct access to the motor cortex after the thalamus (ex, proprioceptive)
Premotor areas
Regions projecting to the motor cortex and determine the sequence of activation of synergies
Premotor cortex vs motor cortex
Motor cortex: mainly somatosensory inputs
premotor cortex: receives all sensory input
Broca’s area
Premotor zone for sequencing language elements for speech/writing. Involves input from Wernickes
Sensorimotor cues
Sensory association areas recognize cues and send signal to frontal lobe (prefrontal and premotor cortex)
When are premotor neurons active
During the preparatory phase of the movement, not during movement
Supplementary motor area
Near the medial hemispheric wall. Controls bilateral coordination and processes internal volitional signals for movement
Cingulate motor area
Below the SMA in the cingulate sulcus. Mediates emotional movements and autonomic functions
Where are the hypothalamus and pituitary located
In the diencephalon
Hypothalamus function
Controls feeding, plasma osmolarity, body temperature, sexual response (4Fs)
Hypothalamic control
Always regulated through negative feedback
Ventromedial and lateral hypothalamic lesions
Ventromedial lesions: mice overeat and become obese
Ventrolateral lesions: mice under eat
Hypothalamic feeding control basic mechanism
Arcuate NPY cells drive feedings, arcuate POMC neurons inhibit feeding
Arcuate NPY cells functions
Release neuropeptide Y, GABA, and agouti-related peptide (AgRP)
Arc-NPY projection
Excite LH neurons, inhibit neurons in paraventricular hypothalamus (tells you you’re full)
PVN
Acts on the sympathetic nervous system to inhibit feeding
Lateral hypothalamus and feeding
Releases orexin which drives feeding and inhibits PVN
Arc-POMC mechanisms
Cleave PMC to make alpha-MSH which is released at synapses to inhibit feeding
Arc-POMC projections
Excited by sympathetic activity, inhibited by Arc-NPY. Project to hypothalamic nuclei
a-MSH function
Released from POMC to excite PVN and VMH neurons which excite the sympathetic neurons
DMH (dorsomedial hypothalamus) function
Inhibits the sympathetic system and is inhibited by Arc-POMC
Leptin production
Released into the blood by fat cells. More fat, more circulating leptin
Leptin function
Inhibits feeding centres Arc-NPY, LH, DMH and excited PVN, VMH and Arc-POMC
What tells you to end a meal
Blood glucose; excites Arc-PMC and inhibits LH. Also sensors in the stomach/intestines
Intestine sensors mechanism
Sense stretch/sugar/protein > release CCK, PYY and GLP-1 that inhibit feeding and excited the vagus nerve
Ghrelin
Released from the stomach to encourage feeding by exciting Arc-NPY, LH and inhibited PVN
Rimonabant
Blocks CB1 receptors leading to weight loss an other bad symptoms
Leptin as a weight loss drug
Ineffective as most obesity is leptin resistant
Liraglutide
A GLP-1 agonist weightloss drug
Autonomic nervous system function
Deals with fight/flight and exercise, emotion, gravity, eating, etc
Preganglionic neurons of ANS
located in CNS and project to ganglion between CNS and the target tissue (axons are autonomic ganglia)
Postganglionic neurons of ANS
Project to target tissue and receive information from preganglionic neurons
Preganglionic neurotransmitters
Sympathetic and parasympathetic neurons release ACh to nicotinic receptors
Postganglionic neurotransmitters
Sympathetic secrete norepinephrine onto adrenergic receptors. Parasympathetic secrete ACh to muscarinic receptors
Sympathetic nervous system
Preganglion in thoracolumbar spinal cord > postganglion in autonomic ganglion > short preganglion to sympathetic chain > long postganglion to effector organs
Parasympathetic nervous system
Preganglion in brainstem > long preganglion to ganglia near effector organs > short postganglion from ganglion to effector organs
Adrenal medulla
SNS neuroendocrine tissue. Preganglionic sympathetic neurons project to postganglion in medulla
Chromaffin cells
Axonless cells in the adrenal medulla that secrete epinephrine into the blood
Duel innervations
Any organ in the body is innervated by both the PSNS and SNS which have opposing effects on target organ
Neuroeffector junction
The synpase between postganglionic autonomic neurons with its target cels
Varicosities
Regions of axon swelling that contain vesicles filled with neurotransmitters
Depression and neurotransmitters
Associated with a lack of serotonin and norepinephrine
Pupillary light reflex location
organized in the pretectal area of the midbrain
Pupillary light reflex function
Light carried by the ON afferent causes pupils to constrict
Baroreflex pathway
Baroreceptors > nucleus solitary tract > VLM > sympathetic output
Baroreflex
Regulates cardiovascular centre in the VLM. Includes noradrenergic vasoconstriction (tonic)
VLM and BP
Caudal half inhibits rostral half, dropping BP and HR (opposite is also true)
Periaqueductal Gray (PAG)
Found in the midbrain and is a premotor centre for autonomic behaviour. Organized in longitudinal columns according to behaviour
Cholinergic modulatory system
Uses ACh. Involved in sleep-wake cycle, arousal, learning, sensory info
Serotonergic modulatory system
Uses serotonin. Mood, emotional behaviour, aggression, depression
Noradrenergic modulatory system
Norepinephrine. Attention, arousal, learning, memory, anxiety, pain, mood
Dopaminergic modulatory system
Dopamine. Reward and addiction
Histaminergic modulatory system
Histamine. Sleep-wake control, supports waking state, allergic reactions
Period gene
Transcribed early in the night, mRNA abundant around 10pm, and PER is abundant 6 hours later
TIM/PER general function
Form a dimer that represses transcription of tim and per. Highest at 4am and gradually falls
TIM/PER mechanisms
Block CLK-CYC binding to DNA to repress per and tim transcription
CLK-CYC
Binds DNA during the day to stimulate per and tim transcription.
Doubletime gene
DBT binds PER, causing breakdown so that levels rise slower. Results in a lengthened cycle of 24 hours
Mammalian cycle-regulation
PER forms a dimer with CRY instead ofTIM. clk, bmal1 and ck1e instead of clk, cyc, dbt
Zeitgeber
Cues that keep cellular clocks in sync. Light, temp, feeding, social interaction, exercise
Master clock
Suprachiasmatic nucleus in the hypothalamus above the optic chiasm. Light sensed by melanopsin is sent here
Entrainment
The process of nudging the clock into synchrony with another rhythm
Melatonin
Secreted by the pineal body at the back of the diencephalon at night. Acts on melatonin receptors in SCN to reset the clock
SCN adjustment
Adjusts itself slowly to a new schedule of light by an hour a day
Chronotypes
Different sleep times within diurnal and nocturnal animals. (ex, early birds/night owls)
SCN in the day
Excited LH neurons to release orexin for arousal
SCN at night
MCH is released from the LH to induce sleep
Adenosine and sleep
Adenosine is created by ATP breakdown and increased during the day
REM
30-40Hz brainwaves, vanished muscle tone, dreaming.
When does REM occur
First stage after 90 minutes for 10 minutes. Gets longer throughout the night
NREM
2-4Hz brain waves, dreamless, 3 stages
What happens when you sleep after sleep deprevation
You first catch up on NREM but then will have more REM than usual the nights after
3 types of muscle
Skeletal muscle, smooth muscle, cardiac muscle
Skeletal muscle
activated by the somatic nervous system. Contractile filaments are in sarcomeres are striated. Well developed sarcoplasmic reticular
Motor units
motor neurons + associated muscle fibres
Neuro-muscular junction
Chemical signalling between motor neurons and skeletal muscle. The synapse between motor neurons and muscle fibres
Muscle anatomy
Made up of fascicles
Muscle fibres
Made up of myofibril which run the entire length of the muscle
T-tubule system
Invagination of the sarcolemma into the muscle fibre. Transmits APs into the muscle
Sarcoplasmic reticulum
intracellular calcium storage. Assists with reaction time
Slow-twitch oxidative fibres
Slow contraction but with many mitochondria for oxidative metabolism. Non-fatiguing, low levels of force. Innervated by small diameter motor neurons
Fast-twitch glycolytic fibres
Fast twitch time, large amounts of tension, rapid fatigue, few mitochondria. Innervated by large diameter motor neurons
NMJ anatomy
Terminal bouton is the axon terminal and motor end plate is the specialized muscle membrane
Motor neuron mechansism
Excited by the CNS for contraction and release ACh. Activation depends on summation of EPSPs and IPSPs
Nicotinic receptor blocker
Prevents ACh binding, preventing APs
Exocytosis blocker
Inhibits vesicle release, causing no ACh
ACh-esterase inhibition
Prevents ACh breakdown, causing depolarization block from continuous depolarization so APs can’t be generated
Skeletal muscle fibre
Thin filament is made up of actin, thick filament is myosin (creates muscular contraction)
Sacromere structure
Actin and myosin overlap in units called sarcomeres. Contraction shortens these by sliding them
Thin and thick filament structure
Thin filament actin has myosin binding site, thick filament myosin contains actin and ATP binding site
Muscle relaxation anatomy
Myosin binding site on thin filament is covered by tropomyosin which is held by troponin. No crossbridges formed
Muscle contraction anatomy
Calcium binds to troponin to move tropomyosin, allowing myosin and actin to bind. Crossbridges form
Crossbridge cycle summary
How muscles generate force. Myosin head undergoes conformational changes, changing affinity for actin. Relies on ATP
Contraction > relaxation
1) power stroke: myosin head moves thin filament to center of muscle
2) thick and thin filaments detach
3) myosin head returns to initial position
ACh function (skeletal)
Allows Na+ entry > muscle AP > alteration in DHP > RyR release calcium from SR into cytoplasm
Contraction Termination
Calcium most leave binding sites by Ca2+ ATPases in SR
3 phases of muscle twitch + info for each
1) Latent: time require for Ca2+ to be released and bind troponin
2) contraction: Ca2+ high, crossbridge cycling occurs, tension rises
3) Relaxation: intracellular Ca2+ falls, tension falls
Tetanus
Increased AP frequency causes successive twitches that fuse which each other into continuous contraction
Single-unit smooth muscle
Most common, in GI tract, blood vessels. Spontaneous, active in the absence of external stimuli
Multi-unit smooth muscles
Large airways, arteries. Innervated, each fibre is independent, contracts when there is stimuli
Excitation-contraction coupling (smooth)
Ca2+ from ECF and SR, lacks specialized receptors, Ca2+ initiates cascade with phosphorylation of myosin
Smooth muscle relaxation
Phosphatases remove phosphate from myosin. Ca2+ removed from cytoplasm by ATPase or Ca-Na counter transporter
Cardiac muscles
Contractile filaments are striated, intermediate SR development, gap junctions, ANS modulation
Cardiac muscle AP
Lasts 300ms (long), depolarization open Na+ and Ca2+ channels, Ca2+ prolongs AP from Na+. AP lasts as long as contraction and relaxation
How is cardiac contraction force increased
Increasing muscle length by greater stretch (Sterling law)
Systole
Contractile proteins from increased cytosolic calcium powers contraction
Diastole
Calcium pump in SR removes Ca2+ from cytosol, allowing for relaxation
Digitalis
A cardiac glycoside used to treat heart conditions by increasing Ca2+ levels, increasing contraction force
