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Questions and Answers
What results from the destruction of dopamine-containing cells in the pars compacta of the substantia nigra?
Which structure is primarily responsible for receiving input from the cerebral cortex to the basal ganglia?
Which of the following accurately describes the function of the subthalamic nuclei?
What is the primary output pathway of the basal ganglia?
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Which regions of the cortex send projections specifically to the caudate tail?
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What is the function of the Globus Pallidus Interna in the basal ganglia output pathways?
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What type of neurotransmitter is glutamate in the basal ganglia circuit?
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How does dopamine affect the direct pathway in the basal ganglia?
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Which neurotransmitter is primarily inhibitory within the basal ganglia pathways?
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What is the role of the subthalamic nucleus (STN) in the basal ganglia circuitry?
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What type of neurons mainly project to the thalamus from the medial segment of the Globus Pallidus?
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Which impairment is characterized by rapid, jerky, aimless, and constant motions of limbs?
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What is the consequence of lesions restricted to the caudate?
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What type of lesion leads to profound hypokinesia without tremor?
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Which structure is located between the Putamen and the Internal Capsule?
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What characterizes a lesion in the Putamen?
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What type of projections does the Globus Pallidus Lateral segment receive?
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What abnormal movement is caused by carbon dioxide or carbon disulfide intoxication?
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What is the primary role of the indirect pathway in movement regulation?
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Which structure is primarily involved in the output for the motor channel?
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In the context of the direct pathway, what occurs after the excitation of the putamen and globus pallidus?
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The prefrontal channel is crucial for which of the following processes?
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Which nuclei are activated by the subthalamic nuclei in the indirect pathway?
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What role does the limbic channel primarily serve?
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Which channel is responsible for controlling facial and limb musculature?
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How does the direct pathway affect cortical excitation?
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What type of disorder is characterized by excessive inhibition from the basal ganglia?
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What is NOT a characteristic symptom of Parkinson’s Disease?
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In Huntington’s Chorea, what disrupts the normal inhibition within the basal ganglia circuit?
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Which brain region undergoes degeneration in Parkinson’s Disease?
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What results from decreased dopamine in the basal ganglia?
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What is a functional impairment commonly seen in Parkinson’s Disease?
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Which of the following conditions is associated with inadequate inhibition from the basal ganglia?
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What major characteristic defines hyperkinetic disorders?
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What contributes to increased resistance to movement in all muscles in Parkinson’s Disease?
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Which of the following elements is essential for the regulation of muscle tension in purposeful movements?
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Study Notes
Axon Collaterals
- Axons emit several collaterals before the primary branch extends beyond the striatum.
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Local Circuit Neurons
- These neurons are found in the striatum.
- They release GABA.
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Medium Spiny Neurons
- Found in the striatum.
- Make up the majority of neurons in the striatum.
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Giant Spiny Neurons
- Found in the striatum.
Caudate and Putamen Impairment
- Lesions or degeneration of neurons in the caudate and putamen can lead to hyperkinetic states.
- Chorea: Rapid, jerky, aimless, and constant motion of limbs.
- Athetosis: Slow, sinuous motion of limbs.
- Dystonia: Slow, sustained contorting of the body.
- Lesions restricted to the putamen result in motor dysfunction in contralateral limbs.
- The putamen connects to the premotor and motor cortex.
- Lesions restricted to the caudate lead to behavioral defects such as apathy, disinhibition, and/or major affective disturbance.
- Tics: Involuntary, rapid, repetitive movements or vocalizations.
- Tardive Dyskinesias: Involuntary movements of the face, tongue, and limbs.
Globus Pallidus
- Wedge-shaped structure located between the putamen and internal capsule.
- Consists of two segments:
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Medial (Internal)
- Output region of the corpus striatum.
- Projects primarily to the thalamus.
- Receives GABAergic projections from the caudate and putamen.
- Part of the direct pathway through the basal ganglia.
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Lateral (External)
- Projects to the subthalamic nucleus.
- Receives GABAergic projections from the caudate and putamen.
- Part of the indirect pathway through the basal ganglia.
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Medial (Internal)
Globus Pallidus Impairment
- Lesions lead to profound hypokinesia (reduced movement).
- Similar to Parkinsonian rigidity.
- Without tremor (shaking).
- Surgeons have used carefully placed lesions to reduce unwanted movements.
- Carbon dioxide or carbon disulfide intoxication can cause profound rigidity and catatonic posture.
Substantia Nigra
- Located in the anterior midbrain.
- Composed of two nuclei:
- Pars reticulata: Output nucleus of the basal ganglia.
- Pars compacta: Contains dopamine-producing neurons that project to the striatum.
- Contains melanin, a byproduct of dopamine metabolism.
- Axons from the substantia nigra innervate the ipsilateral caudate and putamen.
Substantia Nigra Impairment
- Destruction of dopamine-containing cells in the pars compacta results in Parkinsonian signs and symptoms in the contralateral side of the body.
- Synthetic heroin containing MPTP caused significant Parkinsonism in young users.
Subthalamic Nuclei
- Thin, elongated wedge of gray matter.
- Part of the indirect pathway.
- Receives inhibitory fibers (GABAergic) from the external globus pallidus (GP).
- Excitatory projections to the internal GP.
- Source of excitation to the internal GP that can be modulated by the external GP.
Connections to/from Basal Ganglia
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INPUT:
- All regions of the cerebral cortex project to the basal ganglia.
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OUTPUT:
- Directed towards the frontal lobe, particularly the premotor and supplementary motor cortex, via the thalamus.
Basal Ganglia Inputs
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Striatum (Caudate and Putamen): Main recipient of input to the basal ganglia.
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From Cerebral Cortex:
- Frontal lobe to caudate head and putamen.
- Parietal/occipital lobes to caudate body.
- Temporal lobe to caudate tail.
- Primary motor cortex and primary somatosensory cortex project to the putamen.
- Premotor cortex and supplementary motor areas to the caudate head.
- Intralaminar nuclei of thalamus to putamen.
- Substantia Nigra pars compacta: Dopamine input.
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From Cerebral Cortex:
Basal Ganglia Outputs
- Arise from two structures:
- Globus Pallidus Interna: Body output except for head and neck.
- Substantia Nigra pars reticulata: Outputs for head and neck.
- Output pathways are either excitatory or inhibitory.
- Smooth motor function depends on a balance of both.
- Uses GABA.
- Pathway is through the VL and VA nuclei of the thalamus.
- Thalamic nuclei convey information to the entire frontal cortex (mainly the premotor cortex, supplementary motor area, and primary motor cortex).
Intrinsic Basal Ganglia Pathways
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Direct Pathway:
- Facilitates movement.
- Cortical signals excite the striatum (caudate/putamen) causing inhibition of the internal globus pallidus (GPI).
- This releases inhibition of the thalamus, which then excites the cortex.
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Indirect Pathway:
- Suppresses unwanted movements.
- Cortical signals excite the striatum (caudate/putamen), causing excitation of the external globus pallidus (GPe).
- This inhibits the subthalamic nucleus (STN).
- By inhibiting the STN, the GPi is less stimulated.
- This leads to increased inhibition of the thalamus, reducing motor output.
Neurotransmitters in Basal Ganglia Circuit
- Glutamate (Glu): Excitatory, released by cortical motor areas.
- Gamma-aminobutyric acid (GABA): Inhibitory, released by the striatum, globus pallidus, and substantia nigra.
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Dopamine (DA):
- Direct Pathway: Excitatory, reduces inhibition of the thalamus, promoting movement.
- Indirect Pathway: Inhibitory, increases inhibition of the thalamus, suppressing movement.
Direct Pathway
- Excitatory (less inhibition of the thalamus).
- Increases thalamic output to the cortex.
Direct Motor Loop
- Cortex initiates movement.
- Excitation of the direct inhibitory pathway of the striatum (putamen and globus pallidus).
- Disinhibition of the thalamus.
- Facilitation of the cortex.
- Movement occurs.
Indirect Pathway
- Corticostriatal system stimulated.
- Subthalamic nuclei (STN) releases input into the globus pallidus (GP).
- Increased inhibition of thalamic nuclei.
- Reduces thalamocortical output.
- Suppresses unwanted movements.
Indirect Motor Loop
- Cortex initiates movement.
- Excitation of the indirect pathway of the striatum (caudate/putamen).
- Increased activity in the external globus pallidus (GPe) inhibits the subthalamic nucleus (STN).
- This inhibits the GPi, which leads to more thalamic inhibition.
- Suppresses unwanted movements.
Direct vs. Indirect
- Direct: Cortical excitation, promotes movement.
- Indirect: Cortical inhibition, suppresses unwanted movements.
Initiation and Control of Volitional Movement
- Motivation: "I will sign my name."
- Higher Order Association Cortex: Context, where, how big, how fast?
- Sensory/Motor Association Cortex: Sitting or standing, how fast is the hand moving, where is my wrist?
- Motor Cortex: Execution of the signature.
- Basal Ganglia: Legibly, how much resistance from pen and paper, looking at paper or elsewhere?
- Cerebellum: Smoothness of movement, timing, coordination.
- Spinal Cord: Muscle activation.
Four Parallel Channels Through the Basal Ganglia
- Somatomotor Channel: Control of body movements.
- Oculomotor Channel: Control of eye movements.
- Prefrontal Channel: Cognitive control and planning.
- Limbic Channel: Emotional regulation and motivation.
Clinical Application: Basal Ganglia Impairment
- Basal ganglia typically inhibits the thalamus.
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Hypokinetic Disorders: Too little movement.
- Parkinson's Disease: Excessive inhibition from the basal ganglia.
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Hyperkinetic Disorders: Excessive movement.
- Huntington's Disease: Inadequate inhibition from the basal ganglia.
- Dystonia: Muscle spasms and cramping.
- Some types of Cerebral Palsy: Motor impairments caused by brain damage.
Parkinson's Disease
- Characterized by:
- Muscular rigidity.
- Shuffling gait.
- Stooped posture.
- Rhythmical muscular tremors.
- Masklike facial expression.
- Functional Impairments: Poor transitions from standing to sitting, gait with flexed posture, shuffling of feet, decreased/absent arm swing.
- Rigidity: Increased resistance to movement in all muscles, caused by direct upper motor neuron facilitation of alpha motor neurons without appropriate inhibition from the basal ganglia circuit.
Parkinson's Pathology
- Degeneration of dopamine neurons in the substantia nigra.
- Loss of about 80% of dopaminergic cells in the substantia nigra can occur without symptoms.
Parkinson's Disease Circuit
- Decreased dopamine results in less disinhibition (direct root) and more inhibition (indirect root) of the thalamus, resulting in hypokinetic movement.
Pedunculopontine Nuclei
- Provide activation of muscle tension.
- The basal ganglia dampens muscle tension for purposeful movements.
- Loss of BS input results in rigid muscles.
Huntington's Chorea
- Characterized by an increase in choreiform movements (involuntary continuous movements of the body).
- Results in cognitive and behavioral deficits.
- Loss of striatal inhibition of the GPe (indirect pathway).
- The subthalamic nuclei no longer facilitate the GPi and SN, resulting in disinhibition of the thalamus.
Huntington Disease Effect on Basal Ganglia Circuit
- Loss of inhibition in the indirect pathway results in hyperkinetic movement.
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Description
This quiz explores the functions of axon collaterals and their significance in local circuit neurons, medium spiny neurons, and giant spiny neurons within the striatum. Additionally, it covers the impact of caudate and putamen lesions on motor function and behavior, including conditions like chorea and dystonia. Test your knowledge of these critical concepts in neuroscience!
