L-4 Contributions of Cerebellum and Basal Nuclei to Motor Function II Flashcards
what does the basal nuclei help do?
helps plan and control complex patterns of muscle movement, controlling relative intensities of the separate movements, directions of movements, and sequencing of multiple successive and parallel movements.
where does the basal nuclei get its input from?
the cerebral cortex and returns most of their output to the cerebral cortex
what is the principal role of the basal nuclei?
to work with the corticospinal system to modulate thalamic output to the motor cortex to plan and execute smooth movements.
what does the basal nuclei consist of?
paired nuclei:
- striatum: (caudate nucleus and putamen)
- globus pallidus
- substantia nigra
- subthalamic nucleus
what are the two major basal nuclei circuits? what are their general functions
- putamen circuit (direct)
«_space;function not clear; inhibitis athetosis or non-volatile movements; suppresses rigidity» - caudate nucleus circuit (indirect)
«_space;motor planning: activating muscles in sequence for motor patterns 5 seconds ahead or more»
what are two things about the putamen circuit?
- for subconscious execution of learned patterns of movements
- overall excitatory - tends to increase motor activity
describe the direct pathway itself
1) cerebral cortex (premotor, supplementary motor, somatosensory); +/acetylcholine
2) putamen (-/GABA)
T/F: the putamen circuit bypasses caudate nucleus
True
what neurotransmitter is used between the connections of the striatum and the substantia nigra?
dopamine
what direct/indirect receptors id dopamine inhibitory/excitatory on?
- dopamine is INhibitory in the INdirect way (D2 receptors)
- dopamine is Excitatory in Direct pathway: (D1)
- action of dopamine is overall excitatory
describe the IGP/SubNigRet
the IGP/SubNigRet is normally active and sends inhibitory signals to the thalamus
exciting the putamen inhibits the IGP/SubNigRet and allows the thalamus to send excitatory signals to the motor cortex
whats to note about this system?
IGP/SNR is normally active and sends inhibitory signals to the thalamus
exciting the putamen inhibits the IGP/SNR and allows the thalamus to send excitatory signals to the motor cortex
describe lesions in globus pallidus:
- results in inability to maintain postural support
- results in continuous spontaneous writhing movements of a hand, arm, neck or face = athetosis
describe lesions in subthalamic nuclei
- results in the release of inhibition on the contralateral side
- results in sudden, flailing movements of an entire limb = hemiballismus
describe lesions in striatum
- results in the release of inhibition
- results in flicking movements in hands, face, or elsewhere = chorea
- occur in patients w Huntington Disease
describe lesions in substantia nigra
- caused by destruction of dopaminergic neurons
- occur in patients with Parkinsons Disease
- results in rigidity, akinesia, and tremors
- since dopamine inhibits the indirect (inhibitory) pathway and excites the direct (excitatory) pathway, destruction of the dopaminergic neurons results in an overall inhibitory effect
describe the purpose of caudate circuit
- indirect pathway
- for cognitive planning of sequential and parallel motor patterns
- plays major role in cognitive control of motor activity
- overall inhibitory– tends to decrease motor activity
delineate the caudate circuit
1) cerebral cortex (pre-m, supplementary-motor, somatosensory) (+/acetylcholine) –>
2) caudate nucleus (-/GABA)
3) globus pallidus (external –(-/GABA)–> globus pallidus (internal) –(-/GABA)–> 4) thalamic relay nuclei (+/glutamate) —> 5) premotor and supplementary motor cortex
*substantia nigra compacta –(-/dopamine d2)–> caudate nucleus
neurotransmitter for substantia nigra –> caudate nucleus and putamen:
dopamine (inhibitory)
caudate nucleus and putamen –> globus pallidus and substantia nigra:
GABA (inh)
cortex –> caudate nucleus and putamen
Acetylcholine (exc)
multiple pathways from brain stem
norepinephrine, serotonin (inh), enkephalin
mutliple glutamate pathways
provide most of the excitatory signals
- in huntintons disease, which neurons are destroyed?
- /GABA
- indirect pathway no longer has inhibitory influence on direct pathway and motor activity is increased
describe parkinsons disease
- aka: paralysis agitas
- results from widespread destruction of pars compacta of substantia nigra that sends dopaminergic fibers to caudate nucleus and putamen
- dopaminergic pathways to direct and indirect pathways are lost. the direct pathway loses some of its excitatory input and the indirect pathway loses some of its inhibitory input. in both cases there is decreased motor activity
what are the characteristics of parkinsons?
- rigidity of much of body musculature
- involuntary tremors; fixed rate
- akinesia (difficulty in initiating movement)
- postural instability
- dysphagia, speech disorders, gait disturbances, fatigue
describe Huntington disease characteristics
- usually becomes symptomatic around 30-40 years of age
- flicking movements of individual muscles
- progressive severe distortional movements of entire body
- severe dementia
- motor dysfunctions
what are the abnormal movements probably caused by?
probably by loss of most of cell bodies of GABA-secreting neurons of caudate nucleus and putamen of Ach neurons in other parts of the brain
- indirect pathway no longer has inh influence on direct pathway and motor activity is increased
- GABA neurons normally inhibit parrts of the globus pallidus and substantia nigra
what gene is the huntington mutated in?
- HTT gene, which produces the huntingtin protein function is unknown but appears to play important role in CNS neuron health
describe DNA changes
- causes DNA segment known CAG repeats (cytosine, adenine, and guanine) that appear multiple times in a row
normally, CAG segment is repeated 10-35 times within the gene.
in huntington disease, CAG repeated 36-120+ times
describe the spectrum
- people with 36-39 CAG repeats may or may not develop the signs and symptoms of Huntington, while people with 40 or more repeats almost always develop the disorder
how?
an increase in the size of the CAG segment leads to the production of an abnormally long version of the huntingtin protein. the elongated protein is cut into smaller, toxic fragments that bind together and accumulate in neurons, disrupting the normal functions of these cells.
