Physiology II Exam 1 - Spring 2023

Membrane Physiology, Somatic Sensation, & Special Senses

Exam 1 Breakdown

60% Somatic Sensation

20% Special Senses

20% Intro Material

Chemical Gradient

Concentration of ions differ across membrane

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High inside cell (K+) vs low outside (K+)

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Low inside cell (Na+) vs high outside (Na+)

Electrical Gradient Defined

Difference of charges across membrane

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Relatively (-) inside cell (proteins are - )

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Relatively (+) outside cell

Electrochemical gradient

Since both gradients across a cell membrane are due to ions (+ & -) we use this term

Equilibrium & Potential

Equilibrium - The natural tendency to return to an even concentration

Flow from higher concentrations to lower concentrations

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Potential - Increase strength is created by larger concentration differences across membrane

Measured in Volts or mV for neurons due to electrochemical gradient

Resting Membrane Potential

Membrane Potential is held at -70mV

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Leakage channels:

K+ moves out (numerous)

Na+ moves in (few)

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Sodium/Potassium Pump maintains…

\-70mV despite leakage

Actively pumps 3 NA+ out of cell

Actively pumps 2 Ka+ into the cell

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Nernst Equation/Potential

Definition: Equilibrium potential that exactly opposes movement of ions across cell membrane

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Determines resting membrane potential (-70mV)

Involves all ions and charges in our cellular environment → most important ions: Na+ and K+

Depolarization

Influx of positively charges ions (Na+) into cell

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Varying magnitude of influx

Small stimulus = small (+) influx, small increase in membrane potential

\-70mV → -65mV (not threshold)

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Large Stimulus = Large (+) influx

Large increase in membrane potential

\-70mV → -55mV (threshold)

Threshold

Threshold for Action Potential = -55mV

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This is an “all or nothing” phenomenon

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Weak stimulus would not increase membrane potential enough to reach threshold

ex. No action potential = no signal reaching next neuron on way to brain from stimulus location

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Strong stimulus would only need to reach threshold on order to cause an action potential

ex. Action potential generated = signal is now able to reach next neuron on way to brain from original stimulus location

Examples of Stimuli

Neuron to Neuron Communication

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Stimulatory

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Inhibitory

Neuron to Neuron Communication

Neurons communicate via synapses

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majority are chemical synapses that rely on neurotransmitters (ligands) that are released from pre-synaptic neuron and then interact with post-synaptic neuron membrane receptors

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This leads to changes in permeabilty of cell membrane to various ions

Neuron to Neuron - Stimulatory

Increase in permeability to cations (Na+) leads to the cell becoming more positive (Depolarization)

Neuron to Neuron - Inhibitory

Increase in permeability to anions (Cl-) leads to the cell becoming more negative (Hyperpolarization)

Sensory Input at a Receptor

Sensation relies on sensory neurons with receptors that detect stimuli in environment

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Stimuli/modalities include: Touch, pressure, vibration, chemical, sound waves, photons of light, and many more.

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These stimuli cause neuron cell membrane to change permeability to various ions.

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Increase in permeability to cations (Na+) leads to the cell becoming more positive (depolarization) = stimulatory

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A depolarized sensory neuron will likely transmit information to the next neuron in a sensory pathway via an action potential

Graded Potential vs Action Potential

Graded (Sensory) Potential

Local incoming signal

Signal degrades due to…


1. No machinery (no voltage gated channels) to send signal long distances
2. Graded potential must be sufficiently strong or summated to reach initial segment of axon

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Action Potential

Begins in the initial segment of axon

Signal does not degrade due to…


1. Axon + initial segment contains voltage gated Na+ channels (needed for AP)
2. Useful for sending long distances.

Chemical Synapse

Vast majority of synapses in the adult human nervous system

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Relies on chemical messengers (ligands/neurotransmitters) that are released by presynaptic neuron and interact with postsynaptic neuron via specific receptors

Electrical Synapse

Most are replaced after early neuronal development

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Exists in adult hippocampus

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Relies on gap junctions with channel proteins that allow flow of ions directly between cells

Chemical Synapses/Receptor Classes

Ionotropic:

Receptor type that regulates “fast” synaptic transmission

Fast speed is due to the receptor being able to initiate immediate changes in membrane permeability

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Metabotropic:

Receptor type that regulates “slow” synaptic transmission

Slow speed is due to the receptor needing to initiate a cascade of biochemical reactions in order to alter membrane permeability

G-Protein coupled receptors

Excitatory or Inhibitory?

Excitatory:

Signal brings neuron towards depolarization

Neuron becomes more +

Na+ moves in (increased permeability)

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Inhibitory:

Signal beings neuron away from depolarization (Hyperpolarized)

Neuron becomes more -

Cl- moves in (increased permeability)

or K+ moves out (increased permeability)

What helps a neuron reach threshold and generate action potential?

Summation

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Increased pre-synaptic input onto post-synaptic neuron

Reaching Threshold

Spatial Summation → Threshold is reached due to increased number of pre-synaptic neurons

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Temporal Summation → Threshold is reached due to increased frequency of firing from pre-synaptic neuron

How is a signal pathway reinforced in the nervous system?

Potentiation

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Repeated activation of neuronal pathways leads to increased responsiveness of post-synaptic neurons

Long Term Potentiation

Regulated by Glutamate receptors NMDA and AMPA

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High intensity stimulation

Results in stimulation of AMPA & NMDA receptors

AMPA recepts let Na+ in

NMDA receptors let Na+ and Ca+

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Influx of CA is theorized to trigger cascade within postsynaptic neurons that leads to increased number of AMPA receptors (increased responsiveness to stimuli)

How is a signal pathway weakened?

Inhibition

Synaptic Fatigue

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Acidosis & Alkalosis

Hypoxia

Drugs

Inhibition

Lateral Inhibition

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Most sensory pathways utilize lateral inhibition to increase localization of stimulus (contrast)

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Increase signal strength near center

Decrease signal strength in periphery

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Better able to tell exact location of stimulus

Synaptic Fatigue

Synaptic Fatigue may result in progressively weaker synaptic activity. Depletion of synaptic vesicles and neurotransmitters.

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ex. measuring withdrawl reflex following painful stimulus

Long Term Depression

Regulated by Glutamate Receptors: NMDA and AMPA

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Low intensity stimulation (monotonous detail)

Opens only AMPA receptors

Result is low intracellular Ca levels

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Theorized to initiate intracellular cascade that removes AMPA receptors. This weakens the neuron’s responsiveness to stimulation

Acidosis and Alkalosis

Normal pH of blood = 7.4

Neurons are highly sensitive to changes

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Acidosis →

decrease neuronal excitability

ex. diabetic ketoacidosis, decrease activity, leads to coma

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Alkalosis →

increase neuronal excitability

ex. hyperventilation causes loss of CO2 and increase pH which then leads to overactivity and seizures.

Hypoxia and Drugs

Oxygen deprivation for only 3-7 seconds leads to unconsciousness

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Caffeine Increases excitabilty by decreasing threshold

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Anesthetics decrease excitability by increasing threshold.

How is a signal speed increased?

Myelination

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Increases speed of signal

Increases capacitance (ability to store electric charge)

Saltatory conduction → nerve impuse “jumps” from one node of Ranvier to the next

Define Somatic Sensation

Nervous mechanisms that collect sensory information from all over the body

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Except - for special senses

Except - for visceral (deep)

Receptor

A specialized structure that detects a change and can relay that to other neurons

Modality

A unique type of sense

ex. vibration, temp, touch, smell, etc

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Transduction

The conversion of an environmental stimulus into a nerve impulse

Adaptation

How quickly a neuron gets used to that stimulus

Localization

Your brain knows exactly where that stimuli came from

Key basic Concepts for Somatic Sensation

Sensory information must be sufficiently strong to excite (depolarize) each neuron in the pathway

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Stimuli that don’t make it to the brain are not processed (we aren’t aware of them)

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We classify each neuron in the pathway as the 1st through 4th order

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1st order means 1st neuron in the pathway and so on

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A synapse between each neuron

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The synapse (in grey matter) is where we find the axon terminal of a pre-synaptic neuron and dendrites/cel body of the post-synaptic neuron

General Characteristics of All Somatic Sensory Receptors

All are highly sensitive to a single specific stimulus (modality)

All must transduce the environmental stimulus

All are located in a specific location (ex. photo receptor in eyes, not feet)

All relay to a specific and repeated location

All are pseudo-unipolar neurons with the cell body in the:

Dorsal Root Ganglion (spinal)

CNS Nuclei (cranial)

Sensory Transduction

Conversion of an environmental stimulus into an electrical impulse

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The language of information, first neuron in pathway responsible for this conversion

Transduction: Cellular Membrane Changes

Activation occurs:

If the change in membrane permeability results in: Na+ influx (depolarization)

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No Activation occurs:

If the change in membrane permeability results in : Cl- influx OR K+ exit

If threshold is not reached, no activation occurs.

Classification of Sensory Receptors by LOCATION

Exteroceptors

Sensitive to external stimuli

Pacinian, Meissner, Ruffini, Merkel

Free Nerve endings

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Interoreceptors

Sensitive to internal stimuli

Free nerve endings

Pacinian

deep - ex. stretch in stomach

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Proprioceptors (specialized interoceptors)

Sensitive to internal stimuli - for body position

Free nerve endings

Pacinian

Ruffini

Muscle Spindle

Golgi Tendon Organ

Classification of Sensory Receptors by Modality

Mechanoreceptors\*

Touch, Vibration, Pressure, Stretch, Equilibrium, Audition

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Nociceptors\*

Pain - free nerve ending (for extreme intensity)

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Thermoreceptors

Warm - free nerve ending

Cold - free nerve ending

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Photoreceptors

Vision

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Chemoreceptors

Tasts, smell, osmolality

O2, CO2

Mechanoreceptors

Respond to a mechanical deformation of the cell membrane

Primarily classified by how quickly they adapt

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Rapidly Adapting (Phasic)

Pacinian Corpuscle

Meissner Corpuscle

Hair Follicles

Rapidly Adapting (Phasic)

Pacinian (Lamellar) Corpuscle

Fastest Adapting

Deep - dermis and intramuscular

Vibration - large receptive field

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Meissner (Tactile) Corpuscle

Rapidly Adapting

Superficial - dermis, especially fingertips and lips

Precise Touch - small receptive field

Mechanoreceptors

Respond to a mechanical deformation of the cell membrane

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Primarily classified by how quickly they adapt

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Slowly adapting (tonic)

Ruffini Corpuscle

Merkel Disc

Tactile Disc

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Slowly Adapting (Tonic)

Ruffini Corpuscle

Slowly adapting

Deep - dermis and joint capsules

Stretch - large receptive field

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Merkel Receptors (Discs)

Slowly adapting

Superficial - dermis and epidermis junction

Light touch/pressure - small receptor field

Adaptation

Decrease in receptor action potentials over time with a constant stimulus

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Basically, how quickly the receptor gets “used to” the stimulus

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Fast Adapting (Phasic)

ex. Meisner Corpuscle (Fine Touch)

You’re not aware of the socks you are wearing

Adaptation

Slow Adapting (Tonic)

ex. Ruffini Corpuscle (Stretch)

You’re probably currently aware of the stretch in your neck as you are looking down

Stimulus Intensity

How does the nervous system determine strength of stimulus?

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Strong Stimulus → Increase frequency of Action Potentials

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Weak Stimulus → Decrease frequency of Action Potentials

Free Nerve Endings

Super generic, not specialized receptors

Free Nerve Endings

Present nearly everywhere in body

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Most common in epithelial and connective tissues

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Connected to Type A-Delta and C fibers → non myelinated fibers

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Nociceptors, Thermoreceptors, Tickle and Itch Receptors

Nociceptors

Receptors that detect potentially harmful stimuli

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Stimulus is capable of causing tissue damage, threshold should be high.

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Multimodal nociceptors → Capable of transducing mechanical, thermal, and chemical

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Mechanical nociceptors → Transduce extreme mechanical intensity. Extreme pressure, stretch, pinching, cutting.

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Thermal nociceptors → Extreme temperatures (greater than 120F or less than 42F)

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Chemical nociceptors → Inflammatory chemicals, markers of ischemia, strong acids/bases

Nociceptors

Dense concentrations within:

Skin, joints, periosteum, arterial walls, falx

ex. tumors that grow into places with dense we can feel them, low concentrations, asymptomatic

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Low concentrations within:

Deep tissues (visceral) - brain, GIT

Pain Receptor/Fiber Pathways

Nociceptors (free nerve endings)

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A delta fibers

C fibers

Fast Pain - aka Pricking Pain

Stimuli that cause fast pain include:

Needle stick, skin cut, heavy impact of object, bone fracture

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Characteristics of fast pain include:

Sharp & well localized

Acute

Travels in A-delta fibers

Nociceptors of A-delta fibers have a smaller receptive field

A-delta fibers (5-40 meters/sec) are faster than C fibers (.5-2 meters/sec)

Slow Pain - aka Aching Pain

Stimuli that causes fast pain include:

Inflammation, ischemia, burned skin, chronic injuries, deep/visceral structures

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Characteristics of slow pain include:

Diffuse and poorly localized, generalized, deep, aching, chronic

Travels in C fibers of Paleo-Spinothalamic Tract

Nociceptors of C fibers have a larger receptive field

C fibers are slower than A delta fibers

Particularly annoying and intolerable when compared with fast pain.

Thermoreceptors

Warmth Receptors

Transduce warm temperatures between

86-120F at 120F nociceptors kick in

utilizes vacilloid transient receptor potential channels

TRPV transduces heat

Also transduces capsaicin found in spicy food

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Cool Thermoreceptors

Transduces warm temperatures between 42-109F

Cool tends to travel faster than heat

Utilizes melastatin transient receptor potential channels

Transduces cool

Also transduces methanol found in additives and topical pain relievers

Tickle and Itch

Free nerve endings

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Tickle →

Almost exclusive to superficial skin

Very thin (c-fibers)

Very low threshold - sensitive to light touch, think mosquito

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Itch Receptors →

Almost exclusive to superficial skin

Very thin (c-fibers)

Respond to chemical stimuli - most importantly histamine

2 Different systems

Erlanger’s →

Both motor and sensory

Know your AAAABCs

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Lloyd’s →

Only sensory

Mostly used in context of proprioception

Dorsal Horn Intersection Large Myelinated Fibers

Medial Branch

Large myelinated mechanoreceptor fibers turn medially and ascend the dorsal column

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Lateral Branch

Fibers enter dorsal horn and travel laterally

Divide many times to provide communicating fibers :

Many travel medially and ascend dorsal columns

Some excite interneurons in the spinal cord reflex arc

Some interneurons also inhibit pain (Gate Control Theory)

Others give rise to spinocerebellar tracts that aid in cerebellar function.

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Essentially the body needs to start sorting information, and this is how it does it.

Ascending Tracts - Pathways

Features of Dorsal Column-Medial Lemniscal:

High Degree of Speed!

Fine touch

Vibration

Proprioception (from joints and muscles)

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Features of Spinothalamic (Anterolateral)

Lower Degree of Speed

2 subdivisions (Neo and Paleo)

Pain

Temperature

Crude (poorly localized) touch

Tickle and itch

Sexual sensation

General Features of Ascending Tracts

Basically they are responsible for relaying sensory information from sensory fibers to the Thalamus for further processing

Checklist for learning sensory pathways

Identify:

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Modality (ex. pain, vibration, proprioception, etc)

Location of stimulus

What ascending tract will carry info to Thalamus?

Fill in other details(receptor type, fiber type, speed of transmission, where fiber/pathways cross, where info ultimately synapses, location of each synapse and cell body)

Dorsal Column-Medial Lemiscal pathway

Modalities Carried

Fine touch (very detailed and localized)

Vibration

Proprioception

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Location:

Gracillis → Carries info below T6, Lower extremities

Cuneatus → Carries info above T6, Upper extremity

Dorsal Column-Medial Lemiscal pathway (pt 2)

Characteristics of Sensory Information →

Composed mainly of A-Beta fibers

Rapid Speed

Generally well localized (except vibration)

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Physical Pathway →

1st order neuron enters cord, enters dorsal columns and ascend to medulla and synapse in their respective nuclei

Neurons stay on same side of cord they entered

Synapse on nuclei in medulla

Crosses and ascends to Thalamus in the medial lemniscus

Synapse in VPL of Thalamus

Then go to cortex

Spinothalamic Pathway (Anterolateral)

Anterior Spinothalamic

Mostly A-Delta Fibers

Crude (poorly localized) touch

Tickle and Itch (C-fibers)

Sexual sensation

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Fibers synapse in dorsal horn ipsilaterally

Cross immediately to contralateral side and ascend

Synapse in VPL of Thalams, then go to cortex

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Lateral Spinothalamic

Some A-delta (fast pain and cold temperature)

Some C fibers (slow pain and heat)

*much of slow pain never reaches, only 10% does*

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Same pathway as anterior spinothalamic, except pain!

Pain Pathways - Lateral Spinothalamic

Neo Spinothalamic →

Fast pain: A-delta fibers

Require tactile sensors

Most ascend to the thalamus (VPL)

Neurotransmitter: Glutamate (stimulatory for the most part)

Nociceptors stimulated by: Mechanical and Thermal

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Paleo Spinothalamic →

Slow pain: C fibers

poorly localized, dull, chronic

Most synapse on small interneurons before crossing and ascending.

Terminate widely in the brain stem.

Useful during pain control

Descending analgesic system

90% terminate in the reticular formation of the brain stem

Not well localized

Neurotransmitter: Substance P

Nociceptors stimulated by: Chemical, mechanical, thermal, think inflammation, Ischemia

Reticular Formation

Extends from Medulla to Midbrain

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Increases arousal of CNS

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Stimulation by chronic pain is known to interfere with sleep

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Slow pain fibers that terminate in the reticular formation do not ascend to the cortex.

*we still feel slow pain even without the primary somatosensory cortex*

Thalamus function in somatic sensation

Nuclei of Thalamus house the cell bodies of 3rd order neurons

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Relay station for all somatosensory fibers on the way to the cortex

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All somatosensory neurons synapse in the VPL

Somatosensory Cortex

Located in the post-central gyrus int he parietal lobe

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Consists of:

Somatosensory area 1

primary region where sensory information is processed and localized

excision only disables localization of stimulus

Sensory Homunculus

Contains 6 layers of neurons

Somatosensory Area 1

Consists of Brodmann’s Areas 3, 2, & 1

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Somatosensory Area 2 and Cortical Association Areas

Somatosensory Area 2:

Poorly understood

Emerging information may point to a role in interpreting whole limb kinematics/proprioception

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Sensory Association Areas

Provide context for sensation

Create memories

Provide emotional context

Pain Categories

Nociceptive →

Traditional view of pain

Activated nociceptors - tissue injury, not nerve injury

Due to potentially damaging stimulus

May be up regulated by inflammatory products derived from arachidonic acid

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Neuropathic →

Caused by damage to sensory nerves

Altered firing of nociceptors due to unhealthy neurons

ex. peripheral neuropathy, MS

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Nociplastic →

New term

Recent additional category: Alternate explanation of pain

Altered processing of pain signals within the CNS

May be altered by fatigue, stress, mental status

Typically responds to different therapies than nociceptive pain

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What is muscle pain a combination of?

Mechanosensitive Nociceptors stimulated by excessive force

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Chemosensitive Norciceptors stimulated by products of ischemia: Lactic acid, bradykinin, proteolytic enzymes, K+

Headache sensitive stuctures

Dura, DVS, blood vessels, Tentorium

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*headaches are usually more altered pain processing than actual injury to the head*

Extracranial Headaches

Referred to head

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Cervical spine dysfunction

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Muscle spasm: Connection to dura in upper cervical spine

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Sinus pressure/irritation through C5

Cervical Myodural Bridge

Anatomical connection between suboccipital muscles/fascia and dura

Cervicogenic Headache

Cervical Spine dysfunction

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Nociception from cervical afferents - especially greater occipital nerve

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Relayed to sensory nucleus of CN 5

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Trigemino Cervical Complex (TCC)

TCC

Occiput - C1

C1-C2

C2-C3

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Share common sensory pathway with opthalmic nerve (Trigeminal)

Intracranial Headaches

Migrane:

Old theory → vasoconstriction/dilation of arteries (middle cerebral)

prolonged vasospasm may lead to ischemia of brain

prodromal auro symptoms

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Meningitis - inflammation of meninges

most commonly either viral or bacterial

extreme headache, nausea, spine/neck ridgidity, fever

Referred Pain

Referred pain from visceral structures

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2 localization pathways for visceral pain

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Visceral Localization → Pathway will refer pain tot he surface of body

Via dermatomal pattern where organ originated embryologically

Mechanism is that both visceral and skin pain pathways share/synapse on the same 2nd order neuron

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Parietal Localization →

Pathway will refer pain to the surface of body near organ

Via highly sensitive nociceptors located in parietal layer of:

Pleura, pericardium, peritoneum

Pathophysiology of Pain

General Sensitization:

Increased membrane excitability in central nociceptive pathways (not at receptors)

Smaller stimulus will be able to cause depolarization

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Allodynia:

Pain with normally non-painful stimulus.

Pain Modulation

Gate Control Theory:

Fast A beta fibers give off communicating interneurons in spinal cord

These interneurons inhibit synapses for the Spinothalamic tracts, likely through lateral inhibition

Fast large A-beta myelinated fibers give off conninicating interneurons within dorsal horn before ascending the dorsal columns. These inhibit slower/smaller C & A delta fibers. Through hyperpolarization of 2nd order neurons in dorsal horn.

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Descending Analgesic System:

When stimulated, 3 regions of brain stem nuclei send fibers to dorsal horn

These inhibit synapses for the Spinothalamic tracts through endorphins and enkephalins

When stimulated by pain, 3 regions of nuclei in brain step communicate with dorsal horn of the cord to supress pain signals

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Periaqueducatal and Periventricular gray area

Raohe magnus nucleus

Nucleus reticularis paragiganocellularis

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Descending Analgesic System

Descending fibers stimulate inhibitory interneurons in cord

Release endogenous opioids on incoming C & A delta fibers

Sensory Innervation of Joints and Muscles

Proprioception and Pain

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Sensory Innervation of Joints →

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Proprioception:

Heavily innervated

Mechanoreceptors (ex. Ruffini)

Large myelinated fibers

Found in joint capsules

Low threshold

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Pain:

Heavily innervated

Nociceptors

Very high threshold

Completely inactive physiologically normal joint

Activated through:

Significant mechanical pressure

Increased capsular pressure

Chemical irritation

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Proprioceptive Innervation of Muscles

Muscle spindles → Innervated by both sensory and motor neurons

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Sensory:

Intrafusal muscle fibers - minimally/non-contractile

Type 1a fibers: Monitors speed of the changing length, large and myelinated, innervated both nuclear bag and chain

Type II: monitors only length, Intermediate size and myelinated, innervated only nuclear chain

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Motor:

A gamma motor fibers - smaller than alpha motor

Should be in coordination with extrafusal muscle fibers

Job is to keep muscle spindle the same length as the rest of the muscle .

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Sensory:

Golgi tendon organs

found in tendons

Relays information to inhibit interneurons that synapse on alpha motoneurons - results in relaxation of homonymous muscle

Type 1b fibers - slightly smaller than 1a fibers in muscle spindles - monitors tension of muscle/tendon

Pain innervation of muscles

Nociceptors →

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Mechanosensitive Nociceptors

Stimulated by excessive force

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Chemosensitive Nociceptors

Stimulated by products of ischemia or inflammation: lactic acid, bradykinin, prostaglandins, proteolytic enzymes, K+

Proprioceptive Pathways

Dorsal Columns →

Previously discussed

Allows for conscious interpretation of proprioception

Ex. Joint capsule stretch, pressure on weight bearing joint surfaces

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Spinocerebellar Tracts →

Allow for subconscious processing of proprioception by cerebellum

Ex. Muscle length, tension on tendons

Spinocerebellar Tracts

Dorsal →

Carried majority of proprioceptive input:

Muscle spindles

Some input from tactile and golgi tendon organs

Informs the cerebellum instantly of:

Changes in muscle length, tendon tension, Position and rate of change in joints, outside forces put on body.

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Ventral →

Carried minority of proprioceptuve input.

Mainly informs cerebellum of activity at the ventral horn of the spinal cord.

How is light processed in the nervous system?

Retina houses specific light receptors →

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Rods: respond to small changes in light (no color)

highly sensitive to light, low threshold, low acuity, about 100 million rods in each retina

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Cones: respond to large changes in light and 3 wavelength ranges (color)

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low sensitivity to light, responds to light in 3 wavelength ranged (red, blue, green), high threshold, functions in bright/daylight conditions, color vision, high visual acuity, present in fovea and macula, about 3 million cones in each retina.

Internal Anatomy of Eye

In order to reach the photoreceptors of the retina, light must pass through: Cornea, aqueous humor, lens, vitreous humor

Allow light to pass through multiple neural layers in the retina.

Layers of the Retina

Light must pass through all layers before striking the most posterior cellular layer called the pigmented cells

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Pigmented cells: Utilize melanin to help absorb light

Photoreceptor cells: Rods and Cones

Bipolar cells: Relays information to ganglion cells -- one cone per bipolar cell, many rods per bipolar cell

Ganglion Cells: Axons make up the optic nerve

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Horizontal Cells

Communicate with multiple rods/cones and bipolar cells

Provide for lateral inhibition, increases contrast/clarity

Amacrine Cells

Communicate with multiple bipolar and ganglion cells.

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About 30 types - not well understood, generally help analyze and sort visual signals

How do Rods and Cones work?

Transduction: Conversion of light energy to electrical signals

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Opposite of what we normally thing: Photoreceptors are constantly releasing an inhibitory neurotransmitter (glutamate) at synapse with bipolar cells

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Transduction involves a hyperpolarization: Turning off release of inhibitory neurotransmitter (glutamate)

Signal pathway from photoreceptors

Photoreceptors are hyperpolarized when stimulated by light

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Stop releasing inhibitory neurotransmitter (glutamate)

Bipolar cells depolarize and stimulate ganglion cells

Ganglion cells depolarize and carry signal via optic nerve (CN 2) to thalamus and eventually reaching visual cortex

Signal pathway to cortex

Once visual information has been passed to the ganglion cells

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Ganglion axons form each optic nerve

Exit the eye at the optic disc

Pass through the optic chiasm (crossing)

Synapse on the Lateral Geniculate Nucleus (Thalamus)

Travel to the primary visual cortex via optic radiation

Primary visual cortex located in Calcarine fissue of occipital lobe

Optic Chiasm

Temporal - Visual fields cross at the optic chiasm

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Nasal - Visual fields do not cross the optic chiasm

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images are flipped: Upside down and right to left

Refraction

Bending of light as it passes through substances

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Convex lens: Focuses light

Concave lense: Diverges light

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Errors in refraction:

Hyperopia - Farsighted, weak refraction, focus is behind retina, convex lens is used to correct

Myopia - Nearsighttedness, strong refraction, point of focus is in front of retina, concave lens is used to correct.

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Hyperopia

Eye is too short or refraction too weak