Lecture 12 - Basal Nuclei Control of Motor Function Flashcards
Basal Nuclei
•Plan and execute motor commands in concert with cerebral cortex; help cortex execute subconscious but learned pattern •Help plan multiple parallel sequential patterns •Control complex patterns of motor activity
Basal Nuclei receive most of their input from __ and return most of their output to __.
cerebral cortex and cerebral cortex
The principal role of the basal nuclei is
to work with corticospinal system to modulate thalamic output to the motor cortex to plan and execute smooth movements
Two major basal nuclei circuits
Putamen circuit (direct)
Caudate nucleus circuit (indirect)
Putamen Circuit
Direct
Function: not clear
inhibits athetosis or non-volitional movements
suppresses rigidity
•For subconscious execution of learned patterns of movement
•Overall excitatory –tends to increase motor activity
BYPASSES CAUDATE
caudate nucleus circuit
indirect
motor planning: activating muscle in sequence for motor patterns 5 seconds ahead or more
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.
Dopamine is __ on the direct pathway and __ on the indirect pathway.
excitatory (D1 receptors)
inhibitory (D2 receptors)
Dopamine’s function overall is __
excitatory
Exciting the putamen ___ the IGP/SbNigRet and allows the thalamus to send ___ signals to the motor cortex. IGP/SubNigRet is otherwise active and sends __ signals to the thalamus.
inhibits
excitatory
inhibitory
Lesions in Globus Pallidus
- Result in inability to maintain postural support.
* Result in continuous spontaneous writhing movements of a hand, arm, neck or face = athetosis
Lesions in subthalamic nuclei
- Result in the release of inhibition on the contralateral side.
- Result in sudden, flailing movements of an entire limb = hemiballismus
Lesions in striatum
- Results in the release of inhibition
- Results in flicking movements in hands, face, or elsewhere = chorea.
- Occur in patients with Huntington disease.
Lesions in substantia nigra
- Caused by destruction of dopaminergic neurons.
- Occur in patients with Parkinson’s 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.
Neurotransmitters
Substantianigra→ caudate nucleus and putamen
Dopamine (inhibitory)
Neurotransmitters
Caudate nucleus and putamen →globuspallidus and substantianigra
GABA (inhibitory)
Neurotransmitters
Cortex →caudate nucleus and putamen
Acetylcholine (excitatory)
Neurotransmitters
Multiple pathways from brain stem
Norepinephrine, serotonin (inhibitory), enkephalin
Neurotransmitters
Multiple glutamate pathways
Provide most of the excitatory signals
Parkinson’s
AKA: Paralysis agitans
•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.
•Characteristics: Rigidity of much of body musculature Involuntary tremors of involved areas even at rest at a fixed rate Serious difficulty in initiating movement (akinesia) Postural instability Dysphagia, speech disorders, gait disturbances, fatigue
Huntington’s
- Usually becomes symptomatic around 30-40 years of age
- Characteristics:
- Flicking movements of individual muscles
- Progressive severe distortional movements of entire body
- Severe dementia
- Motor dysfunctions
- Abnormal movements probably caused by loss of most of cell bodies of GABA-secreting neurons of caudate nucleus and putamen and of Ach neurons in other parts of the brain.
- Indirect pathway no longer has inhibitory influence on direct pathway and motor activity is increased.
- GABA neurons normally inhibit parts of the globuspallidus and substantia nigra.
Huntington Mutation
- Mutations in the HTT gene, produces protein -huntingtin
- Function unknown, it appears to play an important role in CNS neuron health
- Causes DNA segment known CAG repeats (cytosine, adenine, and guanine) that appear multiple times in a row.
- Normally, the CAG segment is repeated 10 to 35 times within the gene.
- In people with Huntington disease, the CAG segment is repeated 36 to more than 120 times.
- People with 36 to 39 CAG repeats may or may not develop the signs and symptoms of Huntington disease, while people with 40 or more repeats almost always develop the disorder.
- 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.