Where are bipolar neurons found in the body?
The eyes
Pseudounipolar: in PNS, sensory/visceral receptors
Multipolar: effector organs
The sodium potassium pump
Pumping sodium and potassium ions against their concentration gradient
Maintaining the resting membrane potential
20% of the resting membrane potential directly due to this pump, 3 Na+ out, 2K+ in,
net +1 out
80% of the resting membrane potential is indirectly due to this pump due to the ion
concentration gradients resulting from the activity of this pump
Lots of potassium channels
As these ions are leaving the cell and going down their concentration gradient,
the positive charge is also leaving
Sodium is voltage gated channels (that channel only opens at a certain
voltage)
Temporal and spatial summation
Synapses creating excitatory or inhibitory post synaptic potentials
Frequency coding
Absolute: can't initiate another action potential bc sodium channels are closed
Relative refractory period
PNS analogue to MS
MS: conduction velocity decreases
PNS: affecting Schwann cells
Question: basaed on the cart showing action potentials, are these synapses inhibitory or
excitatory
VM1: action potential
VM2: no action ptoential
VM3: no action potential
Synapse 1: b/w neuron 1 and neuron 2 is inhibitory
Synapse 2 is inhibitory (when not firing we're seeing action potential)
Bobby has split brain. Based on brain anatomy, what would happen if you showed his left
eye a dog, his right eye a cat, and then asked him what kind of animals he sees?
Corpus callosum is split
Nerves coming from the eye aren't involved with the split of the corpus callosum in
this ase. He can say that he sees a cat bc language centers on left side. You see it but
you can't say that you see it.
He's going to be able to say that he sees a cat but not say that he sees a dog.
He can write his answer
Still have communication with association fibers occurring
Severed brain
A word is flashed to the right field view and the patient is asked what he saw, he is
able to say his answer because the verbal processing is in the left hemisphere
A word flashed to the left field of view and the patient is asked what he saw, he can
not verbally say his answer but can can draw it with his left hand
Involuntary Reflexes
Automatic patterned response to a stimulus
Stimulus --> sensory receptor --> afferent neuron(towards) --> integration center (CNS) -->
efferent neurons (Away) --> effector organ (muscle, gland)
Reflex classification
Level of neural processing Spinal Muscle spindle stretch
Cranial reflex
Pupillary reflex
Efferent division controlling Somatic (to skeletal muscle) Muscle spindle stretch
effector Autonomic (to smooth reflex
muscle, cardiac muscle or Baroreceptor reflex to
glands) control blood pressure
Developmental pattern Innate Muscle spindle stretch
Conditioned reflex
Pavlov's dogs
Number of synapses in the Monosynaptic (2 neurons & a Muscle spindle stretch
pathway synapse) reflex All other
Polysynaptic reflexes
Muscle Spindle Stretch Reflex
The only monosynaptic reflex in the body
Stimulus --> muscle spindle --> afferent neuron --> CNS , collaterals going up to the
brain at the same time
Efferent neurons --> quadriceps --> cause them to contract
Interneuron --> inhibiting signal from going to the hamstrings so there's relaxation
of hamstrings
Result: cause leg to kick out
Withdrawal and crossed-extensor reflexes
Stimulus --> nociceptor (pain receptor) ---> afferent neuron
1st synapse --> contraction of the hamstring
2nd synapse --> inhibition of the signal down to the quadriceps, relaxation of quads
3rd synapse --> activation of contraction of quads and relaxation of hamstrings
Crossed-extensor reflex: initaiated simulatneously as the nocicpetors have branches
that send singals via interneurons to efferent neurons controlling muscles on the
possite leg
Can override this reflex
Have collaterals going up to the brain so brain can interpret what's happening and
can override these reflexes
Pupillary Light Reflex
Stare at a light- pupils contract
Sensory signals going to retina then the visual cortex and the efferent neuron is
going out to the pupils causing the iris to contract
Voluntary Motor Control
Constant feedback is important for smooth movement
Innervation of skeletal muscle
Efferent neurons originate in ventral horn
One motor neuron to each skeletal muscle cell
Also called lower motor neuron
Always excitatory
Activation of motor neuron= contraction
No activation of motor neuron= relaxation
If it's always excitatory, which neurotransmitter is involved? Acetylcholine!
Input to Motor Neurons
From afferents (as with reflexes)
From brain: lateral pathways & ventromedial pathways
Lateral pathways: voluntary movement
Pyramidal tracts: fine control of distal extremities, most cross to contralateral
side in medullary pyramids
Direct pathways from primary motor cortex to the spinal cord
Axons of neurons in these tracts terminate in the ventral horn, called
upper motor neurons
Rubrospinal tracts: join axons of the pyramidal tract
communication to red nuclei of the midbrain primarily from primary
motor cortex
Less important than motor control, pyramidal tracts are more important
Most cross over to the other side and join the axons of the pyramidal
tract
Ventromedial pathways: both voluntary & involuntary movement
Support movement of trunk muscles and proximal extremities
Indirect input to motor neurons
Tectospinal tracts: originate in the superior colliculus of the midbrain, receive
information from the eyes and ears, involved with head and eye movements
that correctly position the yees to look at an object & follow its movement
Vestibulospinal tracts: originate in the vestibular nucleus of the medulla,
coming from inner ear, balance, posture
Posture: involuntary control, input from skin receptors, eyes, ears,
proprioceptors (figuring out where your body is in space), vestibular
apparatus
Reticulospinal tract: originate in the reticular formation of the medulla, also
involved with balance
Ventromedial pathways control large groups of muscles and lateral pathways small
groups
Nerve tracts: pyramidal tract neurons & extrapyramidal tract neurons
Control of pressure
Ventromedial pathways from brainstem
Mostly involuntary control
Input to brainstem from five sources: skin receptors, eyes, ears, proprioceptors,
vestibular apparatus
Motor coordination
Cerebellum: guiding system for controlling movement, a lot inputs coming in and
processing information and altering movements to increase fine motor control
Provides feedback control of motor function
Contributes to muscle tone
Involved with memory
Input from the sensorimotor areas of the cortex, the basal nuclei, brainstem,
spinal cord. Then sends signals back to the cortex via a relay in thalamus so
the cortex can adjust
Damage to cerebellum: intention tremor, clumsy movements
Basal nuclei: feedback control, selecting purposeful movements fine tuning, writing
smoothly
Areas of grey matter inside white matter
Huntington's chorea: genetic disorder of basal nuclei, pathway from basal
nuclei to thalamus is lost
Symptoms: loss of motor coordination, increased involuntary motions
like twitches, jerking motions, in advanced stages (loss of cognitive
functions). Onset is usually 40-50s
Parkinson's: disease of basal nuclei, lack of dopamine in substantia nigra
Symptoms: rigidity, slow stiff movements, involuntary movements or
tremors, stooped, shuffling gait, difficulty initiating and stopping
movements
Language
Spoken, written, sign language
Aphasia: language dysfunction
Broca's area: speech formation (also written and sign speech not just oral), frontal
lobe
Wernicke's area: language comprehension, temporal lobe
Deafness: right auditory cortex doesn't function
Damage to Broca's in deaf people: deficit in forming signs
Damage to Wernickes: difficulty in interpreting signs
Sleep
We need sleep for 30% of our lives, active process
Restorative, enhancing memory, learning, supports immune function
EEG: electroencephalography, a way to visualize the elctrical activity of brain
Two types of sleep: slow-wave sleep, REM sleep
Sleep wake cycles
Ascending reticular activating system ARAS (reticular formation of the
brainstem)
Awakens the cortex, brings you out of sleep
Part of reticular formation
Projections to thalamus, hypothalamus, and forebrain
Forebrain: induces slow-wave sleep SWS
Temperature fluctuations: body is warmer when it's awake
Neurotransmitters
Awake state: acetylcholine, norepinephrine and dopamine (-ARAS)
Nicotine mimicks acetylcholine, and cocaine and amphetamines mimick
catecholamines
Histamine & orexin
Sleep state
adenosine (SWS induced by forebrain)
Caffeine blocks this
Acetylcholine: REM sleep, Pons
Heart rate also coincides with sleep cycles
Ratio of rem to nonrem sleep is increasing with time
REM stage is most similar to stage one in terms of heart rate & brain waves
Emotions
Cortical association areas integrating multiple inputs and sending signals to the
limbic system
Limbic system creates emotion, and goes to cortex and perceived by the cortex
But also goes to the hypothalamus and leads to hormonal changes or goes to the
brainstem leading to motor responses and autonomic responses
Drugs- euphoria by activating dopaminergic systems of basal ganglia
Learning
Associative learning: associate two stimuli
Non-associative learning: habituation (desensitizing to ex construction noise) &
sensitization (become hypersensitive ex construction)
Memory
Procedural (implicit) memory
Learned motor skills and behaviors
Cerebellum is involved
Automatic response: doesn't require a conscious effort
Declarative (explicit) memory
Hippocampus
Learned facts, events, and experiences
Requires conscious effort for recall
Short term vs long-term
Information is first stored as short term memory
Lasts seconds to hours
Information is lost unless consolidated
Short term memory: frontal lobe
Long term memory: temporal lobe including hippocampus
Plasticity
Ability of neurons to restructure themselves as you learn
Develop new synapses
New neurons may be able to develop in areas associated with memory
Long term potentiation: repetitive stimulation increases strength of synaptic
connection
Through increase in the postsynaptic cell's sensitivity to the neurotransmitter
released at that synapse, an increase in the quantity of neurotransmitter
released by the presynaptic cell with each action potential or both
Ex: low levels of activity in the presynaptic cell. Glutamate neurotransmitter is
released and can bind to two receptors, the AMPA receptor which is a sodium
channel and the NMDA receptor which is a calcium channel. It can bind to the
sodium channel easily but not to the calcium channel because there is a magnesium
there.
When there's high levels of activity in the presynaptic cell, the glutamate can bind to
the calcium channel and the magnesium is displaced. Have the 2nd messenger
system activated
AMPA receptor channels become more sensitive to glutamate & the postsynaptic
cell produces a paracrine that causes the presynaptic cell to release more glumate
With repetition, we are increasing the connection at the synapse
