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1 Basal ganglia Sujata Sofat, class of 2009

2 Basal ganglia Objectives Describe the function of the Basal Ganglia in movement Define the BG components and their locations Describe the motor loop of the BG Describe the direct motor circuit of the BG and how it functions Understand how the indirect motor circuit influences BG function Describe how the substantia nigra influences BG circuits Describe the symptoms of BG diseases and understand the vocabulary of movement disorders Describe the types of BG diseases, nuclei involved, and current treatments for Parkinson s Dis.

3 Overview 1. UMN activity in cortical motor areas is not great enough by itself to cause movement. So, it must get a boost by the Basal Ganglia. 2. Basal Ganglia - 5 nuclei in cerebral hemispheres and brainstem. Chris Cohan, Ph.D. Dept. of Pathology/Anat Sci University at Buffalo

4 Overview 3. Basal Ganglia interconnected by excitatory and inhibitory synapses. precision of circuit makes them difficult to analyze 4. Basal Ganglia diseases upset the balance of excitation and inhibition, leading to 2 paradoxical symptoms: Difficulty starting movements Spontaneous movements at rest Consequences of UMN needing a boost!

5 What is Function FUNCTION COMPONENT DEFICITS Start Start Basal Ganglia Spontaneous Move Movements Move Coordinate Cerebral Cortex Weak/Paralyzed Brainstem, Sp cord Adjust Plan Cerebellum Ataxia Maintain balance and posture Adjust Cerebellum Ataxia Balance/EyeMove Cerebellum Falling/nystagmus

6

7 Basal Ganglia- Booster How it Works Thalamus UMN Cerebral Cortex Basal Ganglia Cerebellum head muscles Brainstem body muscles Spinal Cord

8 The Basal Ganglia FACILITATE movement

9 Terminology Extrapyramidal (ie not the pyramidal system) Basal Ganglia are NUCLEI Basal Ganglia diseases are called MOVEMENT DISORDERS

10 1. Caudate 2. Putamen }Striatum 3. Globus Pallidus 4. Substantia Nigra 5. Subthalamic Nucleus Components caudate GP putamen subthalamic nuc

11 3D Shapes Caudate + Putamen

12 Pathway Summary A loop from cortex to basal ganglia to cortex CST CBT VL putamen GPi GPe

13 Output of Basal Ganglia Thalamic Fasciculus VL Lenticular Fasciculus

14 Basal ganglia control the activity of VL. Pathway Function no effect VL CST CBT putamen on VL activity UMN Movement off off off on on on Subthalamic nuc

15 Pathway Function What Lesions if there of BG was components a lesion in the disturb BG a that very resulted sensitive in the switch circuit that being causes permanently VL to be turned ON continuously on! = continuous movement. VL CST CBT putamen on VL activity UMN Movement off off off on on on Subthalamic nuc

16 Direct and Indirect Circuits VL direct circuit STN indirect circuit BG utilize a direct and indirect circuit to control VL. Subthalamic nucleus is involved in the indirect circuit.

17 Direct and Indirect Circuits VL direct circuit accelerator Direct and indirect circuits have competing effects on GPi to control VL activity. brake STN indirect circuit Accelerator increases VL activity Brake decreases VL activity

18 Direct and Indirect Circuits VL direct circuit accelerator When movement is desired, the competing effects of these circuits are resolved by help from substantia nigra. brake STN indirect circuit

19 Role of Substantia Nigra unstained Substantia Nigra pars compacta releases dopamine into putamen dopamine binds to 2 different receptors on putamen neurons: brake putamen STN D1 receptors cause excitation VL accelerator SN c dopamine SN D2 receptors cause inhibition

20 Circuit Summary SN c VL accelerator CST CBT dopamine brake STN SN c The thought to move initiates a small amount of activity in cortical motor areas. Axons from cortex excite putamen neurons. Simultaneously, SN releases dopamine into putamen, which increases the effect of the accelerator and removes the brake. VL activity increases and its axons further excite cortical motor areas where CST/CBT neurons now have enough activity to cause movement.

21 Circuit Details tonic VL accelerator tonic SN c brake STN SN c Disinhibition the tonic inhibition of VL by GPi is stopped when Gpi activity is inhibited by putamen neurons in the direct circuit.

22 Circuit Details ACh tonic VL accelerator tonic SN c ACh brake STN SN c Compared to dopamine, ACh has opposite effects on the direct and indirect circuits. A balance between dopamine and ACh is important for BG function.

23 Parkinson s Disease Hypokinetic disorder SNc degenerates Dopamine is lost from putamen tonic VL accelerator X SN c tonic brake STN X SN c 1. ß Effect of direct pathway 2. Effect of indirect pathway ß Accelerator Brake 3. Abnormal rhythmic activity in neurons Slowed movement Resting Tremor

24 Putamen neurons in indirect circuit degenerate (also caudate nuc) Huntington s Disease tonic VL accelerator tonic SN c Hyperkinetic disorder brake STN SN c chorea In Huntington s Disease: D2R cells GPe degenerate 1. ß Effect of indirect pathway ß GPi, VL = movement

25 Degeneration of STN Hemiballismus Hyperkinetic disorder tonic VL accelerator tonic SN c brakex STN Occurs from a lesion of STN effects are similar to Huntington s except more violent ß Effect of indirect pathway ß GPi, VL = movement X SN c

26 SUMMARY tonic VL accelerator tonic SN c brake STN SN c Lesions in Huntington s, Hemiballismus increase VL activity by removing the brake. Lesion in PD decreases presence of dopamine, causing the accelerator and brake circuits to compete and result in difficulty starting movement.

27 Symptoms of BG Disease 1. Involuntary movements (dyskinesias) hemiballismus chorea Huntington s Disease dystonia/athetosis resting tremor Parkinson s Disease 2. Decreased voluntary movement Hypokinesia / Bradykinesia 3. Change in posture/muscle tone superimposed tremor Rigidity lead pipe with cogwheeling An increase in muscle tone different from spasticity Increased muscle tone in both flexors and extensors

28 Putamen and Globus Pallidus are supplied by branches of the middle cerebral artery. Occlusion of these branches can cause BG symptoms. Blood Supply

29 Basal Ganglia Diseases (movement disorders) Disease Lesion Site Symptoms Ballism STN Wild,flailing movements Parkinson s most common movement disorder Huntington s autosomal dominant adult onset Tardive dyskinesia SNc Putamen D2R neurons/caudate Drug-induced block of D2 and other receptors (eg antipsychotics) Resting tremor, ßmovement, rigidity, altered gait/posture Chorea; caudate damage causes personality changes and dementia Facial chorea/athetosis Tourettes s unknown Motor and verbal tics.

30 PD Treatments 1. Dopaminergic Drugs L-Dopa; ßdopamine metabolism 2. Pallidotomy surgical lesion of GPi reduces inhibition of VL irreversible danger of lesion in nearby internal capsule 3. Deep Brain Stimulation implant stimulator into Gpi, STN STN stim gives best result; stim inhibits STN! best effect: reducing tremor Meds for other symptoms non-damaging, reversible, adjustable procedure! 4. Implant dopamine secreting cells into BG - abandoned in 2003, but new trial underway using stem cells.

31 Basal Ganglia have Other Functions Basal Ganglia diseases eventually involve cognitive and emotional deficits in addition to motor deficits. The former arise from connections with prefrontal cortex (PFC): dorsolateral PFC working memory, executive functions orbitomedial PFC emotion and motivation Motor Loop Cortical motor areas Putamen Globus Pallidus i /SN Cognitive/Emotional Loop Prefrontal Cortex Caudate Globus Pallidus i /SN VL of thalamus VA of thalamus

32 9. Modulation by presynaptic receptors 8. Recycling vesicles Amantadine? 7. Reuptake transporter COMT inhibitors 6. Degradation in cleft, metabolism, or diffusion Agonists 5. Binding to Receptors G Postsynaptic membrane Levodopa, MAO inhib 1. Neurotransmitter synthesis 2. Storage in Vesicles 3. Ca entry 4. Neurotransmitter Release Review catecholamine synthesis and metabolism pathway to understand Silvestri lecture.

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