Exam 3 Flashcards
(76 cards)
1
Q
Lower Motor Neuron
A
- Any cell in the somatic nervous system that has a cell body in the SC/brainstem
- Synapses directly onto skeletal muscle
- Does not originate in the braun
2
Q
Two Types of Motor Neurons in the Spinal Cord
A
- Alpha Motor neurons- innervate skeletal muscles
- Gamma motor neurons- innervate muscle spindles
3
Q
Alpha Motor Neurons
A
- Project from the spinal cord onto extrafusal muscle fibers
- Cell body located in the ventral horn of the SC; immediately exit the SC (don’t move rostrally or caudally)
- Can synapse onto multiple muscle cells, but each muscle cell is innervated by only one alpha motor neuron
4
Q
Mototopy of the Ventral Horn
A
- Organization of cell bodies in the spinal cord are based on the muscles that are innervated
- Proximal muscles= more medial
- Distal muscles= more lateral
- Figured out using retrograde tracers (horseradish peroxidase)
5
Q
Local Circuits
A
- When we move, there is a complex interplay btwn excitation and inhibition
- Local circuits of interneurons project rostrally, caudally, and across the midline to coordinate multiple muscles together
- –Organization is very important because one we stimulate one LMN, the whole chain is stimulated
6
Q
Anatomy of skeletal muscle
A
-Muscle–> muscle fascicles–> muscle fibers (cells)–>myofibrils
7
Q
The Motor Unit
A
- Within each muscle, we have tons of muscle fibers
- An alpha motor neuron will synapse onto a group of fibers, but not all fibers
- Each fiber recieves innervation from only one alpha motor neuron
* All of the muscle fibers innervated by a single alpha motor neuron= motor unit
* Motor units=organized my muscle fiber type
8
Q
Muscle Fiber Types
A
- 3 types:
1. Fast fatiguable– Large force, not long lasting
2. Fast fatigue-resistant- Medium force, medium lasting
3. Slow-Low force, but long lasting - We recruit the different muscle fiber types based on the level of intensity
- –We recruit small and weaker motor units first, and gradually work our way up to larger, stronger motor units until we reach the necessary amount of force
9
Q
Temporal Summation
A
- Method of increasing force
- The amount of ACh released from one presynaptic AP causes a twitch of the muscle
- –If we stimulate at high enough frequency, we get a fused tetanus
- Muscle fibers are activated by the next AP before they have time to relax, therefore the forces are summed
10
Q
Gamma Motor Neurons
A
- Stimulate intrafusal muscle fibers around which muscle spindles are wrapped
- –Muscle spindles- detect length/stetch of muscle
- W/o gamma motor neuron innervating the muscle spindle, the spindle will not change length along w/ muscle–> won’t be able to detect changes in muscle length at new length of the fiber
- W/ GMN- intramural and extrafusal are same length, and the muscle spindle will be reactive
11
Q
Why is muscle stretch so important?
A
- Changes in the length of the muscle detected by muscle spindles can directly regulate the contraction of muscle
- If the load on a muscle increases, the muscle will stretch
- -This stretch/lengthening of muscle is detected by the muscle spindles and projected back to the SC
- –Directly synapses to:
1. AMN to the same muscle to contract the muscle
2. An inhibitory interneuron that will inhibit the alpha motor neuron of the contradictory muscle
12
Q
The GAIN theory
A
- We can modulate the excitability of this muscle spindle reflex based on the situation we are in
- High gain- very excitable
- –Ex: on the bus, we want to be reactive
- Low gain- low excitability
- –Ex: passive stretching, you don’t want to be reflexively contracting muscles as you are stretching them
13
Q
Golgi Tendon Organs
A
- Detect change in tension of the muscle
- As tension increases, the sensory fiber directly synapses onto two interneurons
- –1. Inhibitory interneuron that will inhibit the alpha motor neuron projecting to that muscle
- –2. Excitatory interneuron that will excite the contradictory muscle to relieve some tension
14
Q
Muscle Spindles and Golgi Tendon Organs combined
A
- Spindles are reactive to muscle length and have local reflexes to increase the force generated by the muscle
- GTOs are reactive to muscle tension and have local reflexes to decrease the force generated by the muscle
15
Q
Guillen-Barre Syndrome
A
- An autoimmune disorder in which the body develops antibodies that attack Schwann cells
- Leads to peripheral demyelination
- Not specific to LMN, but rather targets all peripheral neurons
- Course is so rapid that motor becomes a problem
- –Ex: innervation of the muscles involved in breathing
16
Q
Upper Motor Neurons
A
- Synapse onto lower motor neurons
- Cell bodies located in:
- –Cortex of the cerebrum
- –Cranial nerve nuclei or brainstem nuclei
17
Q
Descending Tracts from the Brain
A
- One cell originates in the primary motor cortex of the brain, descends through the cerebrum and brainstem, then synapses onto LMN
- Exerts the main voluntary control over LMNs
18
Q
Lateral Corticospinal Tract
A
- Descending tract for limb muscles
- Cell bodies in the primary motor cortex
- Axons cross midline at caudal medulla
- Synapse directly and indirectly onto LMN in contralateral ventral horn
19
Q
Anterior Corticospinal Tract
A
- Descending pathway for trunk muscles
- Cell bodies in primary motor cortex
- Axons do not cross midline in medulla
- Synapse onto bilateral LMN in ventral horn
20
Q
Corticobulbar Pathway
A
- Descending pathway for muscles of the face and neck
- Cell bodies in the primary motor cortex
- Don’t synapse directly onto LMN (local circuit neurons)
- Some will synapse bilaterally
21
Q
Cortico-pontine tract
A
- Not an UMN
- From the primary motor cortex to the pons, then into the cerebellum
- Originate in the brain but don’t synapse onto a LMN
22
Q
Vestibulospinal Tract
A
- UMN tract
- Synapse onto a LMN but doesn’t originate in the brain
- Involved w/ reflexes and originate in cranial nerve nuclei of the brainstem
23
Q
The Primary Motor Cortex
A
- Precentral gyrus- anterior to primary somatosensory cortex
- Mototopy organization- diff areas are responsible for controlling diff movements, NOT FOR DIFF MUSCLES
24
Q
Motor cortex organization
A
- If single cells in the cortex are stimulated, we observe the increase in response of several muscles
- –Single UMN can influence multiple LMNs
- —Therefore, one cortical cell can influence many diff muscles
25
Cortical Circuitry for Specific Movements
- Within a given region, there are multiple cells
- Each cell is "broadly tuned" to perform a set of fxns
- --Rather than one cell performing all diff fxns, it is different subsets of cells that provide variety in fxn
- -Ex: moving your arm in diff directions
- -----Combination of cells dictate which way arm moves
26
Cortical Motor Programs
- The primary motor cortex encodes "motor programs" for complex movements
- ----Supported by local circuits
- Stimulation of one component in a local circuit leads to a cascade that coordinates multiple diff muscles
- --Therefore, we don't need the PMC to encode single muscles- we can just coordinate downstream
27
Multiple Sclerosis
- Autoimmune disorder in which the body develops antibodies that attack oligodendrocytes
- Leads to central demyelination (brain, brainstem, and SC)
- Slow, relapse-remitting progression of the disease that can take years to develop into noticeable symptoms
- Treated with: Immunosupressant drugs, cold therapy, corticosteroids to relieve inflammation
28
Main Functions of the Cerebellum
1. Correct movement errors in real time
2. Learn new complex movements
* Any time a movement is performed the cerebellum needs to know about it
- Recieves input about:
- --The original motor plan that was sent to the body (UMNs)
- --The movement pattern that is occurring in the body (proprioception feedback)
29
3 Components of the Cerebellum
- Cerebrocerebellum
- Spinocerebellum
- Vestibulocerebellum
30
Cerebrocerebellum
- Most lateral aspect
- Recieves input from the motor cortex
- Fine motor control of limbs and digits
31
Spinocerebellum
- Medial aspect
- Recieves input from the spinal cord and brainstem
- Proprioception input from the body
32
Vestibulocerebellum
- The caudal aspect
- Receives input from the vestibular nucleus
- Vestibulo-occular reflexes and vestibulospinal reflexes
33
Anatomy of the cerebellum
- Grey-white-grey interface
- --Cortical grey, white matter, and deep grey nuclei
- Inputs into the cerebellum are going to project into the cortex of the cerebellum
- Outputs of the cerebellum are going to project from the deep nuclei of the cerebellum
34
Inputs to the Cerebellum
- Original motor plan is coming from the cortex by way of pontine nuclei and the inferior olive (crosses the midline)
- Information about what the body is doing is coming from muscle spindles and golgi tendon organs by way of proprioception tracts
35
Descending Pathways into the Cerebellum
- Motor program descends from the primary motor cortex to muscles and the pons; pons relays to the cerebellum
* Cerebellum knows what the body is supposed to do
36
Ascending Pathways into the Cerebellum
- Proprioception from the column of Clarke and external cuneate nuclei communicate with the cerebellum about how the body is positioned
- Vestibular nucleus provides info about balance and gait
* Tells what the body is doing
37
Outputs from the Cerebrocerebellum
- Projecting from deep cerebellar nuclei to:
- --The cortex for motor planning and future correction
- --Red nucleus and the inferior olive for motor learning and real-time corrections of movements
- --Superior colliculus for visual reflexes
* All cross to reach cortex on contralateral side
38
Outputs of the Spinocerebellum
- Project from deep nuclei into:
| - --The superior colliculus and reticular formation for real-time correction of body movements and eye movements
39
Outputs of the Vestibulocerebellum
-Project to the the vestibular nucleus to initiate vestibulo-occular reflexes as well as descending vestibulospinal reflexes
40
Appendicular Ataxia
-The inability to guide motor output towards a directed goal smoothly
41
Intention Tremor
-No tremor at rest, but emerges when goal-directed movement begins
42
What is the main functional cell of the cerebellum?
- The Purkinje cell
- Flat, sheet-like cells with many dendrites and one axon
- Dendrites project out towards the surface of the cerebellar cortex, and an axon that projects down to the deep nuclei of the cerebellum
* Other cells modulate the activity of the Purkinje cell
43
Three Layers of the cerebellar cortex
1. Purkinje layer= middle; houses the cell bodies of purkinje cells
2. Molecular layer- houses the dendrites of Purkinje cells; will be the site of most synapses onto Purkinje (superficial)
3. Granule layer- deepest layer, will form connections btwn non-purkinje cells; Purkinje axons project through
44
Mossy Fibers
- Input to Purkinje cells
- Projections into the cerebellum from the cortex (via pons), the spinal cord, and the vestibular nucleus
- Synpase onto granule cells in the granule layer, which will then project to the molecular layer to synapse with Purkinje cells
- ---Granule cells have sideways projections called parallel fibers that help reach multiple purkinje cells
45
Climbing Fibers
- Input to purkinje cells
- Project into the cerebellum from the inferior olive
- Synapse directly on to Purkinje cells and wrap around like a vine
- --Intricate connections btwn climbing fibers and Purkinje cells is through to play a major role in motor learning
46
Other cells in the cerebellar cortex
- Stellate cells
- Basket cells
- Golgi cells
* Similar to interneurons in the SC-- have inhibitory and excitatory influence over the Purkinje cell to modulate this system
47
Communication within the Cerebellar cortex
- Deep cerebellar nuclei have tonic (constant) output
- When a message is sent to the cerebellum, via mossy fibers or climbing fibers, it leads to:
1. Excitation of the purkinje cell
2. Further excitation of the deep cerebellar nuclei
- Excitation of the purkinje cell will inhibit the tonic activity of the deep cerebellar nuclei. This is the functional projection of the cerebellum
48
Basal Ganglia Fxn
- Selection and initiation of movements (direct pathway)
| - Inhibition of movements (indirect pathway)
49
Structures of the Basal Ganglia
- Collection of deep grey nuclei
1. The Striatum--> the caudate + the putamen
2. The globus pallidus--> external and internal aspect
3. the substantial nigra--> pars compacts and pars reticulata
4. The sub thalamic nuclei
50
Cortico-striato thalamo-cortical circuit
- The main projection into the basal ganglia is the cortex projecting into the striatum
- Series of projections of basal ganglia to the thalamus
- Thalamus relays into the cortex
- Series of excitatory glutamatergic synapses and inhibitory GABAergic synapses
51
The Striatum
- Composed of medium spiny neurons
- --Dense spines on their dendrites, so able to integrate multiple different synapses
- --GABAergic cells--> send inhibitory projections to the globes pallidus internal segment
52
Inhibiting Inhibition
- The globus pallidus is sending tonic inhibition to the VA and VL complex of the thalamus
- If we want to move, we have to inhibit this inhibition so that the thalamus can stimulate the upper motor neurons in the cortex--> disinhibition
53
The Direct Pathway
- Increased excitation of the motor cortex
| - Increased muscle movement
54
Indirect Pathway
- Helps avoid unwanted movement
| - Helps you stop a movement
55
Dopamine on the Indirect and Direct Pathways
- Dopamine will:
1. Enhance activity of the direct pathway via excitatory D1 receptors
2. Inhibit the activity of the indirect pathway via inhibitory D2 receptors
* Dopamine facilitates movement through mechanisms involving both the direct and indirect pathway
56
Parkinson's disease
- Caused degeneration of substantial nigra pars compacta neurons
- W/o DA projection into the striatum, we are less able to stimulate the direct pathway and less able to inhibit the indirect pathway
* Leads to hypokinesia
57
Huntington's Disease
- Caused by a degeneration of medium spiny neurons in the striatum
- Leads to a selective impairment of the indirect basal ganglia pathway
- The inability to inhibit movements w/ the indirect pathway leads to hyperkinetic movement (excess movements)
58
Different types of muscle
- Skeletal muscle- innervated by the somatic NS
| - Cardiac and smooth muscle- innervated by the autonomic NS
59
Hypothalamus
- Key for regulating homeostasis
- Stimulates activity in the autonomic NS for:
- --Blood flow and cardiac output
- --Energy metabolism
- --Reproductive activity
- --Coordinating responses to threats
- Collection of multiple nuclei that are involved in different homeostatic set-points and systems in the body
60
Parasympathetic NS
-Rest and digest
61
Sympathetic NS
-Fight or flight
62
Similarities between Parasymp. and Symp. NS
- Both a 2-cell system
- --1st= preganglionic, 2nd=postganglionic
- Synapses between pre and post occur in PNS
- Preganglionic releases ACh
63
Differences between the Parasymp and Symp NS
- Where the ganglion (synapse between pre and post) occurs
- --Para= in organ wall (long 1st, short 2nd)
- --Symp= sympathetic chain ganglion (short 1st, long 2nd)
- NTM released by 2nd cell
- -Para= ACH
- -Symp= Epi and Norepi
- Where in the CNS the preganglionic cell body resides
- --Parasymp= brainstem and S1-S5
- --Symp= T1-L3
64
Sympathetic NS organization
- Cell bodies of preganglionic neurons= in the lateral horn of the SC
- --Only exists in SC segments T1-L3--> so sympathetic preganglionic cell bodies are only found at this level
- Get throughout the body via sympathetic chain ganglia
- --Runs along the entire length of the spinal cord--> allows symp output to entire body
65
Pregang and Post Gang of Sympathetic NS
- Pregang symp. edit the SC via the ventral root, then enter the sympathetic chain via white communicating ramus--> move until they reach their post-gang target at cholinergic synapse
- Post-gang= exit symp chain via gray communicating ramus, fiber will then communicate w/ target organ or smooth muscle
66
Parasympathetic NS organization
- Preganglionic cell bodies found
- -In cranial nerve nuclei in the brainstem
- -In the intermediate gray zone btwn S1-S5
- Preganglionic cell bodies exit via ventral root and synapse onto organ or smooth muscle target onto postganglionic cell via cholinergic synapse
67
Peripheral convergence
- Sympathetic and parasympathetic fibers get to the same target organ in diff ways
- Sympathetic post-gang fibers reach the organ and directly synapse (release epi and norepinephrine)
- Parasympathetic pregang fibers reach target, synapse onto postganglionic fibers in the target wall, posting synapses onto target (Releases ACh)
68
Balancing Act between Parasympathetic and Sympathetic systems
- Para and sympathetic systems have a tonic level of activity that are constantly competing with one another
- If one inhibited, the other will take more control over that system
69
Cardiovascular Control
- It is important that we regulate cardiac output to provide sufficient oxygenated blood to tissues throughout the body
- Process involves autonomic reflexes that respond to chemical and pressure stimuli in the body
- --Tightly coupled by para and sympathetic systems
70
Detection of the Cardiovascular system
* Step 1 of cardiovascular control
- Baroreceptors located in the aorta--> detect mechanical pressure of blood volume
- Chemoreceptors located in carotid body--> detect oxygen and CO2 content of blood
71
Projection of Baroreceptive and Chemoreceptive Information into CNS
- Chemoreceptive afferents will come in through CN 9
- Baroreceptive afferents will come in through CN 10
- Converge on the Nucleus of the Solitary Tract--> communicates with the hypothalamus and other control centers
72
If baroreceptors indicate BP is high...
- This will excite descending inhibitory projections to sympathetic centers in the SC to reduce sympathetic output
- --Decreases norephi--> lowers excitation of heart rate and contraction
- --Decreases simulation of peripheral vasculature--> BVs dilate
- Excites preganglionic parasympathetic fibers projecting out as the vagus nerve
- --Increases release of ACh in heart--> decreases heart rate and contraction
73
If baroreceptors indicate that blood pressure is low
- Excite descending excitatory projections to sympathetic centers in the SC to increase sympathetic output
- --Increases norepinephrine--> increases excitation of heart rate
- --Increases stimulation of peripheral vasculature which allows BVs to constrict
- Inhibits preganglionic parasympathetic fibers projecting to vagus nerve
- --Decreases ACh on heart, allows sympathetic drive to increase heart rate and contraction
74
Hypovolemic Shock
- Insufficient oxygen getting to the brain and other organs of the body due to decreased volume of blood
- Treatment= epinephrine and IV fluids
- --Increase blood volume, epidemic constricts BVs (increases BP)
75
What do sympathetics and parasympathetic do in the eyes and face?
Sympathetic:
---Dialate pupil to see more
---Raise eyelid and surrounding skin to see more
---Causes perspiration and constriction of blood flow to cool skin
------Without this, BVs dilate (flushed skin) and no sweating
Parasymp:
---Contrict pupil to take in less light
---Lower eyelid to take in less light
76
Horner's Syndrome
- Caused by damage to sympathetic output to the eye; no parasympathetic damage
- ---SC damage around T1-T3
- On affected side:
- --Constricted pupil (miosis)
- --Ptosis (drooping of eyelid)
- --Enophthalmos (Apparent sinking of eyeball)
- --No sweating
- --Flushed skin
