Propogation of Electrical Signal, Neuro Flashcards
Depolarization
Typically is a process that turns on most electrically excitable cells.
Refers to a process where inside the cell is becoming more positively charged, so because it’s a deviation from the normal negative resting membrane potential we say that that is depolarized.
Changing polarity in opposite directions
Hyperpolarization
The process that the body uses to suppress activity
Making the cell even more negative than it is usually at rest
Repolarization & its affect on Na+/ Ca+ Channels (Think heart for Ca++)
The return back towards resting membrane potential.
This process is super important because repolarization is required for the resetting of the fast Na+ channels. We need to come back down to “near normal” Vrm before fast Na+ channels will reset, resulting in fewer Na+ channels involved in an action potential or no action potential at all.
This process is also very important in the heart with our L-Type Ca+ channels (slow).
**Dihydropyridine Ca+ Channel Antagonists work on L-type Ca+ Channels **
Permeability of Cl- During Action Potential
-Cl- permeability is adjusted to hyperpolarize or suppress electrical activity in excitable cells
-This happens through GABA receptors in the nervous system. Cl- channels open in neurons, making the cell more negative, and thus more difficult to excite
Action Potential & Positive Feedback Loops
An action potential is an example of a positive feedback loop. We have an initial stimulus that causes Na+ to come in, which then activates fast Na+ channels that allow more Na+ to come in. This process continues until the action potential spreads along the entire length of the cell
Propagation of Electrical Signal (How an action potential spreads along the cell)
-Stimulus causes depolarization, triggering more fast Na+ channels to open.
- Action potential/depolarization waves spreads in both directions away from the area where it was initially stimulated (as long as there is room for it to spread).
-Can be a two way process as described above, or can have a one way process in some cells.
-Two way propagation is going to speed up the process of exciting the entire cell
-Repolarization typically happens in the same manner/pattern that the cell was depolarized
Ex. given in class: Electrode stuck directly on the muscle, shocking it.
Skeletal Muscle & NMJ Connection
-Skeletal muscle (striated) and the motor neuron are two distinct figures.
-It is not a continuous structure. There is space that separates the two cells, and neurotransmitters are used to transmit the message from the motor neuron to the muscle.
-Brain or spinal chord makes the decision to contract a muscle. The motor neuron is activated somewhere along the spinal chord. That activation produces an action potential that moves from the brain and spinal chord all the way out to where the motor neuron and skeletal muscle meet.
A neurotransmitter is released from the motor neuron.
The skeletal muscle has neurotransmitter receptors on the neuro-muscular junction
Stimulation Ex: Nicotinic ACh Receptor
-ACh is the neurotransmitter released from the motor neuron
-ACh binds to nACh receptors on the skeletal muscle (there are some nACh receptors in the brain as well)
-There are two ACh binding sites on the nACh-R, and both must be bound simultaneously for the channel to allow current through it
-nACh-R is a donut-shaped protein stuck in the cell wall. Lined with AA with (-) charges to repel (-) ions so that only positive ions flow in
-Once both nACh-R are bound, Na+ flows into cell
-Some K+ can leak out through these channels. Na+ typically knocks it out of the way
-Small amount of Ca++ also sneaks through the Na+ channel
-Initial current of Na+ through the nACh-R sets off the fast Na+ channels (next to nACh-R) –> depolarization
Robust system, there are significantly more Na+ channels than we actually need, so the skeletal muscle should always respond (normal physiology)
Inhibition (Hyperpolarization) Example: Muscarinic ACh-R
ACh Mediated Hyperpolarization
-Located in the heart and smooth muscle of the lungs
-GPCR that mediates K+ permeability at the nodal tissue
-Named after a mushroom found in the rainforest
-Mediate and adjust pumping levels of the heart, as well as electrical activity of the heart by controlling how hyperpolarized the cell is
SA & AV Node: Action potential spreads from SA node -> atria -> AV node -> ventricles
The vagus nerve comes into contact with the pacing cells of the heart
R. Vagus nerve predominantly affects the SA node
L. Vagus nerve predominantly affects the AV node
The vagus nerve releases ACh –> binds to mACh-R on nodal cells -> GPCR changes conformation -> Alpha subunit communicates w/ K+ channels nearby and causes additional K+ channels to open (cell becomes more polar, hyperpolarized)
-Increased electronegativity causes the cell to be more difficult to excite, influencing how fast the pacemaker activity works in the heart
-ACh mediated hyperpolarization; this is how our body pumps the brakes on our heart rate. Otherwise, it would be beating ~110bpm.
-Blocking this with a muscarinic antagonist would mean that the alpha subunit on the GPCR does not activate the K+ channels, the K+ channels would close causing the Vrm to be more positive leading to a faster heart rate
Pressure & Action Potential
-Physical pressure on a sensor causes a change in electrical activity
-When there is enough of a stimulus, the electrical activity at the sensor turns into an action potential. Typically these are repeated action potentials
How does this happen?
Pressure is applied to sensor –> pressure sensitive Na+ channels–> Na+ channel becomes flattened out, widened, and Na+ permeability is increased. Na+ comes in –>Vrm becomes more positive–> action potential is generated
This is a method the nervous system uses to “keep an eye” on what’s going on
Action Potential & Several Types of Stimuli
-We will not generate an action potential unless the stimulus causes the cell to depolarize to its threshold
-Vrm and threshold are based on what type of tissue we are looking at (heart, skeletal muscle, or neuron)
-A weak stimulus, that barely passes the threshold, will have a delayed/slow action potential
-A strong stimulus will have a quicker/stronger action potential
Action Potential in the Heart
-Longer action potential than we see in neurons (millisecond vs seconds)
-An action potential is going to be specialized to fit whatever role that cell is responsible for
-The action potential plateaus/ is sustained to allow the heart to pump efficiently
-This is due to the slow L-type Ca++ channels (will pick that apart in cardiac)
Extracellular Ca++ Effects
-Ca++ tends to stabilize membrane potential and settle down irritable tissue
-Ca++ causes massive depolarization because of its high concentration gradient and its two positive charges
-Because of the high concentration gradient, Ca++ typically sits along the cell membrane in the ECF.
-Because of the large, clunky nature of Ca++, it limits the resting permeability of Na+ because it blocks the entrance to the Na+ leak channels
- Ca++ is inhibiting electrical activity of the cell at rest
What happens if we have hypocalcemia?
There will not be enough Ca++ to block the Na+ leak channels. The cell will become more positively charged, and depending on the type of cell, increasing that cell’s excitability. Or if the cell becomes significantly more positive, it may not work at all
Extracellular Effects of Ca++ & Hyperkalemia
-High K+ in the ECF causes a decrease in the concentration gradient.
-Less K+ is leaving the cell, making the membrane potential more positive
-Ca++ can be given to block Na+ leak channels, making the cell less positive
Motor Neuron, Skeletal Muscle, & Ca++
(Also, two important factors when the nervous system wants a skeletal muscle to contract)
Two important factors when the nervous system wants a skeletal muscle to contract
1. The action potential in the motor neuron
2. The action potential in the skeletal muscle
If there is not enough Ca++ surrounding our motor neuron, the membrane potential of the motor neuron will be more positive than they would be otherwise
Why is this a problem?
With really bad hypocalcemia, we expect to increased activity of the motor neurons that in turn increases the amount of contraction happening at our skeletal muscles.
We are not too worried about the direct effect hypocalcemia has on the muscle. What we are worried about is how this affects the activity of the motor neuron.
Trousseu’s sign is what we see with hypocalcemia
Mg++
-Works similar to Ca++, but Dr. Schmidt does not have a good explanation for it
-Reduces the electrical activity of a cell
Cl- & The Nervous System
-Cl- channels keep the brakes on the nervous system
-When there is increased Cl- moving into the cell, the membrane potential becomes more negative which hyperpolarizes the cell causing it to be more difficult to excite
-If we were to remove Cl- permeability from the nervous system, it would result in massive amounts of electrical activity within the nervous system resulting in seizures
What Affects the Rate of Electrical Propagation?(Neurons)
Rate of action potential is affected by:
Length of the nerve: The longer the nerve, the longer it takes to send this information
Diameter of the nerve: A neuro wider in diameter will conduct an action potential quicker because there is less resistance
A small neuron will have more resistance and the action potential will travel slower
Insulation of the neuron (myelin sheath): Myelin is an insulating compound on the neuron. The higher the insulation, the faster the action potential spreads
Myelin Sheath:
What is it?
-Made from sphingomyelin in the cell membrane
-Begins as a Schwann cell (PNS) or an Oligodendrocyte (CNS). Over time, it grows and wraps itself in a spiral around the neuron
-These layers become compacted, and the water that was initially in the cell gets squeezed out
-We are left with a lipid compound that has been wrapped around the neuron providing protection (less prone to crush injuries), speed, and efficiency
Myelin Sheath: What are the support tissues? (Oligodendrocyte vs Schwann)
Glial Cells:
-In the CNS (CN II, Brain, Spinal Cord, Retinas) myelin is maintained and produced by Oligodendrocytes
-If we lose myelin in the CNS, it is very difficult for the Oligodendrocytes to replace
PNS (Everything outside the spinal cord) myelin is maintained by the Schwann cells.
Schwann cells can regenerate myelin in the PNS as long as its not “too bad,” or a “continuous problem”
Myelin Sheath: How does this effect conduction?
-If a neuron needs to send action potentials quickly, it can add more fast Na+ channels in the cell wall.
-Another way to speed up transmission of action potential is to limit the amount of Na+ pumped out of the cell by the Na+, K+, ATPase pump
-Insulation around the cell can limit the amount of Na+ being let into the cell, but more importantly, it is not allowing the Na+, K+, ATPase pump to push out Na+
-This allows the Na+ to move forward along the neuron, making the action potential quicker, more efficient, and reducing the energy requirements of the neuron because it does not get pumped out of the cell until the next gap (Node of Ranvier) in the myelin sheath
Myelinated Neurons: Why are they less prone to ischemia?
The myelin allows for action potentials to be more efficient by requiring less energy.
By having decreased metabolic demands, the neuron does not require as much direct blood flow
Nodes of Ranvier & Saltatory Conduction
-There is a considerable amount of distance between each gap along the cell wall of the neuron
-Most neurons will have a very high population of fast Na+ channels within each node of ranvier
-The movement of the Na+ from one node to the next occurs in a jumping pattern, and this is referred to as Saltatory Conduction
Nerve Blocks; Does a myelinated or non-myelinated neuron require more anesthetic?
A myelinated neuron requires more anesthetic during a nerve block because of the super high density of fast Na+ channels at the Nodes of Ranvier
Demyelinating Diseases
-Optic Nerve: Our vision is going to be cloudy, can lose our peripheral vision
-Guillain-Barre: The body is generating antibodies to “stuff” that shouldn’t be there (after a viral infection, new vaccine)
-MS: Demyelinating disease that affects our motor neurons
Causes: Genetics, infection (with crazy stuff that our body hasn’t seen before), autoimmune
How does demyelination affect the neuron?
-Our fast Na+ channels, VG K+ channels tend to degrade and disappear underneath the myelin
-There will be Na+,K+,ATPase pumps still in place where the myelin has degraded, meaning that Na+ is going to be pumped out of the neuro prior to reaching the next node of ranvier
-We will not be able to send signals. What happens if this is occurring in a motor neuron? Action potentials will not be able to spread, this can result in paralysis
-The neuron will not look normal and will not function normally
Cell-Cell Signaling; Electrical Synapse
What is it? How does it function? What are they made of?
-Located in some smooth muscle, the heart, and in a few neurons
-Six connexin proteins form two connexons
-Connexons in one cell wall will pair up with adjacent a second connexon in an adjacent cell
-This happens in “rows”
-There is a channel through the connexons that acts as a conduit for small ions
-The ions can move easily and very quickly through the connexons. This is a much faster process than the binding of a neurotransmitter
A downside to this is that the electrical current can move in both directions. In the heart, for example, this can cause re-entry arrhythmias
-These re-entry problems only exist because of electrical synapses. This would not occur with a chemical synapse
Electrical Synapses in the Heart
What are they there for? What issues can this cause?
-There are many gap junctions in the heart to allow action potential to quickly spread
-In some areas of the heart, such as the pacing areas, our body intentionally has fewer gap junctions to allow for some delay
-An issue that can arise because of these gap junctions is that electrical current can flow both directions, allowing for re-entrant tachycardia
Cell-Cell Signaling: Chemical Synapses
What are they? How do they work?
-Electrical signal that is relayed via a chemical intermediary (neurotransmitter)
-The “target” on the receiving cell is going to define what the neurotransmitter does
Ex: ACh is inhibitory on the muscarinic receptors of the heart, and stimulatory on the nicotinic receptors of the skeletal muscle
-Presynaptic terminal: Sending cell
-Post-synaptic terminal: Receiving end
General Nerve Fiber Classification
-A fibers: heavily myelinated (largest)
-B fibers: lightly myelinated
-C fibers: no myelination (smallest)
A Fibers are subcategorized into:
Alpha: Largest
Beta: 2nd largest
Gamma: Third largest
Delta: Smallest of A fibers
-Fiber sizes vary from 20 microns to 0.5 micron
-Important motor neurons (like for skeletal muscle) are going to be large and heavily myelinated
-Tickle, cold, warmth, are typically smaller and unmyelinated
Neuron Structures
What structures make up a neuron? How many neurons do we have?
-Cell body: Soma. Vrm ~-60mv
-Dendrites: Receiving ends, not typically myelinated, project from the soma
-Axon: Sending end. Specialized to send action potential quickly. Usually myelinated. The end of the Axon is presynaptic side of the next connection point
~100million neurons
Post-synaptic neural connections:
Dendrites
-Dendrites are the signal-receiving end of the neuron. Not myelinated because they have so many connections. They can have excitatory or inhibitory connections.
Each “connection” is an individual synapse.
A neuron can connect with greater than 10,000 other neurons
-The Vrm will be less negative near an excitatory connection than the Vrm of the soma (~ -10mv, -20mv)
-Inhibitory connections will be more negative and more difficult to excite
Postsynaptic Neural Connections
Axon Hillock, Gaba
-Axon Hillock: Beginning of the Axon. There are only inhibitory synapses here. Vrm is about -70mv, -75mv This is how we pump the brakes on the nervous system.
Usually the receptors here are Gaba. Gaba receptors on the axon hillock increase Cl- permeability, and this is a key component of controlling the electrical activity of the central nervous system
If we removed all of the gaba, it would result in over-the-top levels of central nervous system activity (seizures).
ETOH is a Gaba receptor agonist. If someone has been consuming massive amounts of alcohol for 10-20+ years, they’re not going to be producing their own Gaba. Take the alcohol away–> massive seizures & over activity of the CNS
We only have inhibitory synapses at the axon hillock because an excitatory connection would mean that we bypass the thousands of connections with other neurons.
Glial Cells
Which is more predominant, neurons or glial?
If you had a brain tumor, what type of cell would it be?
Neurons are the most predominant type of cell in the nervous system. They are not proliferative
Glial cells are proliferative, so if you have a brain tumor it is most likely some type of glial cell.
Macroglia cells:
-Astrocytes: Provide support for the BBB. The appendages of the astrocyte wrap around the endothelial cells and capillaries within the brain.
Maintain pH of CSF (buffer) and electrolyte balance of CSF
-Ependymal Cells: Cilliated. Produce CSF and circulate the CSF with cillia
-Oligodendrocytes/Schwann: Myelin-producing cells
Microglia: Smallest. Immune function in the CSF. Function as macrophages and are able to keep the CSF clean and free of debris.
Types of Neurons: Mulitpolar, Pseudounipolar, Bipolar
Locations & Purpose
-Multipolar: Decision-making cells; whether or not to fire an action potential. Lots of space to receive information
Ex: Motor neuron: Pain sensors are telling the motor neuron that something is painful, the motor neuron makes the decision to pull body part away
-Bipolar: Two projections off of the soma. Bipolar neurons are used in special organs. Do not need extra attachments because they are sensory neurons themselves
Ex: Photoreceptors in the retina that send messages through the optic nerve
-Pseudounipolar: Majority of the sensory cells that are in the spinal cord or immediatly outside the spinal cord. This cell body does not really make decisions. It basically exists as a place to build proteins and to support the rest of the structures
Multipolar, Bipolar, Pseudounipolar Image
Somatic Sensory Receptors (Types of)
Pressure Sensors, Pain Receptors, Golgi & Muscle Spindle
-Somatic = Aware, “Sensible”
-Free Nerve Endings = Nociceptor; pain receptors
-Pressure sensors: (Na+ permeability)
Pacinian Corpuscle,
Meissner’s corpuscle,
Golgi tendon apparatus: A sensor in which the body can figure out how the muscles & limbs are performing. Integrated into our tendons and skeletal muscle
Muscle spindle: Stretch sensors interwoven into our skeletal muscles that can confirm if that muscle has contracted or not
These are considered “mechanoreceptors.” They’re able to take some kind of physical environmental disturbance and turn that into an electrical signal that can be relayed to the rest of the body
Somatic Sensory Receptors & Adaptation (Baroreceptor Ex)
Ex: Baroreceptors
Map is normally 100mHg; Baroreceptors should have some amount of Na+ flooding in, but this is our normal BP
If map increases to 150mmHg, the rate of action potential propagation would increase in the baroreceptors –> information is sent to the brainstem-> brainstem makes adjustments
If our map stays at 150mmHg for greater than 2 days; our baroreceptors become desensitized to prolonged hypertension and adapt to what they think is the new normal.
If our baroreceptors did not adapt, they would be extremely limited in their ability to respond to any additional changes from normal.
This is an example of slow adaptation.
Some sensors do not adapt at all. Some are fast, some are slow.
Reverse adaption occurs in some sensors- we stimulate something for a prolonged period of time, we become more sensitive to that stimulus
Pressure Sensor/ Ball Example & how that relates to fast adapting sensors
We have fast adapting pressure sensors because the body is concerned with changes in pressure.
Ex: Holding a ball in your hand; pressure sensors do not need to continuously tell your brain that there is that same, consistent pressure in your hand. It does not help the nervous system accomplish anything or make any decisions. We are only concerned when the pressure changes; like loosening our grip and dropping the ball
Susceptible to block?
Anatomy dictates whether or not the nerve bundles are easy to block
Pain Receptors & Reverse Adaptation
-Free nerve endings or nociceptor
-The more stimulus these receptors are subjected to, the more sensitized those receptors become
-The worse the pain is, for longer periods of time, the worse the pain becomes
-It is very important to tackle pain before it gets out of control
-Creating a nerve block that prevents pain from even starting is a great way to manage pain
Directional Nomenclature; Planes & Cross Sections
Superior/Inferior
Dorsal (Back) / Ventral (Front)
Anterior/Posterior
Medial/Lateral
Rostral (front and towards the top)
Caudal (Low and toward the rear)
These are typically used in neurosurgery
Distal (Further from the CNS)
Proximal (Closer to the CNS)
Sagittal: Left from right
Coronal: Anterior from posterior
Horizontal: Superior from inferior (magician’s cut)
Oblique: Goofy or odd angle
Brain:
Telencephalon- Cerebral cortex
Diencephalon- Thalamus: Important relay center, receives and sends information
Hypothalamus: Sensory area, control center for our osmoreceptors, infection sensors, body temperature regulation
Brainstem:
Midbrain, mesencephalon
Pons (olive shaped)
Medulla Oblongota
Spinal Cord
Locate:
Cerebral hemisphere
Diencephalon
Brain stem
Sulcus, Gyrus, Fissure
Sulcus: Groove
Gyrus/Gyri: Lump of neurons in supporting tissue
Fissure: Very deep groove
Major Brain Divisions (Lobes and landmarks)
Lobes:
* Frontal: Where we do most of our thinking
* Parietal: Primary somatosensory cortex
* Occipital: Where vision is processed
* Temporal: Language comprehension, listening to music & figuring out what the lyrics mean
Landmarks:
* Central Sulcus: Defining groove that separates the frontal lobe from the parietal lobe. Main anatomical marker if dissecting a brain
* Temporolateral Fissue: It’s name describes its function. It separates the temporal lobe from the parietal and frontal lobes
* Longitudinal Fissue: Separates the left and right cerebral hemispheres. Runs from the front of the brain to the back of the brain
Left lateral side of brain
Inferior view of the brain
Coronal- Separating anterior from posterior
Locate:
Longitudinal Fissure
Temporolateral fissure
Corpus Callosum: Where crosstalk takes place
Cerebral Cortex
White matter- Myelinated axons, sending/receiving
Grey matter- Cell bodies, decision making neurons
* The grey matter is superficial, which is odd because the body typically protects important structures by making them “deep structures.” One good thing about this location is that the blood vessels in the brain do not have far to travel to supply grey matter with nutrients
Grey Matter & White Matter in the Brain
How is each protected? Blood flow to the area?
White matter- Myelinated axons, sending/receiving. Located deeper in the brain than the grey matter
Grey matter- Cell bodies, decision making neurons
* The grey matter is superficial, which is odd because the body typically protects important structures by making them “deep structures;” however, the main blood vessels in the brain are also superficial, meaning the blood does not need to travel far to supply the grey matter with nutrients
* If the grey matter hits the inside of the skull (concussion, head injury) the grey matter can be temporarily or permanently damaged
* The body’s way of protecting the grey matter is by suspending the brain in CSF. The CSF gives us a bit of a buffer
What took place to get this view of the corpus callosum? Color?
Sagital, left lateral
We are looking at the inside of the corpus callosum. The only way we’d be able to see that is by cutting the brain in half with a saw. The corpus callosum is lighter in color because it contains a large amount of myelinated neurons
The cerebral hemispheres did not have to bet cut. Those can essentially be pulled apart because of the longitudinal fissure
Brain Subdivisions
Broca’s Area: Word formation, speaking. This is more of a motor function, that’s why it is in the frontal lobe
Wernicke’s Area: Launguage, understanding
Motor cortex: Pre-central gyrus This is where we execute our motor function. Planning motor funtion happens in the frontal lobe
Somatosensory: Post central sulcus
Limbic system: Emotional responses to things that are happening around us. Happens in temporal lobe and throughout the brain
Spinal Cord Cross-section. Grey vs White Matter, Dorsal and Ventral Horn
White Matter:
Generally filled with myelinated axons
Function is to send/receive signals
Grey Matter
Non-myelianated neurons & cell bodies
Cell bodies are where decisions are typically made
Ex: A motor reflex to something that is painful. That decision is made in the spinal cord and typically is not routed up to the brain
- Dorsal Horns: Sensory information goes in here. The cell bodies that reside in the dorsal horn are sensory neurons. Easier to access for anesthesia
- Ventral Horns: Where motor information leaves the spinal cord
Where does crosstalk happen? What are these locations called?
Locations to Find:
Where does the sensory info go in?
Where does motor information leave?
Anterior side of the cord?
Posterior side of the cord?
Posterior median fissue
Anterior median fissure (what goes here?)
Dorsal horns
Ventral horns
Central Canal:Lined with cilliated cells, moving fresh CSF from the brain down the spinal cord until the cord terminates. Then the CSF is allowed to float back up to the brain
Lamina X: An area in the grey matter of the spinal cord where crossover takes place
Anterior White Commisure (AWC) An area anterior to the grey matter where crossover takes place. Commisure means connecting
These are the only two spaces in the cord where the left and right are able to communicate
Which blood vessels feed into the spinal arteries?
There is a large blood vessel that travels beneath each rib.
The intercostal blood vessels feed into the anterior & posterior segmental arteries
Another important area of blood flow comes from the top of the cord, just below the brainsteam
We have autoregulation of both brain & spinal blood flow that is very tightly controlled
General Overview: Motor Pathway
Motor: (Efferent Signals)
A stimulus originating from the brain will need to go through deeper structures such as the thalamus. A portion of the information will have to go through the brainstem in order to enter the cord. Once at the level of the spinal cord, the stimulus exits through the anterior horn, down the anterior rootlets of the cord, and travels to skeletal muscles or motor targets
Afferent Sensory Pathway. How does the stimulus travel throuhg the cord?
-Sensory information travels in through the dorsal horns
-Motor information leaves the cord through the anterior horns
-The rootlets are segmented and attached with a horizontal approach. Sensory information travels through the posterior rootlets and enters the dorsal horn. From the dorsal horn, the information “jumps” over to white matter in the cord where it ascends the spinal cord, travels through the brain stem, and to the brain
This is showing a generalization of where the ascending columns are
The majority of them are in the posterior part of the spinal cord, then the sides of the cord, and lastly the anterior portion.
Pain, pressure, and other sensory messsges are sent this way
Descending signals are primarily what?
These pathways are primarily motor. They are located in the lateral and anterior cord
The rootlets form what? And merge into which structure?
What makes up the spinal ganglion? What kind of information is received in the spinal nerve?
-The anterior roolets lead into the anterior root which merges into the spinal nerve
-Motor cell bodies are located in the anterior horn
-The posterior rootlets feed into the posterior root and form the spinal ganglion before merging into the spinal nerve
-The spinal nerve is where motor and sensory information meet. Most spinal nerves will have mixed motor/sensory function
-The spinal ganglion (located in the posterior root only) is a collection of cell bodies of our pseudounipolar sensory neurons
How many pairs of nerves at each level? Where do they exit?
-We have spinal nerves exiting the spine for each level of vertabra that we have
**-Cervical Spine: **7 cervical vertabrae. There are 8 pairs of spinal nerves, one coming out of the left and one coming out of the right. C1 spinal nerves exit above C1… ending with C8 spinal nerve pair exiting below C7.
The c-spine nerve pairs are named after the cervical vertebrae in which the originate ABOVE
**-Thoracic: **12 Vertebrae, 12 pairs of spinal nerves.
These spinal nerves originate BENEATH the vertebrae for which they are named
Lumbar: 5 lumbar vertebrae, 5 sets of spinal nerves, exiting the cord underneath the vertebra for which they are named.
Sacrum: Originally start off with 5 vertebra at birth. Fuse into one solid bone as we enter adulthood. 5 pairs of spinal nerves associated with each of the original sacral vertebra, exiting the spinal cord underneath the vertebrae they are named after
Coccyx: 1 pair of nerves, two distinct vertebrae. Nerves originate at the base of the spine.
We start off at birth with 4 distinct vertabrae
Dermatone Man
A dermatome is a region of the body that is innervated by a set of spinal nerves
What shape? Shock absorbers?
The spine follows an S-shaped patern in adulthood
There are discs in between each vertebrae that provide cushioning and some degree of shock absorption (springy)
This helps us when we’re walking around all day, we don’t really notice the pressures that are weighing on our spine