Basal ganglia lecture

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A major concentration of the lecture was anatomy and, hence, the basal ganglia lab should be helpful in preparation.


Column 1 Column 2 (memorize)
What are the circuits or loops that go through the basal ganglia? Motor, oculomotor, dorsolateral prefrontal, and lateral orbitofrontal.
What is the generic structure of the basal ganglia circuits? Cortex -> Striatum -> Pallidum, Substantia nigra -> Thalamus ( -> back to Cortex)
What is the general input-output structure of the basal ganglia? Cortical info (excluding primary visual and auditory cortex) is sent to the striatum. Processing is done in the basal ganglia circuit. Output is sent by the GPi (globus pallidus internal) and/or SNpr (substantia nigra pars reticulata) to the cortex (via thalamus).
What is the output structure for eye and face movements of the basal ganglia? SNpr (substantia nucleus pars reticulata)
What is the output structure for body movements of the basal ganglia? GPi (globus pallidus internal)
What does the SNpc do? It exerts a modulating influence on the striatum (through dopamine).
Draw the simplified diagram of the basal ganglia. (simplified diagram of the basal ganglia)
What did Schulz et al (1995) find? That SNpc (dopaminergic) neurons fire in relation to reward and stimuli that predict the availability of reward. With no task, the SNpc responded when the monkey received a reward. In the first task, the SNpc responded when the a trigger indicated to a monkey that a reward was available. In the second task, the SNpc responded when an instruction was given that could eventually lead to a reward.
What did Mink and Thach (1991) do and what did they find? They trained a monkey to make wrist movements that required activation of muscle (against load) or relaxation of muscle (with load). When the basal ganglia was deactivated with muscimol, the monkeys had more difficulty relaxing the muscle. This supports the idea that the basal ganglia helps inhibit muscle activity.
What did Hikosaka and Wurtz (1985) do and what did they find? They inactivated SNpr (output nuclei for eye movements) in monkeys, which were then much less likely to be able to suppress eye movements in order to fixate.
What are some of the hyperkinetic movement disorders caused by lesions of the basal ganglia in humans? Athetosis (slow writhing movements of fingers, hands, feet), chorea (abrupt movement of limbs and facial muscles), and ballism (violent involuntary flailing movements).
What are some of the hypokinetic movement disorders cuased by lesions of the basal ganglia in humans? Akinesis (inability to initiate movement), bradykinesis (slow movements), rigidity, and postural instability.
Draw the simple basal ganglia circuit for Parkinson's disease (symptoms bradykinesia, akinesia, postural instability, resting tremor, and rigidity). Diagram should show deactivation of SNpc and that inhibitory output to thalamus is very strong.
Draw the simple basal ganglia circuit for hemiballismus (violent involuntary flailing movements on one side of body). Diagram should show deactivation of subthalamic nucleus and decreased inhibitory output to thalamus.
What is wrong with the simplified basal ganglia circuit? 1). This model would predict that decreased output from GPi would result in involuntary movements. However, GPi inactivation in monkeys causes bradykinesia (slowness of movement) and there are no involuntary movements. 2). It seems that STN high frequency stimulation activates it. This model would predict that this would increase the inhibition of the GPi, which would result in hypokinesia. However, this works as an effective treatment of Parkinson's (instead of making it worse).

[edit] NeuroCog Lectures

[edit lecture list]

NeuroCog Lectures
Date Time Topic Instructor
Mon 4-Jan10:45-11:45Intro to thalamus and cortexHendry
Wed 6-Jan10:45-11:45Neural Mechanisms of painCaterina
Fri 8-Jan10:45-11:45Molecular mechanisms of painCaterina
Fri 8-Jan1:00-3:00Somatosensory lab 1Schramm, Blue, Wilson/NT/TM
Mon 11-Jan10:45-11:45Trigeminal systemDong
Wed 13-Jan10:45-11:45Somatosensory system: Peripheral MechanismsHsiao
Fri 15-Jan10:45-11:45Somatosensory system: Central mechanismsHsiao
Fri 15-Jan1:00-3:00Somatosensory lab 2Schramm, Blue, Wilson/NT/TM
Mon 18-JanMartin Luther King Jr Day-no classes
Wed 20-Jan10:45-11:45Retina and phototransductionYau
Fri 22-Jan10:45-11:45Olfaction and tasteYau
Fri 22-Jan1:00-3:00Methods: bioinformaticsPevsner
Mon 25-Jan10:45-11:45Early visual processing IHendry
Wed 27-Jan10:45-11:45Early visual processing IIHendry
Fri 29-Jan10:45-11:45Shape perception - ConnorConnor
Fri 29-Jan1:00-3:00Visual systems labSchramm, Blue, Wilson/VM/EG
Mon 1-Feb10:45-11:45Motion perceptionConnor
Wed 3-Feb1:00-2:00Spatial perceptionConnor
5-FebGraduate Program Interviews-no classes
Mon 8-Feb10:45-11:45Attention lectureYantis
Wed 10-Feb10:45-11:45Receptive fields and image segmentationvon der Heydt
Fri 12-Feb10:45-11:45Cross-modal integrationHsiao
Fri 12-Feb1:00-3:00Methods: mathematical tools and conceptsNiebur
Mon 15-Feb10:45-11:45The binding problemNiebur
Wed 17-Feb10:45-11:45Spinal cord circuitry lectureBastian
Fri 19-Feb12:00-1:00Motor cortex lectureBastian
Fri 19-Feb1:00-3:00Motor neuron labSchramm, Blue, Wilson/NT/EG
Mon 22-Feb10:45-11:45Cerebellum lectureBastian
Wed 24-Feb10:45-11:45ALSRothstein
Fri 26-Feb10:45-11:45Basal ganglia lectureStuphorn
Fri 26-Feb1:00-3:00Cerebellum labSchramm, Blue,Wilson/VM/NT
Wed 3-Mar10:45-11:45Parkinson's disease lectureDawson T
Fri 5-Mar10:45-11:45Huntington's DiseaseRoss
Fri 5-Mar1:00-3:00Basal ganglia labSchramm, Blue, Wilson/NT/TM
|March 8-12 Spring Break-no classes
Mon 15-Mar10:45-11:45Oculomotor system lectureZee
Wed 17-Mar10:45-11:45Vestibular lectureMinor
17-Mar2-JanreviewALL TAs
Fri 19-Mar10:30-11:45METHODS: Movement Research **in Bastian lab, note time changeBastian
Fri 19-Mar1:00-3:00Vestibular labSchramm, Blue, Wilson/EG/VM
Mon 22-Mar9:00 AMMIDTERM EXAM
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