KNES 251

dermatome

area of skin that corresponds to neurons of a specific region of the spinal cord

functions of the brainstem

autonomic functions like sleeping, eating and breathing

cerebellum

smooths motion paths

thalamus

sensory highway

cerebral cortex

responsible for higher order function

dendrites

receive signals

axons

APs travel down this part of the neuron

responsible for sending signals

ions present in cell function

inside: K+

outside: Na+, Cl-, Ca2+

current

rate of ion flow

voltage

electric potential difference

ligand gated channels

open when a neurotransmitter binds to it

thermally gated channels

open with heat/lack of heat

mechanically gated channels

open by touch or stretch

Coulomb’s Law

repulsion of similar charges

attraction of opposite charges

forces present in electrochemical equilibrium

molecular diffusion force

electrostatic forces

Nernst potential

voltage at equilibrium

one ion at a time

factors that affect resting membrane potential

K+ leak channels

intracellular K+ \[ \]

Goldman equation

voltage calculation that takes into account several ions and their permeabilities

resting membrane potential = ?

\-70 mV

action potential steps

* voltage-gated channels are closed at rest
* Na+ enters neuron, causing the membrane potential to become more positive in order to reach threshold
* Na+ voltage gated channels open
* Na+ voltage gated channels inactivate, K+ channels open
* hyperpolarization occurs

axonal/saltatory conduction

myelinated neurons

node of Ranvier to node of Ranvier

anatomy of a synapse

* action potential
* depolarization opens Ca2+ channels
* influx of Ca2+
* Ca2+ causes vesicles to fuse w/ the membrane
* transmitter is released via exocytosis
* transmitter is accepted by post synaptic neuron

SNARE protein

complex that helps w/ vesicle fusion

reversible antagonists (neurotoxins)

procaine, lidocaine, novocaine, cocaine

bind w/ voltage-gated Na+ channels to inhibit APs

irreversible antagonists

don’t wear off

e.g. TTX from pufferfish

EPSP

excites post-synaptic neuron

glutamate is the most common

IPSPs

inhibits post-synaptic neuron

GABA (allows Cl- in)

myofilaments

myosin (thick) and actin (thin)

excitation-contraction coupling

* action potential - NMJ
* presynaptic depolarization (volt-gated Ca2+ channels)
* Ca2+ flows in, attaches to vesicles
* SNARE complex activates Ach
* Ach ligand-gated on muscle opens
* muscular depolarization
* triggers AP
* depolarization SR
* Ca2+ flows to myofibrils
* binds to troponin, shifts tropomyosin to expose active site
* myosin/actin bind, hydrolyze ATP

type I muscle fibres

* slow
* oxidative
* least force
* least fatigable
* e.g. walking
* recruited first

type IIa fibres

* fast oxidative
* the “middle ground” fibre

type IIb fibres

* fast glycolytic
* most force
* fatigues the fastest
* recruited last

motor unit

a motor neuron and the fibres it innervates

MU size recruitment principle

turns on first = turns off last

smaller MNs recruited first

bigger MNs get recruited w/ increased force

motor pool

group of motor units in a muscle

surface EMG

pads placed on muscle belly at pennation angle

limited due to cross-talk

amplitude = muscle force produced in MVC

muscle belly

thickest part of muscle

pennation angle

direction of fibres

rectification

taking the absolute value of all the data

smoothing

averaging of all the values noted

indwelling EMG

placed directly into muscle

less cross-talk

limited by misplacement, worse effects than cross-talk

effects of (de) training on EMG

* increases or decreases EMG amplitude

muscle spindles

sensory receptors that provide feedback on the stretch of a muscle

intrafusal fibres

don’t produce force

lengthen/stretch changes muscle length

afferent axons

innervate sensory endings of muscle spindle and send feedback to spinal cord

efferent axons

gamma MNs innervate polar ends (contractile), send inputs FROM spinal cord

GMN endings

stimulate intrafusal muscle fibres

allow for proprioception

w/o them, intrafusal fibres would go slack

allow muscle spindle to keep responding during contraction

sensory endings

sense length

capsule

connective tissue

extrafusal fibres

cause muscle contractions

primary afferents

mostly bag type

annulospiral

more sensitive to DYNAMIC phase (i.e. velocity of the stretch)

secondary afferents

flower/chain type

more sensitive to changes in length (i.e. stretch)

proprioception

perception of limb position

kinesthesia

perception of limb movement

cutaneous receptor classification

based on receptive field size and responses to sustained indentation

Merkel Cell

* type 1 (superficial)
* high concentration at fingertips
* slow adapting
* texture
* highly sensitive to edges and curvature
* irregular discharge when stimulated
* Merkel Cell-Neurite Complex: sensory neuron + Merkel cells contacted
* moderately low threshold

Meissner’s Corpuscles

* fast adapting
* type 1 - extremely superficial
* fast response to indentation changes
* velocity of skin indentation
* motion across skin
* 40% of hand innervation
* low thresholf
* sensitive to low frequency vibration
* slip/motion detection + grip
* e.g. holding a glass of beer

Ruffini Endings

* type 2 (deep)
* larger receptive fields
* equally distributed in hand
* humans only
* slow adapting
* continuous firing
* skin stretch
* regular discharge when stimulated
* high mechanical threshold

Pacinian Corpuscles

* most sensitive
* vibration
* extremely low mechanical thresholds
* acceleration of indentation
* high frequency
* vibration through objects

mechanical threshold

skin indentation needed to trigger APs

di/polysynaptic

2+ synapses

convergent pathway

many receptors, one target neuron

divergent pathways

one source, many effector neurons

reciprocal inhibition

relaxes agonist while contracting antagonist

feedback inhibition and excitation

\-ve and +ve feedback

pre-synaptic neurons send only EPSPs/IPSPs

muscle stretch reflex pathway

1. Stimulus stretches sensory receptors in extensors
2. Sensory afferent neuron synapses w/ and excites motor neuron in the spinal cord
3. Sensory neuron also excites spinal interneuron
4. Interneuron inhibits motor neuron to flexor muscles
5. Motor neuron synapses onto extensor muscles and causes it to contract
6. Flexor muscle relaxes
7. Leg extends

tonic excitatory input

* sensory (cutaneous stimulation)
* descending (corticospinal stimulation)
* excitatory (facilitatory input) - meaning that same stimulation allows the threshold to be crossed

cutaneous withdrawal receptors

* sudden and painful cutaneous stimulation
* wired in a way that withdrawal occurs in the correct direction
* longer to sense inflammation
* neurodiameter for proprioception is larger

cutaneous flexed-crossed-extension reflex

retracts injured leg but compensates w/ the other leg

weight transfer

e.g. stepping on a nail

Babinski’s sign

* dorsiflexion of big toe when bottom of foot stimulated
* should only be +ve in babies
* can indicate neurological problems

GTO autogenic inhibition reflex

* shuts down muscle during MVC as a protective reflex if force output becomes dangerously high
* prevents ruptured tendon'
* GTO becomes more active at higher force levels

Renshaw cell

inhibitory interneuron

inhibits the same motor neuron and its neighbours

activated by a small “collateral” branch

recurrent inhibition

neuroscientific negative feedback loop

final common path

all the inputs go through MNs to produce movements

premotor cortex

planning motion

Betz cells

layer 5 neurons

send APs down descending spinal tracts (LCST + VCST)

motor homunculus

* “map” that shows correspondence between regions of the brain and the regions of the body in motion
* undefined borders
* lack of accuracy and lots of overlap
* stimulation can lead to specific movements
* differentiation between movements is hard

population vectors

* M1 neurons fire more in certain directions
* peaks in tuning curve indicate which direction neurons are tuned to
* complex movements: predict movement vectors

circular vector diagram

shows which neurons like which directions

preferred directionality

somatopic maps

* similar to motor homunculus
* goes around from head to toes
* bigger regions = more sensitive

plasticity

* remodelling depending on use
* change with things like amputation

phantom limb

occurs during S1 remodeling

dorsal root ganglion

all sensory afferent cell bodies

dorsal column medial leminiscus

* ascending tract
* mechanosensory inputs travel up the spinal cord
* cutaneous receptors/proprioception
* decussates at caudal medulla
* long axons

ventral spinothalamic/anterolateral

* sensory inputs from nociceptors and thermoreceptors
* decussations at level it enters the spine

lateral corticospinal

* motor info to distal muscles
* decussates at caudal medulla
* refer to motor homunculus

ventral corticospinal

* motor info to proximal muscles
* innervates bilaterally

contralaterally

other side

ipsilateral

same side

factor in ascending vs descending

paraplegia

lower body paralysis

hemiplegia

paralysis of one side of the body

tetra/quadriplegia

paralysis of all four limbs

brown-sequard syndome

if the lesion is below the caudal medulla:

* reduced pain/temp on opposite side (vst decussates immediately)
* reduced mechanosensory on same side
* loss of sensation at site of lesion

causes of SCI

* tumours
* ischemia
* disease
* \

signs of SCI

* Babinski’s sign
* hyperreflexia

ASIA scale - SCI diagnosis

* mechanosensory = Q-tip
* pain = pin prick
* motor control = strength test
* neurological scans
* tests each dermatome

SCI therapies (incomplete severance)

supported treadmill walking

exoskeleton supported walking

gross motor skills

* low accuracy
* large, whole-body movements
* large muscle groups
* e.g. dance

fine motor skills

* precise
* small muscle groups, small movements
* e.g. surgery, writing

closed motor skills

* predictable environment
* e.g. typing, brushing your teeth