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Afferent Division
carry nerve impulses from peripheral receptors and special sense organs to CNS
small round cell body, dingle dendrite, short axon
dendrites extend to periphery and act as axon
found in clusters called ganglia (external to spine)
axons extend to dorsal horn
Receptor Physiology: Threshold
located at peripheral ending of afferent neurons
respond to stimuli (externa and internal)
conversion of environmental signal to electrical (transduction)
Receptor Properties- Modality
photoreceptors: responsive to visible length of light
mechanoreceptors: respond to mechanical E
thermoreceptors: sensitive to heat
chemoreceptors: sensitive to certain chemicals
Receptor Properties- Intensity
action potentials are all or nothing
strong signal can trigger increased frequency of action potential
nerve cells code intensity of info by frequency of action potential
Receptor Properties- Location
receptive field: sensitive regions of neuron, if stimulus in this region, neuron will fire and the location will be communicated to the brain
multiple sensors: compare input from more than one sensor
gradients: with smell, determine location based on gradients, neurons encode duration of stimulus and communicate
they fire as long as stimulus is present (some as stimulus goes on), stop, and then start again when stimulus is gone
Transduction; Receptor and Generator Potentials
receptors can be specialized ending or separate
receptor activation is similar in both
stimulation of receptor alters permeability, causing opening of non-selective cation channels to open
depolarization
receptor potenial: change in potential due to incoming signal
in socialized receptor cells or generator cells
Receptors Create Graded Potential
receptors and generator potentials are graded potentials
separate receptor cell:
specialized afferent ending:
separate receptor cell:
receptor potential can cause afferent nerve fibre to reach threshold and trigger action potential
when receptor potential is strong enough it will release chemical messengers that diffuses to afferent neuron and opens chemically gated Na+ channel
if threshold achieved then the afferent nerve fibre will initiate and propagate action potential
Receptor Adaption
Tonic Receptor
Phasic Receptor
slow or no adaption, impotent when near constant signal from stimulus is necessary (muscle stress receptors)
rapid adaptions, strips generating action potential rapidly even in presence of stimuli
off response: depolarization even when stimuli is removed
important monitoring changes in stimuli intensity
Pain:
nocieption:
unpleasant sensation (internal or external)
Nociceptors: specialized nerve afferent nerve fibres
Nocieption
mechanical
thermal
chemical
fast pain fibres
slow pain fibres
respond to physical damage
respond to temp
respond to noxious chemicals (external or internal )
A-delta fibres (temp, chemical, mechanical stimuli)
C-fibres, unmyelinated, polymodal receptors (burning,aching,throbbing)
bradykinin which is activated by enzymes that are released damaged cell
once once activated it can directly stimulate nociceptors (explain ling lasting pain)
Processing Pain
action potential reaches end, it releases neurotransmitter
substance pressure coexists with glutamate to activate ascending pathways and transmit the pain signals
How does the brain process pain?
Hypothalamus(limbic)receive input from thalamus and reticular formation, allows for behavioural and emotional responses to pain
Cortex localizes pain in one area of the body
Thalamus allows for perception of pain
reticular formation increases the level of alertness and the awareness of painful stimuli
Glutamate
amino acids that functions as a neurotransmitter, it activates post synaptic receptors in dorsal horn
AMPA Receptors
activation leads to permeability change
generate action potential and send signal to higher brain centres
as Na+ enters, depolarization occurs
Certain level of depolarization means Mg2+ channel can be dislodged and NMDA channel can be activated
NMDA Receptors
once activated aslope Ca+ to enter neuron
activates 2nd messenger pathway resulting in neuron being more excitable
this is why injured areas are more sensitive
Endogenous Analgesic System:
opiates: chemicals produces by body (pain killing)
opioids: substances not produced by the body (pain killing)
activates descending pathway that activates inhibitory neurons in dorsal horn
released opiates to act on opiate receptor and reeled in suppression of neurotransmitter being released from afferent pain fibres
exogenous opioids activate opioid receptors to decrease perception of pain
Vision
reacts to light and function
Light entering the eye:
centre of isis is pupil and it allows right to enter the eye
size of opening can be adjusted by 2 sets of smooth muscles in iris
regulation of the muscles is under control of autonomic nervous system
Pupillary constriction
Pupillary dilation
caused by parasympathetic stimulation, one set of muscles is organized in circular fashion
make pupils constrict (less light in)
caused by sympathetic stimulation, one set of muscles is organized in a radical fashion
from pupil to edge of iris
contract to dilate rot allow more light to go through
The focusing of light:
light rays made of photons that travel in wavelike patterns
waves vary in wavelengths and intensity, and need to be bent
when light passes through transparent media with different densities of air wavelength decreases unless it enters perpendicular then direction changes (refraction)
Cornea:
contributes to most refractive ability (stays constant)
some ppl have uneven level of contra and therefore have astigmatisms
Lens
convex structure located behind pupil
shape has ability to focus light rays
adjustable
Accommodation
ability to adjust lens and maintain
controlled by ciliary muscle and suspensory ligaments
relaxed means more flat and less convex
Distant Light Source:
Near Light Source:
Blind Spot:
more than 6m away (light rays parallel to one another)
less than 6m away (light rays diverging)
optic disk where ganglion axons bundle to form optic nerve
one per eye
no rods or cones so can’t see
Retina
extension of CNS (optic nerve)
goal of lens is to focus light rays on retina to convert light E to electrical signals to send to CNS
3 layers pop excitable cells
photroreception
bipolar
ganglion cells
Cells of Retina
Rods and Cones: rods- vision low light, cones-colour
Bipolar Cells: middle layer, involve in transmission from rods and cones to ganglion cells
Ganglion Cells: neurons at inner surface, axons of ganglion cells makeup optic nerves
Central Processing of vision
thalamus
separates visual stimuli and relay to diff zones of cortex
visual cortex organized into function columns (alternating dedicated to left and right eyes)
vision takes up 30 percent of cortex capacity
Visual Processing:
eyes apart to process different visual input
improves depth and perceptions
Visual Pathway:
optic nerve made of right visual field and left visual field
cross over
left side processed on right side of brain
right side processed on left side of brain
Sound Waves:
vibrations of the air travel outwards from source
transfer energy from molecule to molecule
Pitch:
Intensity:
Timbre:
tone: frequency of vibration (incr frequency = incr pitch)
loudness: depends on aptitude of the sound waves and the greater the amplitude the greater the sound
quality: overtones at same pitch, allows one to locate the source of the sound
external ear
pinna
ear canal
tympanic membrane
channel sound waves to middle ear
external skin covers cartilage that collects sound waves (hear and localize)
conducts sound waves towards tyrannic membrane, guarded by fine hairs that produce earwax
stretches averse entrance to middle ear, vibrates when hot by sound waves
P on both sides need to be even or won’t vibrate
connected pharynx via eustachian tube, P in middle equalizes with atmospheric pressure
Middle ear:
malleus —> incus —> stapes
transfer movement of. tympanic and amplify sound to transit to cloud of inner ear
Inner Ear
oval window —> sounds converted to mechanical E and transferred to here
cochlea is corgis organ and supported by basilar membrane
fluids move, the hair cells mechanically deform and generate neuronal signals
Inner Hair Cells transform fluid to membrane potential therefore auditory msg sent to cortex
change in membrane potential matches frequency of go sound stimuli
Outer Hair Cells: odn’t transmit sound signals to Brian but they modify electrical signally of the inner hair cells
inhance response of inner hair cells (making them more sensitive to intensity and pitch )
Inner Ear - Pitch Discrimination:
depends on the shape of basilar membrane (narrow to oval, spiral shaped)
higher pitch detected at narrow end
stapes moves oral window at certain pitch, wave to basilar membrane
hair cells undergo most deformations
afferent neurons pick to auditory signals from hair cells to form auditory nerve
way to cortex signals pass through brainstem and thalamus
thalamus sorts signals and send to higher processing centres
Vestibular Apparatus
equilibrium and coordination
neuronal signals don’t reach conscious awareness (motion sickness, dizzy, nausea)
Chemoreceptors
needed for taste and smell
can trigger appetite and erase of digestive juices, detect pleasurable and undesirable
human smell isn’t that sensitive
Taste
tongue, oral cavity and throat
tastebuds
taste receptors cells
afferent neurons
most chemoreceptors found, esp tongue
papillae = small bumps (each has hundreds of taste buds)
cluster of nerve endings, each haas about 50 receptors
renewed every 10 days
each bud has opening that allows fluid to come out
tasant binds to receptors, ion channels depolarize initiating action potential
signal to brainstem and thalamus before going to cortical gustatory area (in parietal lobe)
brainstem to hypothalamus limbic system to be able to distinguish pleasant and unpleasant Tas
Taste Discrimination
salty
sour
sweet
bitter
umami
Na+ channels, direct entry for na+, depolarization of cell
Free H+ blocks K+, decreases k+ and produce depolarization
Glucose binding activates G protein, generating cAMP, inhibits K+ channels and produce depolarization
receptor maybe be invited in protective mechanism (works like sweet cells)
triggered by amino acids, 2nd pathway unknown, known to detect meaty flavours
Smell:
olfaction
chemoreceptor found at top of nasal cavities
olfactory mucosa- small patch of skin ceiling of nasal activity
supporting cells
secret mucous and basal cells (precursor)
2 months life span
axons from olfactory receptor cells form olfactory nerve
Olfaction Process
odourants dissolve in mucous layer and interact with cilia on olfactory receptors
binding odourants activates G protein and mobilize 2nd messenger CAMP to Na+ channel opening to depolarize and action potential in afferent fibre
5 mill raptors, divided into 2 thousand types
cortex can identify over 1000 different smells
Overview of Autonomic Nervous System
influences heart, smooth muscles and glands through sympathetic and parasympathetic systems
AMS output is form hypothalamus, brainstem, spinal cord sent to periphery through sympathetic and parasympathetic systems
Sympathetic: fight or flight
Parasympathetic: rest and digest
Autonomic Nerve Pathway
2 neuron chain, connects CNS to effector
Body of first neuron his within CNS, axon called preganglionic fibre, synapses w cell body of second neuron
second neurons cell body is with ganglion, axon called postganglionic fibre, innervates effector organ
Sympathetic:
originate in thoracic and lumbar
preganglionic fibres- short and terminate in ganglia located chains down both sides of spinal cord
long postgangionic fibre terminate on effector organ
some preganglionic fibres pass and terminate in collateral gingival (located halfway btwn CNS and effector organ)
Parasympathetic:
preganglionic fibres arise from brain and lower spinal cord
long and terminate in terminal ganglia (close to effector organ)
postgangionic fibres are very short
Neurotransmitters
preganglionic fibres use neurotransmitter acetylcholine (Ach)
both systems have diff neurotransmitter
Sympathetic- Ach called cholinergic fibres
Parasympathetic- norepinephrine called andergenic fibres (someones epinephrine)
Autonomic Regulation
almost all effector organs receive input from sympathetic and parasympathetic systems
most afferent nerve traffic from visceral organs like digestion, sweating and circulation
regulated by autonomic
Autonomic Innervation of Organs
sympathetic excitatory
increases heart rate and decreases gastric motility
parasympathetic system in inhibitory
decrease heart rate, increase gastric motility
Sympathetic or Parasympathetic Tone:
relative contributions
sympathetic dominance: fight or flight
parasympathetic dominance: rest and digest
Dual Innervation Exception
most arterioles and veins receive sympathetic stimulation, regulation is achieved by increases or decreasing sympathetic activity
penis and clitoris are dual
sweat glands receive sympathetic stimulation (post ganglionic fibres reteach Ach not norepinephrine)
Salivary glands receive dual
Role of Adrenal Glands in the ANS
arena medulla functions like sympathetic pregangionic fibre
sympathetic stimulation- adrenal medulla releases chemical transmitters (qualify as hormones) into blood
20% norepinephrine, 80% epinephrine
During stimulation acts like an amplifier
ANS Receptors
Cholinergic: respond to neurotransmitter Ach
Andergenic: G-protien coupled receptors respond to catecholamine neurotransmitters
catecholamine: epinephrine and norepinephrine
Muscarinic Receptors
activated by mushroom poison
respond to Ach released by parasympathetic postganglionic fibres
Binding of Ach or receptors open cation atoms
depolarizes
Nicotine Receptors
activated by tobacco plant
found on post ganglionic cells in all autonomic ganglia, bind to Ach
release from Sympathetic and Parasympathetic preganglionic fibres
cation channels open
Adrenergic - Alpha Receptor
increases sensitivity for norepinephrine and epinephrine
all activated by G proteins
a2 activation suppresses the cAMP pathway
a1 activations activates Ca2+ 2nd messenger system
Adrenergic - Beta Receptors
B2 greater affinity for epinephrine
B1 respond equally to norepinephrine and epinephrine
Active g protein
enhance cAMP pathways
Somatic Nervous System
axons innervate skeletal muscle under voluntary control
cell bodies of all motor neurons located in the ventral horn of the spinal cord and their axons terminate directly on the effector/target (exception of the head)
stimulation releases acetylcholine making muscles contract
no inhibition of skeletal muscle contraction just excitation
relaxing is when excitability of motor neurons is decreased
Motor Neurons
covering point for sensory input
cortex, basal nuclei, cerebellum, brainstems- send info to upper morrow neurons
receive sensory input for reflexes directly
accept bot inhibitory and excitatory signals to decide whether or not action potential should be generated and if it should contract muscles
damage to these neurons can cause irreversible health problems (paralysis/spasticity)
Neuromuscular Junction:
terminal end of motor neuron m
small space in between called cleft located btwn studctures
action potential propagated
action protection reaches Ca2+ gate, gate opens, Ca2+ increases = exocytotic release of vesicles containing Ach into cleft
released Ach binds to nicotine receptor, depolarization, end plate potential increases
initiation of action potential, end plate potentiona; depolarizes motor end, influencing muscle membrane surrounding end plate and Na+ channel open
enough Na+ means there will be a contraction
Stimulated Motore neuron released Ach, which needs to be removed from cleft or there will gee constnat state of excitation
acetylcholinesterase inactivates in milliseconds
Black Widow Spider Venom
excessive release of Ach
acetylcholinesterase can’t inactivate
prolonged depolarization
Na channels inactive, can’t be stimulated
Diaphragm has no contraction = respiratory failure
Botulinum Toxin
form of food poisoning
not enough Ach, therefore no contraction = respiratory failure
need 0.0001 mg to kill a human
Curare
when binded to Ach doesn’t cause end plate potential
skeletal muscles not excited, respiratory failure