Phgy 215 - Module 3

• 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

• located at peripheral ending of afferent neurons

• respond to stimuli (externa and internal)

• conversion of environmental signal to electrical (transduction)

• photoreceptors: responsive to visible length of light

• mechanoreceptors: respond to mechanical E

• thermoreceptors: sensitive to heat

• chemoreceptors: sensitive to certain chemicals

• 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

• 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

• 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 and generator potentials are graded potentials

• 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

• 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

• unpleasant sensation (internal or external)

• Nociceptors: specialized nerve afferent nerve 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)

• action potential reaches end, it releases neurotransmitter

• substance pressure coexists with glutamate to activate ascending pathways and transmit the pain signals

1. Hypothalamus(limbic)receive input from thalamus and reticular formation, allows for behavioural and emotional responses to pain

2. Cortex localizes pain in one area of the body

3. Thalamus allows for perception of pain

4. reticular formation increases the level of alertness and the awareness of painful stimuli

amino acids that functions as a neurotransmitter, it activates post synaptic receptors in dorsal horn

• 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

• 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

• 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

• reacts to light and function

• 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

• 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

• 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)

• contributes to most refractive ability (stays constant)

• some ppl have uneven level of contra and therefore have astigmatisms

• convex structure located behind pupil

• shape has ability to focus light rays

• adjustable

• ability to adjust lens and maintain

• controlled by ciliary muscle and suspensory ligaments

• relaxed means more flat and less convex

• 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

• 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

• 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

• 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

• eyes apart to process different visual input

• improves depth and perceptions

• 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

• vibrations of the air travel outwards from source

• transfer energy from molecule to molecule

• 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

• 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

malleus —> incus —> stapes

• transfer movement of. tympanic and amplify sound to transit to cloud of 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 )

• 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

• equilibrium and coordination

• neuronal signals don’t reach conscious awareness (motion sickness, dizzy, nausea)

• needed for taste and smell

• can trigger appetite and erase of digestive juices, detect pleasurable and undesirable

• human smell isn’t that sensitive

• 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

• 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

• 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

• 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

• 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

• 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

• 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)

• preganglionic fibres arise from brain and lower spinal cord

  • long and terminate in terminal ganglia (close to effector organ)

  • postgangionic fibres are very short

• preganglionic fibres use neurotransmitter acetylcholine (Ach)

• both systems have diff neurotransmitter

• Sympathetic- Ach called cholinergic fibres

• Parasympathetic- norepinephrine called andergenic fibres (someones epinephrine)

• 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

• sympathetic excitatory

  • increases heart rate and decreases gastric motility

• parasympathetic system in inhibitory

  • decrease heart rate, increase gastric motility

• relative contributions

• sympathetic dominance: fight or flight

• parasympathetic dominance: rest and digest

• 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

• 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

• Cholinergic: respond to neurotransmitter Ach

• Andergenic: G-protien coupled receptors respond to catecholamine neurotransmitters

  • catecholamine: epinephrine and norepinephrine

• activated by mushroom poison

• respond to Ach released by parasympathetic postganglionic fibres

• Binding of Ach or receptors open cation atoms

• depolarizes

• 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

• increases sensitivity for norepinephrine and epinephrine

• all activated by G proteins

• a2 activation suppresses the cAMP pathway

• a1 activations activates Ca2+ 2nd messenger system

• B2 greater affinity for epinephrine

• B1 respond equally to norepinephrine and epinephrine

• Active g protein

• enhance cAMP pathways

• 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

• 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)

• terminal end of motor neuron m

• small space in between called cleft located btwn studctures

1. action potential propagated

2. action protection reaches Ca2+ gate, gate opens, Ca2+ increases = exocytotic release of vesicles containing Ach into cleft

3. released Ach binds to nicotine receptor, depolarization, end plate potential increases

4. 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

5. Stimulated Motore neuron released Ach, which needs to be removed from cleft or there will gee constnat state of excitation

   • acetylcholinesterase inactivates in milliseconds

• excessive release of Ach

• acetylcholinesterase can’t inactivate

• prolonged depolarization

• Na channels inactive, can’t be stimulated

• Diaphragm has no contraction = respiratory failure

• form of food poisoning

• not enough Ach, therefore no contraction = respiratory failure

• need 0.0001 mg to kill a human

• when binded to Ach doesn’t cause end plate potential

• skeletal muscles not excited, respiratory failure