Neuroscience 4

Outputs from cerebellum to brainstem nuclei

Superior peduncle: cerebellar cortex>deep cerebellar nuclei (dentate/interposed)>superior coliculus>reticular formation>through anterior-medial white matter of spinal cord to lower motor neurons in medial ventral horn cerebellar cortex and inferior cerebellar peduncle: cerebellar cortex>deep cerebellar nuclei (fastigial)>superior and reticular formation>through anterior-medial white matter of spinal cord to lower motor neurons in medial ventral horn Cerebellar cortex>vestibular nuclei>anterior medial white matter of spinal cord>lower motor neurons in medial ventral horn. **All signals from deep cerebellar nuclei travel down inferior cerebellar peduncle

How does negative feedback regulation work for the Golgi Tendon Organs? (GTO)

The 1b afferents from tendon organs contact inhibitory interneurons that decrease the activity of alpha motor neurons innervating the same muscle. The 1b inhibitory interneurons also receive input from other sensory fibers, as well as from descending pathways. This arrangement PREVENTS MUSCLES FROM GENERATING EXCESSIVE TENSION.

Cerebellar dysfunction

VESTIBULOCEREBELLAR DISEASE/DAMAGE -disturbed equilibrium -ataxia -problems coordinating movement of eye and body, BUT eyes move fine when lying down SPINOCEREBELLAR DISEASE/DAMAGE AFFECTS EXECUTION AND FEEDBACK FOR MOVEMENT -hypotonia = decreased muscle tone -decreased activity of y motor neurons CEREBROCEREBELLUM DISEASE/DAMAGE AFFECTS PREPARATION FOR MOVEMENT -delays in initiation and termination of movement -terminal tremor at end of movement -disorders in temporal coordination of movements involving multiple joints -problems with spatial control of hand and fingers

Upper motor neurons - Brainstem

Vestibular nucleus (body posture and position) -reticular formation (body posture and position, autonomic and somatic stereotyped motor behaviors) -superior colliculus (orienting movement of head and eyes)

Organization of synaptic connections in the cerebellum

climbing fibers and mossy fibers activate purkinje cells which inhibit deep cerebellar neurons. Precerebellar nucleus cells (spinocerebellar pathways, brainstem reticular nuclei, pontine nuclei) and INFERIOR OLIVARY NUCLEUS CELLS cn activate deep cerebellar neurons which excite descending motor systems.

Dorsioflexor training resulted in...

increased peak torque strength -increased surface EMG (neuronal activity) -increased initial firing rate of alpha motor neuron (asterisk = repeat firing)

Spatial organization of motor neuron pools

inject dye (retrograde tracer) into soleus and gastrocnemius (indiv muscles) of cat. Lower motor neurons from distinct clusters in the ventral horn. Many neurons may innervate same muscle = motor neuron pool. -Motor neurons innervating axial(proximal) structures =medial -Motor neurons innervating distal musc. more lateral

primary motor cortex vs pre-motor cortex

motor cortex: -major cortex has topographic representation of body=homunculus -disproportionate rep. of face and hands -individual neurons may have directional selectivity pre-motor cortex: -reciprocal connections with the motor cortex -also projects to local circuits in the spinal cord -neurons MAY have direction selectivity -involved in CONDITIONAL movements (press lever after bell rings) -impt for the initiation/selection of motor activity NOTE LOCATION OF CORTICOSPINAL AND CONRTICOBULBAR TRACT

A series of nuclei that play an important role in modulating

movement, motivation, reward receive inputs from: cortex, substantia nigra pars compacta (SNc)

Motor components of the human basal ganglia

striatum (caudate + putamen) RECEIVE input Globus Pallidus and SNr OUTPUT +=excite (glutamate) -=inhibit (gaba) circle=DOPAMINE cerebral cortex=motor movement superior colliculus = eye movement

Striatum (caudate + putamen) receive inputs from...

the SNc and almost all cortical areas. DOES NOT receive from auditory or visual

Upper and lower motor neuron lesions

upper motor neuron syndrome: -weakness -spasticity (increased tone, hyperactive stretch reflex, clonus (oscillatory contract/relax) reflexes -decerebrate rigidity -babinski's sign -loss of voluntary movement Lower motor neuron syndrome: -weakens or paralysis -decreased superficial reflexes (stimulation of skin) -hypoactive stretch reflexes -decreased tone -muscle atrophy

Golgi-tendon organ stretch vs contraction

(Golgi compared to muscle spindle) Both afferents discharge in response to passively stretching the muscle, although the Golgi tendon organ discharge is MUCH LESS than that of the spindle. When the extrafusal muscle fibers are made to contract by stimulation of their motor neurons, however, the spindle is unloaded and therefore falls silent, whereas THE RATE OF THE GOLGI TENDON ORGAN FIRING INCREASES.

Principal input and output pathways of the cerebellum

**Vestibulocerebellum. Vestibular inputs lead to vestibulocerebellum which lead to vestibular nuclei. Involved in balance (axial control and vestibular reflexes) and eye movement. **Spinocerebellum -Vermis (medial) inputs: visual and auditory>FASTIGIALnucleus>to medial decending systems in motor execution (axial and proximal motor control, ongoing execution of movement, muscle tone -Intermediate part of hemisphere inputs: spinal afferents (distal body parts, trigeminal inputs). >INTERPOSED NUCLEI>lateral descending systems (distal motor control, ongoing execution, muscle tone (latter two part of Spinocerebellum function anyway) **Cerebrocerebellum -Lateral part of hemisphere with corticopontine inputs>cortical afferents>DENTATE>to motor and premotor planning. Precision and fine dexterity. Planning.

Upper motor neurons - cortical

-motor cortex -premotor cortex -planning and precise control of complex voluntary movement

The muscle spindle and the monosynaptic stretch reflex

-Alpha motor neuron regulates muscle tone -y motor neuron regulates sensitivity of spindle. When muscle contracts, the spindle shortens, reducing tension of the spindle and decreasing firing rate of 1 a afferents. To retain sensitivity of the spindle, the y motor neuron synapses on the contractile poles of the spindle, causing the poles to contract, thus stretching/increasing tension on the spindle. Stretching a muscle spindle leads to increased activity in 1a afferents and an increase in the activity of alpha motor neurons that innervate the same muscle. 1a afferents also excite the motor neurons that innervate synergistic muscles, and inhibit the motor neurons that innervate antagonists. Stretch reflex functions on a negative feedback loop

Spinocerebellar Ataxia 1 (SCA1)

-Caused by CAG repeat expansion in the ataxin1 gene -Function of the ataxia 1 protein not well understood -age of onset usual in the 40s -death within 10-15 years

Cerebellar lesions

-Lesions in the cerebellum produce defect ipsilaterally -Lesions in SPINOCEREBELLUM **affect body trunk - "drunken sailor" **tremors **ataxia w/ wide leg stance **facial muscle control problems affect speech **alcoholism cause degeneration of anterior vermis **impaired gait in legs, but arms normal **wide gait remains abnormal when lying down -Lesions in VESTIBULOCEREBELLUM **eye movement affected **impaired wide leg gait, improved when lying down -Lesions in CEREBROCEREBELLUM **impaired initiation of movement, especially in distal joints during multi-joint movement

Cerebellar circuitry and the coordination of ongoing movement

-Neuronal activity in the cerebellum changes continually during movement (e.g. flip wrist back and forth) -Neurons respond selectively to various aspects of movement **extension vs contraction of specific muscles **position of joints **direction of NEXT movement -Important for experience-dependent modification of reflexes -Involved in real-time error correction of movement IMAGE: Both classes of cells are tonically active at rest. Rapid alternating movements result in the transient inhibition of the tonic activity of both cell types.

Cerebellar Hypoplasia

-Underdeveloped or missing cerebellum -Rare in humans, often associated with other congenital diseases. Rare cases linked to mutations in the VLDL receptor -More common in cats (caused by utero exposure to virus feline distemper)

upper motor neurons in cerebral cortex vs upper motor neurons in brainstem

-Upper motor neurons in cerebral cortex reach to LATERAL white matter of spinal cord (ventral horn) which leads to innervation of distal limb muscles (skilled movements) -Upper motor neurons in brainstem lead to anterior-medial white matter of spinal cord and control axial and proximal limb muscles (posture and balance).

How many motor units per muscle correlates with

-correlates with "dexterity" of the muscle. smaller motor unit = more dextrous. The more precise the movement the muscle makes, the smaller the motor units will be.

Motor unit size correlates

-larger motor units usually associated with a larger motor neuron (larger cell body and axon diameter) -larger motor units associated with increased dendritic complexity (more inputs to the motor neuron) -more axonal branches -decreased excitability of the neuron

Brainstem: reticular formation

-many small nuclei -cardiovascular and respiratory control -coordination of eye movements -regulation of sleep and wakefulness -temporal and spatial control of limb and trunk movements -primarily synapse on local circuit neurons -maintain posture in response to disturbances in posture

Upper motor neurons...

-signals from brainstem and cortex -descend to lower motor circuits Brain stem: body position/posture, eye and head orientation Cortex: voluntary movements -upper motor neurons connect to lower motor circuits DIRECTLY and INDIRECTLY (via local circuits)

Ongoing movement Expected load, increased load, adapted stages

1) Expected load. flexion of wrist causes complex spikes 2) Increased load causes increased complex spike freq., decreased simple spike freq. 3) Adapted load complex spike freq. returns to baseline, simple spike freq. remains decreased

small motor units (S) vs Fast fatigable motor units (FF) vs Fast Fatigue Resistant (FR) motor units

1. slow motor units (s) -small -muscle fibers contain lots of mitochondria and blood vessels (energy!) -slow to fatigue -for sustained, low force muscle movements (upright posture) -low threshold, therefore tonic activity 2. Fast fatigueable (FF) -large -relatively few mitochondria and blood vessels -fast to fatigue -for brief, high force contraction -high threshold 3. Fast Fatigue Resistant (FR) -intermediate size -high threshold

Basal ganglia: activation through disinhibition

A is transiently excited, B is transiently inhibited, C is disinhibited, so other inputs can excite it, leading to excitation of D

Stretch reflex circuitry

A negative feedback loop. Disturbance (addition of liquid to glass) changes length in muscle fiber, which activates the spindle receptor, leading to an increase spindle afferent discharge which leads to activation of the alpha motor neuron which innervates the muscle and this changes the force required to hold the glass.

Effect of stimulation rate on muscle tension

A) low freq single muscle twitch B)higher frequencies = sum of twitch force. C) higher frequency yet. force product greater, but individual twitches still apparent. D) At highest rates of motor neuron activation, individual twitches are no longer apparent (fused tetanus)

Afferent, efferent, interneurons in the cerebellum

Afferent: -mossy fiber(parallel fiber) -climbing fiber Efferent: -Purkinje Interneurons -Basket -Golgi -Stellate

Nuclei of the basal ganglia

Caudate and Putamen: -medium spiny neurons (MSNs) -GABAergic -Dopamine receptors(D1 coupled to Gs and D2 coupled to Gi) -Low basal activity Globus Pallidus -GABAergic neurons -High tonic activity STRIATOPALLIDAL PATHWAY

Output from cerebellum to cortical motor systems

Cerebellar cortex >> deep cerebellar nuclei. Cerebrocerebellum> Dentate nucleus Spinocerebellum > interposed and fastigial nuclei vestibulocerebellum > vestibular nuclei NOT PART OF DEEP CEREBELLAR NUCLEI DEEP CEREBELLAR NUCLEI go to upper motor neurons **dentate nucleus > premotor cortex (motor planning) **interposed and fastigial nuclei>motor cortex and brainstem (motor execution) VESTIBULAR NUCLEI go to lower motor neurons in spinal cord and brainstem (balance and vestibulo-ocular regulation)

Anatomy & organization of the cerebellum

Cerebellar cortex: -cerebrocerebellum -spinocerebellum which consists of: **vermis AND intermediate -vestibulocerebellum Deep cerebellar nuclei: -Dentate nucleus -interposed nucleus (2) -Fastigial nucleus Cerebellar peduncles: -superior -middle -inferior

Component of the brainstem and diencephalon that "interact" with the cerebellum

Components of the brainstem and diencephalon related to the cerebellum. This sagittal section shows the major structures of the cerebellar system, including the cerebellar cortex, the deep cerebellar nuclei, and the ventroanterior and ventrolateral (VA/VL) complex (which is the target of some of the deep cerebellar nuclei).

Corticospinal tract vs corticobulbar tract

Corticospinal Tract: -90% of axons cross to the contralateral side in pyramidal decussation and form the lateral corticospinal tract -cortical neurons controlling forearm and hand may synapse directly on alpha motor neurons (most synapse on local circuit neurons) -10% remain ipsilateral and form the ventral corticospinal tract that is important for control of axial and proximal limb muscles Corticobulbar tract: -synapse on local circuit neurons that control cranial nerve nuclei -Most axons of the corticobulbar tract terminate bilaterally -EXCEPTION: CORTICOBULBAR NEURONS CONTROLLING LOWER FACE

anatomy: corticospinal vs corticobulbar tract

Corticospinal tract: -90% of axons cross to the contralateral side in pyramidal decussation and form the lateral corticospinal tract -cortical neurons controlling forearm and hand may synapse directly on alpha motor neurons -most synapse on local circuit neurons -10% remain ipsilateral and form the ventral corticospinal tract that is important for control of axial and proximal limb muscles Corticobulbar tract: -synapse on local circuit neurons that control cranial nerve nuclei -most axons of the corticobulbar tract terminate bilaterally -exception: corticobulbar neurons controlling lower face

Medium spiny neurons

Diagram showing convergent inputs onto a medium spiny neuron from cortical neurons, dopaminergic cells of the substantia nigra, and local circuit neurons. The PRIMARY output of the medium spiny cells is to the GLOBUS PALLIDUS and to the SUBSTANTIA NIGRA pars reticulata.

Striatopallidal output of the basal ganglia

Direct pathway: SNc>d1 neurons in putamen>Gpi>VA/VL>cortex Indirect pathway: SNc>D2 neurons in putament>GPe>STN>Gpi>VA/VL>cortex (D2 PROJECTS EXTERNAL, NOT INTERAL...ROUTES THROUGH SUBTHALAMIC NUCLEUS, THAN FOLLOWS REST OF PATH)

direct vs indirect movements

Direct: move distal limb, activate lateral corticospinal tract, and lateral ventral horn activated Indirect: postural adjustment. Activate reticular formation and ends in medial ventral horn.

Parkinson's basis

Due to loss of the dopaminergic neurons in the substantial nigra -Because the nigrostriatal pathway excites the direct pathway and inhibits the indirect pathway, the loss of this input tips the balance in favor of activity in the indirect pathway (inhibition)

postural control during voluntary movement

Example: hear bell, pull lever -voluntary movement: contract biceps POSTURAL CONTROL: contract gastrocnemius occurs BEFORE bicep contraction conclusion: this movement involves a feed forward (anticipatory) mechanism

Excitatory and inhibitory connections in the cerebellar cortex and deep cerebellar nuclei

Excitatory and inhibitory connections in the cerebellar cortex and deep cerebellar nuclei. The excitatory input from mossy fibers and climbing fibers to Purkinje cells and deep nuclear cells is basically the same. Additional convergent input onto the Purkinje cell from local circuit neurons (basket and stellate cells) and other Purkinje cells establishes a basis for the comparison of ongoing movement and sensory feedback derived from it. The Purkinje cell output to the deep cerebellar nuclear cell thus generates an error correction signal that can modify movements already begun. The climbing fibers modify the efficacy of the parallel fiber-Purkinje cell connection, producing long-term changes in cerebellar output.

Chronic electrode stimulation of the MG muscle resulted in...

FF motors converted to S. Properties of the innervating alpha motor neuron also shifted to be similar to those of neurons that normally controls S motor units

What is reduced in pre symptomatic SCA1 mice?

Firing frequency of PCs is reduced in SCA mice. SCA mice also show lower response to conditioned response.

Cerebellar cortex anatomy & organization

Flocculus AND nodulus part of the vetibulocerebellum

Overall organization of neural structures involved in the control of movement

Four systems - local spinal cord and brainstem circuits, descending modulatory pathways, the cerebellum, and the basal ganglia make essential and distinct contributions to motor control. basal ganglia-gating proper initiation of movement (brake and release) cerebellum-sensory motor coordination of ongoing movement (error correction) (only 2 ways to control muscles, spinal cord and brainstem circuits)

Inputs to the cerebellum via the MIDDLE and INFERIOR cerebellar peduncles

Frontal/parietal cortex sends info to the pons (red nucleus and pontine nuclei) which sends info to the Inferior olive and the cerebellar cortex/deep nuclei. **The Inferior Olive, spinal cord and vestibular nuclei all make up the inferior cerebellar peduncle and contribute to the cerebellar cortex/deep nuclei. Info crosses midline.

The Golgi-tendon organ function

Golgi-tendon organ senses alpha motor unit CONTRACTION -GTO insensitive to stretch -functions in a negative feedback loop to maintain steady level of FORCE

basis for Huntington's

Huntington's disease results from the selective loss of striatal neurons in the indirect pathway (Figure 4.10). Thus, the balance between the direct and indirect pathways becomes tipped in favor of the direct pathway. Without the normal inhibitory influence on the thalamus that is provided by the indirect pathway, thalamic neurons can fire randomly and inappropriately, causing the motor cortex to execute motor programs with no control by the patient.

Categories of cerebellar dysfunction

Hypotonia : decreased resistance to passive limb movement Ataxia: disorders in voluntary movement (coordination) -delays in initiating response -errors in range of movement -disdiadochokinesis: errors in rate and regularity of movement (tap one hand with the other) Action tremor: problems with movement (not initiation) -most problem at the end of movement

y (gamma) motor neuron

INNERVATES MUSCLE SPINDLES -encapsulated -regulates sensitivity of spindle -When muscle contracts, the spindle shortens, reducing tension on the spindle and decreasing firing rate of 1a (spindle) afferents. -To retain sensitivity of the spindle, the y motor neuron synapses on the contractile poles of the spindle, causing the poles to contract, thus stretching/increasing tension on the spindle.

Alpha motor neuron

INNERVATES STRIATED MUSCLE -Not encapsulated -force generators -regulates muscle tone

Cerebellum cell layers

Know Granules, white matter, Purkinje cell layer, molecular layer

Basal ganglia structures

Know basal ganglia structures and how they relate to the other structures featured here.

Treatments for parkinson's

L-DOPA crosses the blood brain barrier, then is converted to dopamine by SNc neurons -used in combination with MAO or COMPT inhibitors -prolonged use of L-DOPA may cause the cells to either not convert it to dopamine (in SNc) or to stop responding to dopamine (in striatum) -Eventually the dopaminergic neurons all die and there are few/no remaining cells to convert L-DOPA into dopamine -GROWTH factor GDNF to prolong survival of remaining SNc neurons (in canala) -transplant stem cells that express GDNF -surgical ablation of the STN -deep brain stimulation of the STN

Simultaneous activation by PF and CF can cause...

LTD in the Purkinje neuron. -Climbing fiber depolarizes Vm, synapse is weakened between PF and Purkinje dendrite. EPSP amplitude decreases.

Parkinson's disease activity

Loss of 90% of Dopaminergic input = hypo kinetic In Parkinson's disease, the inputs provided by the substantia nigra are diminished (thinner arrow), making it more difficult to generate the transient inhibition from the caudate and putamen. The result of this change in the direct pathway is to sustain the tonic inhibition from the globus pallidus (internal segment) to the thalamus, making thalamic excitation of the motor cortex less likely (thinner arrow from thalamus to cortex).

Huntington's disease activity

Loss of D2 neurons in the striatum = hype kinetic In hyperkinetic diseases such as Huntington's, the projection from the caudate and putamen to the globus pallidus (external segment) is diminished (thinner arrow). This effect increases the tonic inhibition from the globus pallidus to the subthalamic nucleus (larger arrow), making the excitatory subthalamic nucleus less effective in opposing the action of the direct pathway (thinner arrow). Thus, thalamic excitation of the cortex is increased (larger arrow), leading to greater and often inappropriate motor activity. (After DeLong, 1990.)

MPTP and Parkinson's Disease

MPTP = 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine -accidental byproduct when making synthetic heroin -selectively kills dopaminergic neurons -renders person unable to move -acute poisoning can be treated with MAOIS

The type of AP produced by a Purkinje cell depends on the input cell

Mossy fiber > granule cell PF (parallel fibers) > Purkinje -PF synapses generate simple spike AP in Purkinje cells -fire at high frequency (50-100 spikes/sec) -summation required to generate AP in Purkinje cells climbing fiber (CF) > Purkinje -CF synapses generate complex spike AP in Purkinje cells -fire at low frequency (1 spike/sec) -unlikely to directly modulate Purkinje cell output -may modulate the synaptic efficacy of the parallel fibers (concurrent stimulation of CF and PF reduces strength of PF input in Purkinje cell = LTD)

motor and non motor loops

Motor Loops: -Body movement loop cortical input: motor, premotor, somatosensory cortex striatum: putamen pallidum: lateral globus pallidus, internal segment thalamus: ventral lateral and ventral anterior nucli -Oculomotor loop cortical input: posterior parietal, prefrontal cortex striatum: caudate (body) pallidum: globus pallidus, internal segment, substantia nigra pars reticulata thalamus: mediodorsal and ventral anterior nuclei NONMOTOR loops: -Prefrontal loop: cortical input: dorsolateral prefrontal cortex striatum: anterior caudate pallidus: globus pallidus, internal segment; substantia nigra pars reticulata thalamus: mediodorsal and ventral anterior nuclei (same as oculomotor) -Limbic loop: cortical input: amygdala, hippocampus, oribitofrontal, anterior cingulate, temporal cortex striatum: ventral striatum pallidum: ventral vallidum thalamus: mediodorsal nucleus

Initiation of movement - motor vs pre-motor cortex

Motor cortex: -motor cortex has a topographic representation of the body = homunculus -disproportionate representation of face and hands -individual neurons may have directional selectivity Premotor cortex: -reciprocal connections with the motor cortex -also projects to to local circuits in the spinal cord -neurons may have directional selectivity -involved in "conditional" movements (e.g. press lever after the bell rings) -important for the initiation/selection of motor activity

Diseases of the basal ganglia

Parkinson's Disease (many causes, some genetic) -resting tremor -difficulties in movement initiation -cased by death of dopaminergic neurons in SNc (symptoms only appear after >90% death, natural, age-related death of the SNc neurons occurs Huntington's Disease (autosomal dominant genetic disease) -Choreiform (doll-like) movements -cognitive disfunction -caused by a single gene mutation in the Huntington gene -CAG repeat that causes poly-glutamine repeats in the protein (protein function not well understood)

Only purely excitatory pathway among the intrinsic pathways of the basal ganglia

Pathways involving the subthalamic nucleus

order of activation of different types of motor units

S>FR>FF Fast fatiguable = highest grams of force and highest tension in response to repetitive stimulation of motor neurons. Fatigue rates much faster in FF. Slow doesn't get affected in force after 60 minutes. FR slowly does. FF does right away (<2 minutes)

Time courses of motor behavior, morphological alterations, and cell death in SCA1 mice

SCA1 mice show morphological alterations and decreased latency to fall

Spinal cord circuits in flexion-cross extension reflex

Spinal cord circuitry responsible for the flexion reflex. Stimulation of cutaneous receptors in the foot (by steppin on a tack) leads to activation of spinal cord local circuits that withdraw (flex) the stimulated extremity and extend the other extremity to provide COMPENSATORY support.

Cerebellum Hypothesis

The cerebellum is a "comparator" that compensates for errors in movement by comparing intention and performance. Cortex- "plans for movement" which sends info to motor AND cerebellum, motor sends info to sensory systems which sends info to cerebellum. Cerebellum compares info from sensory systems and cortex, then relays info to cortex.

Cerebellum hypothesis revisited

The cerebellum is a "comparator" that compensates for errors in movement by comparing intention and performance. Cerebellum sends info via superior cerebellar penduncle to relay nuclei and then to thalamus and back up to cortex.

Inputs to the cerebellum via the MIDDLE and INFERIOR cerebellar peduncles cont.

The cortical projections to the cerebellum are made via relay neurons in the pons. These pontine axons then cross the midline within the pons and run to the cerebellum via the middle cerebellar peduncle. Axons from the inferior olive, spinal cord, and vestibular nuclei enter via the inferior cerebellar peduncle.

Patterns of facial weakness and their importance for localizing neurological injury

Weakness of lower (inferior) face muscles due to damage in motor cortex(middle cerebral artery stroke) or damage to corticobulbar projections (anterior cerebral artery stroke) (MOSTLY AFFECTS LOWER CONTRALATERAL FACE MUSCLES) Damage to facial nerve effects an entire half of the face (contralateral) Projections arise from the cingulate cortex, which is associated with emotional processing

Role of y motor neurons in modulating afferent sensitivity

When alpha motor neurons are activated without activation of y motor neurons, the response of the 1a fiber decreases as the muscle contracts. -When BOTH alpha and y motor neurons are activated, there is no decrease in 1a firing during muscle shortening. Thus, the y motor neurons can regulate the gain of muscle spindles so they can operate efficiently at any length of the parent muscle. -y for more complex movements

Cerebellum: function & dysfunction

about 10% of brain volume (develops post-natally) -contains >50% of the neurons in the brain (granule cell) -neurons arranged in a regular pattern -divided into distinct regions that make connections with different areas of the brain **What we know about cerebellar function** -NOT required for perception or muscle contraction -Indirectly regulates movement by adjusting the output of major descending motor systems of the brain -LESIONS in the cerebellum: **disrupt coordination of eye and limb movements **impair balance **DECREASE muscle tone

motor unit

all muscle fibers innervated by the same neuron. -1 muscle fiber is innervated by 1 neuron -1 neuron can innervate multiple muscle fibers =motor unit=smallest unit of force -size of motor unit is proportional to size of motor neuron

output from cerebellum to cortical motor systems via the superior cerebellar peduncle

cerebellar cortex>deep cerebellar nuclei>thalamus (VL) and superior colliculus > motor and pre motor cortex

age and disease-associated death of dopaminergic neurons

green = healthy individual pink=parkinsons? black= huntington's?

indirect pathway basal ganglia

leads to LESS movement. << If cerebral cortex is activated, but SNc is not, the caudate/putamen sends inhibitory signals to both external and internal segments of the globus pallidus. b/c the ext. globus pallidus is inibited, STN is disinhibited and sends an excitatory signal to the internal segment of the globus pallidus. REMEMBER that internal segment is receiving BOTH inhibitory and excitatory signals, so only a few lines show up, the signal still carries through to the VA/VL which still semi carries through the the frontal/motor cortex second sitch: caudate/putamen AND SNc inactive, caudate/putamen no longer send inhibitory signals, activates both external and internal segments. However, the external segment inhibits the internal, so the internal is receiving BOTH excitatory and inhibitory signals. This leads to partially activated VA/VL thalamus which partially activates the motor cortex third sitch: cerebral cortex is inactivated, leads to inhibition of internal global pallidus, which leads to disinhibtion of VA/VL thalamus, which leads to excitation of frontal/motor cortex

reticular formation functions

many small nuclei, functions divided into 2 categories: -modulatory -premotor

medial v lateral local circuits

medial local circuits -project long distances -innervate multiple segments -make ipsilateral and contralateral connections -postural adjustment lateral local circuits -innervate only a few segments -make ipsilateral connections -fine control of distal extremities (fingers)

motor control center in the brainstem: medial vestibular vs lateral vestibular

medial vestibular nuclei: -regulate head position by reflex movement of neck muscles -respond to stimulation of semi-circular canals lateral vestibular nuclei: -facilitates of limb extensor muscles -responds to activation of the otolith organs both nuclei maintain posture in response to disturbances in posture