Unit 3 Flashcards
Are there any absolutes in why we move?
no
What are the arguments for why we move?
- shows the adaptive value of the advanced NS
- moving in a coordinated manner lets us pursue mates and food as well as reacting to environmental stimuli (very adaptive for us)
What is the simplest explanation for why we move?
- all movements are based on ion channel activity
How do paramecium move?
- if it bumps into an object on anterior, Ca2+ channels open causing an AP and reversing motion
- if it bumps into an object on posterior, K+ channels open, hyperpolarizing cell, causing forward movement
Is the primary motor cortex ipsilateral or contralateral?
- contralateral
What broadmans’s area is the primary motor cortex?
- broadmans area 4
Where in the brain is the primary motor cortex?
precentral gyrus (precentral sulcus on a gyrus)
What does the primary motor cortex do?
-executes the move
-population coding for direction of muscles
What are the UMN of the primary motor cortex?
- pyramidal neurons in layer V
- axons project to brainstem and spinal cord
- each can influence multiple muscles
Where is the premotor area?
-in the premotor cortex
What broadman’s area is the premotor cortex?
6
What does the Premotor area do?
-plans movements, ideas for movement before movement happens
- Select appropriate movements based on external cues
Where are the premotor cortex and the supplementary motor area?
-anterior to M1
What is the order of activity between M1, SMA, PMA,
- PMA,
- SMA
- M1
What broadman’s area is the supplementary motor area?
medial portion of Broadman’s area 6
What does the supplementary motor area do?
- selects appropriate movements based on internal cues
What are the monkey motor experiments?
-Red light tells monkey where to hit
- Blue light tells them when to hit
- while it’s anticipating the movement we can see correlated activity in premotor cortex
- activity in M1 would correlate wit movement itself
What is apraxia?
- selective inability to preform complex (but not simple) motor acts
Does damage to M1 cause Apraxia?
no, it would cause paralysis
Where does apraxia com from?
- an inability to perform learned movements on command even tho the command is understood and there is willingness to preform the movement
What are the two types of apraxia?
- ideomotor
- ideational
What is the difference between paralysis and paresis?
- paralysis there is no movement
-paresis there is weak movement
What is ideomotor apraxia?
- impaired ability to perform a skilled gesture with a limb upon verbal command and or/ imitation
What does ideomotor apraxia look like?
- it can be shown with meaningful motor acts that don’t imply objects and gestures
or that imply object use - different events based on the area affected
Are people with apraxia aware that they have it?
yes
What is ideational apraxia?
- unable to plan movements related to interaction with objects because they’ve lost perception of the object’s purpose
-disturbance in the concept of sequential organization of voluntary actions (no sequential actions)
What would idational apraxia look like?
- “pick up something that would have coffee”
- can’t pick up mug
How is the tomographic map of M1 organized?
- movements and population coding more than muscles or body parts
- not as cleanly segregated as S1
- some organization (fingers grouped near hand)
Where does the basal ganglia receive input from?
-almost all of the cerebral cortex with most from the prefrontal cortex and motor cortex and least from sensory cortex
Where does the basal ganglia motor loop get projections from?
- projections from basal ganglia, through the thalamus, back to the premotor cortex (area 6)
- thalamic nucleus involved is a portion of the ventral lateral nucleus
Where does the basal ganglia motor loop project to?
- superior colliculus to influence head and eye movements
What is special about the cerebellum?
-only part of the brain that gets to review itself
Where does the cerebellum get its projections from?
- cerebellum, through thalamus, back to motor cortex
- The thalamic nucleus involved is the caudal portion of the ventral lateral nucleus
-cerebellum gets some sensory info more directly (vestibular and proprioceptive)
Where does the cerebellum motor loop project to?
- all UMN areas (not just cerebral cortex)
What does the basal ganglia do?
- function varies by which part of the basal ganglia is being considered, but in general, it evaluates and modulates cortical commands
- Evaluate and filter motor commands
- consistent with lots of input from prefrontal cortex and association cortex (involved in planning)
Are the dorsal, caudate and putman area all together?
- in humans they are all separate but animals have caudate and putamen together
What is required for normal initiation of voluntary movements?
dorsal, caudate, putamen area
What does the dorsal caudate putamen do?
helps in switching movement on and off and controlling and modulating various motor patterns
Is the basal ganglia bilateral or unilateral?
-bilateral, two different basal ganglia
What is disinihbition?
-limiting inhibition
What helps the basal ganglia function?
parallel circuits
What are parallel circuits involved in?
- cognition (executive loop)
- emotion (limbic loop)
- ventral striatum and nucleus accumbens core and shell really help with this
What is the direct pathway?
- acts to facilitate motor output and stimulate particular motor diagrams
What is the indirect pathway?
- acts to inhibit motor output and suppress competing motor pathways
Why do the indirect and direct pathways happen at the same time?
- to trigger wanted movements and supress unwanted ones
What causes the indirect and direct pathways to be different?
-its more about output, but indirect has an extra step that is going to change the result
What is the overall effect of dopamine in the direct pathway?
excitatory, encourages output
What is the overall effect of dopamine in the indirect pathway?
- inhibition
What happens if you get rid of the SNPC in the direct and indirect pathway?
- swings pathway to indirect and has an overall decrease in motor output
-less excitation of direct - less inhibition of indirect
- causes parkinsons
Describe dopamine?
-small NT
- catecholamine (like NE and E)
- reuptake is degraded in synaptic cleft
- 5 types of receptors
Describe the dopamine receptors?
- 5 types
-all metabotropic - d1 and d2 are highly expressed in striatum
- cell bodies not in striatum just terminals
What does D1 activation cause?
- increases in CAMP and is excitatory
What does D2 activation cause?
- decreases in Camp and is inhibitory
What is parkinson’s caused by?
- a loss of neurons in the SNPC, locus coerulus (NE) and dorsal raphe (serotonin)
- not a decrease in tonic output of BG, but a change in the pattern of activity leading to increased synchronization of oscillatory discharge leading to a tremor
What percentage of neurons are gone before a parkinson’s patient will have symptoms?
-typically 30-50%
- sometimes 70%
When does parkinson’s typically onset?
60s
What are the symptoms of parkinsons?
- resting tremor
-bradykinesia
-loss of smell
-cognition changes (depression) - mood disorders
- loss of bowel control
-akenisia
What is bradykinesia?
-slow movements
What is akenisia?
- lack of movements/ difficulty starting movements
What is the most common treatment for parkinsons?
LDOPA
How does LDOPA work?
- only works while there are still some neurons left
- dopa decarbozylase bypases RLS compared to other products, producing dopamine
- paired with a peripheral DOPA decarbozylase inhibitor becasue it can’t cross blood-brain barrier, limiting effects to brain only
What are the problems with LDOPA?
-loses efficacy as neurons die
- side effects like dyskinesia, psychiatric disturbances, impulse control
What is dyskinesia?
uncontrollable abnormal movements
Why does LDOPA create impulse control problems?
- due to synapse, circuit plasticity, and other dopamine pathways
What are LDOPA alternatives?
- transplants of Dopamine producing neurons from fetal tissue
- inactive subthalmic nucleus or internal globus pallicidus (deep brain stimmulation
Why can’t you use tyrosine for parkinsons?
-involved in rate limiting step
Why can’t you just inject more dopamine to fix parkinon’s?
-blood-brain barrier problems
What does a lesion that diminishes the indirect pathway do?
- increases motor output
How does deep brain stimulation work?
- disrupts the atypical electrical patterns in a way that allows the neurons to communicate more smoothly to lessen symptoms
- especially helps resting tremors and muscle stiffness (another Parkinson’s symptom), bradykinesia, and gait problems
- can be long-lasting but there is still a debate on when to do it
What are the drawbacks to deep brain stimulation?
- expensive and invasive
What is Huntington’s caused by?
- caused by a loss of neurons that project from striatum to external GP
- mutant form of HTT gene leads to neuronal death
How long until huntingtons causes death?
10-20 years
When does huntington’s onset?
50s-40s
What does huntington’s cause?
- chorea
- death of neurons elsewhere (frontal and temporal lobe) leading to personality disorders and dementia
- death due to associated complications (pneumonia, heart failure, choking, malnutrition) and increased risk of suicide
What is chorea?
- involuntary, rapid, jerky movements
-more subtle than dyskinesia
Compare ballism and huntingtons?
- Ballism: much more violent involuntary sudden movements
- Huntington - starts more subtle and increases intensity overtime, chorea, involuntary, rapid jerky movements
What is ballism?
- violent, involuntary (but you can try and direct) limb movements usually caused by a stroke
Where does the cerebellum develop from?
-hindbrain
Where does the cortex develop from?
-diencephalon
Why does cerebellum structure differ from species to species?
-different origins so different structure
What is unique about the electric fish cerebellum?
-cerebellum hypertrophies
- they sense prey and communicate through electrical signals and the cerebellum has to process sensory signals
What does the cerebellum do?
-process sensory signals and tell the brain when movement has occured
What is the cerebellom made of?
-3 layers
- 2 hemispheres, vermis along midline, deep cerebellar nuclei
What creates cerebellar layers?
purkunje fibers
What are the three layers of the cerebellum?
- purkunje cells/layers
- granule cells/layer
- molecular layer
What is the molecular layer of the cerebellum?
- outermost layer
- has dendritic arbors of purkunje fibers
What are dendritic arbors of purkunje fibers?
- dendrites covered with dendritic spines
- a Purkinje neuron receives as many synaptic inputs as any other neuron in the NS
- fan-shaped, almost 2D
- 100,000s of synapses
What do different regions of the cerebellum do?
serve different functions
What kind of somatotopic map does the cerebellum have?
- a fractured one
-maps are typically of ipsilateral body
Where does the cerebellum get its info from?
- ipsilateral sensory cortex
Where do parallel fibers come from?
granule layer
Describe parallel fibers?
- from the granule layer
- run perpendicular
- synapse onto many Purkinje fibers
How do climbing fibers work?
- go from contralateral inferior olivary nucleus in the brainstem then leading to one synapses many times onto a single purkunje cell leading to a very strong excitatory output
What is the difference between parallel and climbing fibers?
- carry proprioceptive info from muscles while parallel fibers carry info from cerebral cortex
What happens when climbing gibers and parallel fibers are active at the same time?
- parallel synapses et weaker and less effective, a form of LTD
What is parallel fiber input specificity?
- only parallel fiber synapses that are active at the same time as climbing fibers show LTD
-80% of purkunkje fibers are for error correction, primary role of cerebellum is error reduction - error reduction happens during a given moment and is a part of learning overtime
What is cerebellar ataxia?
- jerky inaccurate, poorly coordinated movements
What kind of causes does cerebellar damage have?
-many causes with many different effects
- autoimmunity to purkunje fibers, stroke, toxin damage, genetic disorders
What is an intention tremor?
-only a tremor when making movements, an expression of ataxia
What do lesions of the vestibulocerebellum lead to?
-impaired eye function
What is korsakoff’s syndrome?
- due to alcohol abuse
- degeneration of the lower body (anterior spinocerebellum)
- results in wide, staggering gait, later difficulty with walking at all
What are the four groups of UMNs?
- body posture (axial and proximal limb muscles)
- movements of the arms (Proximal arm muscles)
- orienting movements of eyes and head
- complex sequences of voluntary movements
Describe the body posture UMN group?
- axial and proximal limb muscles
- vestibular nuclei in brainstem (Feedback)
- axons run vestibulospinal tract
- axons run reticulospinal tract to spinal cord
- reticular formation in brainstem (Feed foward)
Describe the arm movement UMN group?
- proximal arm muscles
- red nucleus in midbrain
- axons run rubrospinal tract
Describe the orienting movements of head and eyes UMN?
- superior colliculus (optic tectum) in midbrain
- axons run in tectospinal tract
Describe the complex sequences of voluntary movements UMN?
- cell bodies in the contralateral frontal lobe
- primary motor cortex
- axons project to the spinal cord in corticospinal tract
Describe alpha motor neurons?
- LMN
- cell bodies arse in the ventral horn of the spinal cord
- axons in ventral roots and then spinal nerves
- typically innervate a large number of muscle fibers
What is ALS?
-neurodegenerative neuromuscular disease that causes muscle weakness and atrophy
How long does ALS take?
over 1-6 years voluntary movement is lost
Does ALS affect cognition, sensation, or intellect?
no
How does ALS cause death?
- failure of respiratory system
What is the main pathology of ALS?
- death of AMN, death before axon retraction occurs 1st
- in some cases UMn in M1 also dies, but axon retraction occurs first
What causes ALS?
- in 10% of cases its inherited, the rest are environmental/ unknown
- environmental cases are well documented (such as exposure to pesticides and cyanobacteria, most causes are not)
- ELEVATED GLUCOSE LEVELS IN THE SPINAL CORD, excitotoxicity caused death of MN
- anything that can slowly and selectively kill alpha MN can induce ALS
Why are ventral horns larger at enlargements?
- there are more alpha motor neurons there, thoragic region has small ventral horns and fewer AMNS
Why is there less white matter at the lumbar level than the cervical level?
-fewer axons
What do MN that innervate the same muscle have in common?
- cell body together in nuclei
- MN location represents an orderly representation of muscles innervated
What is a motor unit?
smallest functional unit of the skeletal motor system
What is the motor neuron pool?
- group of MN cell bodies that innervate a given muscle
What properties to motor units vary in?
-fatiguabilty
- speed of contraction
- size
How do motor units vary in size?
- fine motor control is optimal in small MU
- small MU tend to get recruited first and larger MU later
- more moter units= stronger contraction
What are the types of motor unit stimulation?
- muscle twitch
- summation of contractions
- sustained contraction (tetanus)
What system are muscle spindles a part of?
proprioceptive
What is the strect reflex innervated by?
-1A afferents
Do reflexes involve the brain?
no
How does the stretch reflex work?
- stretch activates mechanically gated channels in 1A afferents that are Na (possibly Ca) permeable
- contains small muscle fibers (intrafusal muscle fibers)
What are intrafusal msucle fibers)
- small muscle fibers
- innervated by gamma MN
- don’t directly contribute to muscle contraction
- critical
- to stretch receptor function, maintains tension on spindles for stretch detection
monosynaptic
What is an agonistic muscle?
- generates desired movement
What is an antagonistic muscle?
- opposes movement
What type of synapses are ipsilateral flexion and contralateral extension?
not monosynaptic
