Exam 3: Motor system and Basal ganglia Flashcards
somatosensory system
controls striated skeletal muscles ⇒ this is how you move
2 components of the somatosensory system
- Moves the bones of your body around
- Controls posture, limbs, and face
autonomic motor system
sympathetic and parasympathetic control of heart, blood vessels, (GI) digestive tract ⇒ background processes
2 main sets of neurons
- upper motor neurons
- lower motor neurons
upper motor neurons (UMNs)
cell bodies are in the brain mostly that descend to various places in the brainstem and spinal cord
- start in the cerebral cortex and target the lower motor neurons
- Control lower motor neurons
Lower motor neurons (LMN’s)
actually leave the CNS and go out into the body and touch muscles to cause physical contractions
- start in brainstem (cranial nerves) or spinal cord (spinal nerves) and directly target muscles
- Brainstem is head and face while spinal cord is everything else
where do the soma of LMN’s sit and where do they synapse?
Their soma sit in the ventral horn of the spinal cord and brainstem cranial nerve motor nuclei
- these leave the spinal cord via the ventral root and make their way out to the periphery to contact a muscle in the tissue
- motor neurons synapse directly onto skeletal muscles
neuromuscular junction/synapse
the motor neuron muscle connection
- Similar to a synapse that happens in the brain between different neurons
how do motor neurons signal muscle contractions?
via acetylcholine
acetylcholine
neurotransmitter chemical release that acts on the muscle tissue to cause muscle contractions
- Like an action potential but instead is a muscle contraction
fascicles
large circles of what muscles are made up of and contain bundles of muscle fibers
fiber
small round portions that make up a fascicle unit in the muscles
how do muscles connect to bones?
via tendons
each adult muscle fiber is targeted by what?
by one neuromuscular junction
where are acetylcholine receptors concentrated?
on the muscle fiber membrane at the neuromuscular junction
what do muscle fiber membranes do?
allow the flow of ions in and out like normal cell membranes
- Muscle fibers are more than one cells but has a collective property of a membrane with cell like properties ⇒ mm-inches possible
- This limits the possibility of contraction because contractions have to spread throughout the whole muscle to contract at once
botox (botulism toxin)
blocks acetylcholine release at the neuromuscular junction
- Injection into muscles causes paralysis ⇒ cosmetic approach to reduce wrinkles
how does contraction work?
- Acetylcholine released from the motor neuron activates acetylcholine receptors on the muscle
- Acetylcholine receptors are ligand-gated ion channels
- Activation of the receptor causes depolarization so sodium enters the muscle fiber and potassium exits
- This spread across the fiber like an actin potential ⇒ calcium is released inside the fiber
ligand gated ion channels
determined by the presence of a certain molecule such as acetylcholine on the receptor which opens the depolarization of the muscle cell/other type of cell
what do muscle fibers contain?
alternating bands of motor proteins (actin and myosin) that form stripes in striated muscle
what is calcium released in response to?
acetylcholine binding to the muscle fiber activating the protein complex that causes muscle contraction
- Once acetylcholine binds then calcium can come into the cell to create the muscle contraction
how does myosin work in muscle contraction?
myosin molecules slide across actin molecules, shortening the muscle fiber
- Myosin requires energy (ATP) to produce muscle contraction
- The head of the myosin make contact with the fibers and they have a conformational change to physically pull the actin bands together
- The protein complexes synch together and there are millions collectively working together to pull the chunk of tissue together
- ATP is the rate limiting step since they need it for energy
type 1 muscle fibers
thin, slow, low force, and slowly fatigue
type 2A muscle fibers
thick, intermediate speed, intermediate force, intermediate fatiguability
type 2B muscle fibers
thick, fast, high force, and rapidly fatiguable
slow sustained exercise increases the proportion of which types of muscles?
type 1
short high intensity exercise increases the proportions of which types of muscles?
type 2 => A and B
motor unit
motor neuron and the muscle fibers it innervates
muscle groups with fine dexterity
(hands, face) have smaller motor units ⇒ more neurons devoted to these areas with fine level control than other types
course control muscles
(thighs, back) have large motor units
lower motor neurons are controlled by? (2)
- local circuits
- upper motor neurons
local circuits
LMN’s
- sensory neurons (reflexes)
- interneurons in the spinal cord
upper motor neurons contain? (2)
- cortical (pyramidal tracts) control
- noncortical control
cortical (pyramidal tracts) control
mostly voluntary motor control
noncortical control
mostly non voluntary motor control
types of noncortical control
- Vestibular nuclei
- Superior colliculus
- Red nucleus
- Reticular formation of the pons and medulla
reflex circuits
local and fast that don’t need a signal to come from the brain
- Triggers relapse circuits that go to the spinal cord and back out to the periphery as a reflex due to it happening so fast
why don’t reflex circuits use the brain?
If the brain came in to play it would be too slow
How does the motor cortex influence movement?
biggest descending input to lower motor neurons comes from upper motor neurons in layer V of the primary motor cortex
where is the primary motor cortex and what is it necessary for?
on the precentral gyrus of the frontal lobe
- necessary for voluntary movements
- organized somatotropically so more space is given to face and hands
what does the upper medial of the motor cortex control?
the lower body
- as you move down you get to hands and face
premotor cortex
essential for planning movements and executing learned movements
- your body is one step ahead of what movement you will do next
how does somatosensory cortex and association cortexes influence movement?
integrating other sense into movement and planning (such as somatosensation)
how is the thalamus involved in movement?
relays basal ganglia and cerebellar information for movement coordination
corticobulbar tract
control head and neck muscles ⇒ reference to brainstem
components of the corticobulbar tract
- Bilateral brainstem cranial nerve motor nuclei
- Targets LMNs in cranial nerve nuclei in brainstem
- All cranial nerves except olfactory, optic, and vestibulocochlear have a motor function
- Control of the eyes, face, mouth, larynx, and neck
corticospinal tract
control body/limb muscles
components of the corticospinal tract?
- lateral
- ventral/anterior
- Descending route from motor and premotor cortex
lateral corticospinal tract
to entire contralateral spinal cord (mostly limb)
- Lateral tract crosses the midline (decussation)in lower medulla
what is the descending route from the motor and premotor cortex through the corticospinal tract? (4)
- Internal capsule
- Cerebral peduncle (midbrain)
- Pons
- Pyramids (medulla)
ventral/anterior corticospinal tract
to bilateral cervical and upper thoracic spinal cord ⇒ mostly central body
- ventral/anterior tract descends uncrossed
- controls muscles on both sides of the body compared to lateral which is contralateral
- depending on damage, it may affect different muscle groups ⇒ lateralization vs not
everything neck down is controlled by which tract?
corticospinal tract
initiation of voluntary movement control comes from what?
upper motor neurons
internal capsule
white matter tract in the brain that helps connect parts of the brain including the cortex
- The descending motor system is important coming from the primary motor cortex
where does the internal capsule tract go?
They keep going to the cerebral peduncle which is another band of axon fibers connecting the brainstem and the cerebrum together
are more neurons in the lateral corticospinal tract or the ventral?
more neurons in the lateral
where does the corticospinal tract cross the midline and synapse on?
crosses the midline at the lower medulla, descends in the spinal cord, and synapses on LMNs in the ventral horn of the spinal cord ⇒ go down the other side of the spinal cord
what does the lateral corticospinal tract mainly control?
limb muscles
how do LMNs receive information via the corticospinal tract?
the muscles are receiving information in a very controlled and specific way (lateral on outside and midline on inside)
LMNs for limb muscles are in the lateral ventral horn (targeted by the lateral corticospinal tract)
- LMNs for the trunk muscles are in the medial ventral horn (targeted by the ventral/anterior corticospinal tract)
damage to the motor cortex produces paralysis ___ vs. damage to the spinal cord produces paralysis primarily ____
contralateral; ipsilateral
4 non pyramidal motor pathways for unconscious movements?
- rubrospinal
- vestibulospinal
- reticulospinal
- tectospinal
→ mixture of crossed and uncrossed pathways
rubrospinal tract
red nucleus to spinal cord for coordinating fine limb movements
vestibulospinal tract
vestibular nucleus to spinal cord for balance and head position adjustment
reticulospinal tract
reticular formation to spinal cord for postural control and learned limb movements
tectospinal tract
superior colliculus to cervical spinal cord for coordinating head and eye movements
amyotrophic lateral sclerosis (ASL) aka Lou Gehrig’s disease
progressive loss of motor control due to degeneration
- Symptoms follow from which motor neurons die
primary lateral sclerosis
affects only UMNs
progressive muscle atrophy
affects only LMNs
paralytic polio
motor neurons are directly targeted and killed by the virus, causing muscle atrophy and paralysis
basal ganglia
subcortical nuclei critical for information processing related to decision making and movement selection (diencephalon)
components of the basal ganglia function (3)
- Sit in the middle of the brain under cortex
- Relay and process information but also regulate output as the animal experiences the world
- Important for decision making, movement, action, motivation, learning, etc.
structures in the basal ganglia (4)
- striatum (caudate, putamen, nucleus)
- globus pallidus
- sub thalamic nucleus
- substantia nigra
what is the main input and output to and from the basal ganglia?
input is from the cortex and main output is thalamus
general functions of the basal ganglia (3)
- Voluntary movements and action selection
- Skill learning
- Motivation and emotion ⇒ to express this we must move
where is the nucleus accumbens?
only present in the anterior/rostral striatum
striatum
receives dense inputs from cortex and dopamine neurons in the midbrain
- anterior and a big entry part for BG
internal capsule
divides the striatum and is a white matter tract with axons from cortex
2 divisions of the globus pallidus?
- external (GPe) => intrinsic nucleus
- internal (GPi) => part of the output of the basal ganglia
globus pallidus
control conscious and proprioceptive movements
lies medial to the putamen and is part of the diencephalon
2 divisions of the substantial nigra?
- pars compacta (SNc) => major dopamine center
- pars reticulata (SNr) => part of the output of the basal ganglia
substantia nigra
important for connectivity and communication
- part of the midbrain/mesencephalon
- positioned between the subthalamic nucleus and cerebral peduncle
- dopamine neurons are concentrated in the SNc where they project to the dorsal striatum
- SNc dopamine neurons contain high levels of neuromelanin, pigment them black/brown
where is the striatum located compared to substantial nigra and sub thalamic nucleus
striatum is telencephalon and the other two are in the diencephalon
where in the basal ganglia do cortical neurons project to?
to the striatum and then to the internal unit which has specific output to the thalamus (SNr and GPi)
corticostriatal neurons
signal with glutamate to excite medium spiny neurons (MSNs) in the striatum ⇒ excitatory cortex info
striatal MSN’s
project to multiple BG structures for information processing
- MSNs signal with GABA to inhibit target neurons
- Dopamine input from SNc can modify MSN activity ⇒ different kind of neurotransmitter that sends dopamine (can have different effects) => excitatory via D1Rs and inhibitory via D2Rs
what are the main output centers for the BG?
the GPi and SNr which signal ventral anterior and ventral lateral nuclei of the thalamus with GABA
what integrates BG signals and sends excitatory projections to the cortex; what is it critical for?
the thalamus
- Activity in cortico-strioato-thalamic loops is critical for movement and control and basic learning/motivational processes
general functions of the basal ganglia? (3)
- learning
- motivation
- action selection
what can BG pathology result in?
cognitive and learning deficits that contribute to psychiatric diseases
hypokinesia
reduced movements
akinesia
impaired initiation ⇒ can’t start a movement vs expression as it moves
bradykinesia
slowed and reduced ⇒ cannot make fluid movements vs control
rigidity
stiffness and resistance
hyperkinesia
increased movements
chorea
rapid/jerky movements
athetosis
slow writhing
ballism
flailing
nigrostriatal dopamine neurons
are concentrated in the SNc, where they project to the dorsal striatum
- Goes from SNc to striatum in the caudate and putamen area
- These are what die off in parkinson’s disease
Parkinson’s disease
(hypokinesia) symptoms arise from degeneration of dopamine neurons in substantia nigra pars compacta ⇒ substantia nigra are the dark band (light in parkinson’s bc they died)
symptoms of Parkinson’s
(dopamine neuron dies) Impaired movement in 1% of people over 60
- Akinesia
- Bradykinesia
- Resting tremor
- Muscle rigidity
Oral levodopa (L-DOPA)
dopamine precursor molecule that crosses the blood brain barrier and is converted to dopamine
- Less effective in late stage Parkinson’s and can produce unwanted involuntary movements
- Parkinsons has no cure but there are treatment options that improve motor control
deep brain stimulation
surgical treatment for Parkinson’s, OCD, and other diseases
- Stimulating electrodes are implanted usually into the GPi or subthalamic nucleus
- Can restore movement control in Parkinson’s patients
Huntington’s
degeneration of medium spiny neurons in striatum ⇒ dying of striatal neurons
- Genetic origin from inheritance of a dominant mutation producing a mutant protein that kills MSNs
- Produces hyperkinesia ⇒ involuntary random, rapid movements
- Gets worse over time and ends up being deadly
tourettes syndrome
dysfunction in striatal and frontal cortical circuits ⇒ hyperkinesia (more promising research)
dystonia
uncontrollable sustained muscle rigidity and contortions
how do most BG diseases progress?
from motor impairments to cognitive/decision making deficits
- basal ganglia systems are critical for learning, reward, cognition, in addition to movement
