Sunteți pe pagina 1din 6

 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

S-ar putea să vă placă și