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NSCI 324* Systems Neuroscience. Doug Munoz Centre for Neuroscience Studies Botterell Hall, room 226 x32111 doug.munoz@queensu.ca Tutorial: Monday Jan 23, 2012 10:30am Botterell B147 TA: Jay Jantz (j.jantz@queensu.ca). NSCI 324* Systems Neuroscience.
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NSCI 324* Systems Neuroscience Doug Munoz Centre for Neuroscience Studies Botterell Hall, room 226 x32111 doug.munoz@queensu.ca Tutorial: Monday Jan 23, 2012 10:30am Botterell B147 TA: Jay Jantz (j.jantz@queensu.ca)
NSCI 324* Systems Neuroscience Vision and Oculomotor Control (Dr. Munoz) January 10 The retina January 13 Central Visual Pathways January 16 Dr. Munoz Tutorial: January 16 Higher Visual functions January 17 Oculomotor System I. Basic organization January 20 Oculomotor System II. Vestibulo-ocular reflex January 23 Dr. Munoz tutorial: January 23 Oculomotor System III. Saccades January 24 Basal Ganglia for cognitive and motor control January 27 review of Dr. Munoz lecture material January 30 Dr. Munoz exam in tutorial period
Basal Ganglia • Collection of nuclei deep in telencephalon, diencephalon, and midbrain • Play a very important role in cognition and motor control
Basal Ganglia • Caudate Nucleus (CN)
Basal Ganglia • Caudate Nucleus (CN) • Putamen (P) } Striatum
Basal Ganglia • Caudate Nucleus (CN) • Putamen (P) • Globus pallidus (GP) } Lentiform nucleus
Basal Ganglia • Caudate Nucleus (CN) • Putamen (P) • Globus pallidus (GP) • external segment (GPe) • Internal segment (GPi)
Basal Ganglia • Caudate Nucleus (CN) • Putamen (P) • Globus pallidus (GP) • external segment (GPe) • Internal segment (GPi) • Sustantia nigra (SN) • pars reticulata (SNpr) • pars compacta (SNpc)
Basal Ganglia • Caudate Nucleus (CN) • Putamen (P) • Globus pallidus (GP) • external segment (GPe) • Internal segment (GPi) • Sustantia nigra (SN) • pars reticulata (SNpr) • pars compacta (SNpc) BG Output
Basal Ganglia • Caudate Nucleus (CN) • Putamen (P) • Globuspallidus (GP) • external segment (GPe) • Internal segment (GPi) • Sustantianigra (SN) • pars reticulata (SNpr) • pars compacta (SNpc) • Subthalamic nucleus (STN)
Basal Ganglia • Caudate Nucleus (CN) • Putamen (P) • Globuspallidus (GP) • external segment (GPe) • Internal segment (GPi) • Sustantianigra (SN) • pars reticulata (SNpr) • pars compacta (SNpc) • Subthalamic nucleus (STN) } Striatum } Lentiform nucleus BG Output
Cortex GLU GPe Caudate Putamen GLU SNpc STN SNr GPi GABA Simplified Basal Ganglia Circuit Thalamus
Cortex GPe Caudate Putamen SNpc STN SNr GPi Simplified Basal Ganglia Circuit GLU GLU DIRECT PATHWAY GABA SubstanceP GABA Thalamus
Cortex GPe Caudate Putamen SNpc GABA Enkephalin STN SNr GPi GABA GLU Simplified Basal Ganglia Circuit GLU GLU INDIRECT PATHWAY GABA Thalamus
Cortex GPe Caudate Putamen SNpc STN SNr GPi Simplified Basal Ganglia Circuit GLU GLU GABA Enkephalin GABA GABA SubstanceP GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc STN SNr GPi Simplified Basal Ganglia Circuit HYPERDIRECT PATHWAY GLU GLU GABA Enkephalin GABA GABA SubstanceP GLU GABA Thalamus GLU
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Simplified Basal Ganglia Circuit GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus DA-D1: increase excitability in DIRECT pathway DA-D2: decrease excitability in INDIRECT pathway
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Simplified Basal Ganglia Circuit GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus
Parkinson’s Disease • progressive degenerative disorder • degeneration in substantia nigra pars compacta • leads to reduced dopamine release in striatum (caudate and putamen) • affects motor function
Cortex GPe Caudate Putamen SNpc STN SNr GPi Parkinson’s Disease: Loss of DA from SNpc GLU GLU GABA DA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc STN SNr GPi Parkinson’s Disease: Loss of DA from SNpc GLU GLU GABA DA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc STN SNr GPi Parkinson’s Disease: Loss of DA from SNpc GLU GLU GABA DA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc STN SNr GPi Parkinson’s Disease: Loss of DA from SNpc GLU GLU GABA DA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc STN SNr GPi Parkinson’s Disease: Loss of DA from SNpc GLU GLU GABA DA D2 D1 GABA GABA GLU GABA Thalamus Leads to reduced excitability in cortex inability to initiate movement
Parkinson’s Disease What Causes Parkinson’s Disease? • Exogenous toxins • Oxidative stress • Genetic Predisposition • Infection • Drug-induced loss of DA neurons in SNpc
PD at 95+ PD at 50+ Loss of DA neurons leads to Parkinson’s 100 Viable DA Neurons (%) 20-25 Threshold for diagnosis 100 Age (yrs)
Sudden Insult PD at 95+ PD at 55+ Loss of DA neurons leads to Parkinson’s 100 Viable DA Neurons (%) 20-25 Threshold for diagnosis 100 Age (yrs)
Cortex GPe Caudate Putamen SNpc STN SNr GPi Parkinson’s Disease: Loss of DA from SNpc GLU GLU GABA DA D2 D1 GABA GABA GLU GABA Thalamus Leads to reduced excitability in cortex inability to initiate movement
Huntington’s Disease • Inhereted (genetic) disorder that manifests in midlife • Autosomal dominant trait • Restlessness and choreiform (rapid, jerky) movements in arms and face • Starts with degeneration in Indirect pathway • Degeneration spreads through basal ganglia
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Simplified Basal Ganglia Circuit GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Huntington’s Disease: Degeneration in Basal Ganglia GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Huntington’s Disease: Degeneration in Basal Ganglia GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Huntington’s Disease: Degeneration in Basal Ganglia GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Huntington’s Disease: Degeneration in Basal Ganglia GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus
Cortex GPe Caudate Putamen SNpc DA STN SNr GPi Huntington’s Disease: Degeneration in Basal Ganglia GLU GLU GABA D2 D1 GABA GABA GLU GABA Thalamus Leads to increased excitability in cortex inability to inhibit movement