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![• The cortical signal results in MORE inhibition
from striatum to GP(internal)
• More inhibition of GP(internal) means LESS
inhibition of motor thalamus (VA/VL)
• Since the motor thalamus receives LESS
inhibition, the VA/VL cells will INCREASE their
firing
• (VA/VL cells are receiving other excitatory
inputs [one source is cerebellar]). This decrease
in inhibition is called dis-inhibition.
• This results in INCREASED FIRING OF VA/VL
NEURONS AND IN TURN MOTOR CORTEX.](https://image.slidesharecdn.com/basalgangliaaiyegbusi-241217182825-964a4126/75/Basal-Ganglia-Anatomy-by-Dr-Aiyegbusi-ppt-23-2048.jpg)
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Basal Ganglia Anatomy by Dr Aiyegbusi.ppt
- 1. THE BASAL GANGLIA DRA.I AIYEGBUSI
- 2. • Collection ofnuclei (gray matter)on both sides of the thalamus within the temporal lobes. • Control voluntary movements and establish postures. COMPONENTS • Caudate nucleus ("tail") • Putamen ("shell") • Globus pallidus ("pale globe"), • and the nucleus accumbens • Subthalamic Nucleus • Substantia Niagra
- 4. • The Caudatenucleus + Putamen along with the interposed anterior limb of the internal capsule = Striatum (i.e. striated body) • Globus Pallius = Pallidum - GP interna = GPi: main outflow of basal ganglia - GP externa = GPe • Putamen and Globus pallidus resembles a lens, and they are collectively called the Lenticular nucleus.
- 5.
- 7. THE CAUDATE • Beginsjust behind the frontal lobe and curves back towards the occipital lobe. • The caudate curves around with the lateral ventricle. The head of the caudate is most anterior • It gives rise to a body whose “tail” extends with the ventricle into the temporal lobe • The “ball” at the end of the tail is the amygdala
- 8.
- 9. THE PUTAMEN • Liesjust under and behind the front of the caudate. • Medial to the putamen is the globus pallidus (GP). Anatomically, the putamen and globus pallidus are shaped like a lens. For this reason, they are referred to as the lenticular nucleus. • However, the functions of the putamen and globus pallidus are different.
- 10. GLOBUS PALLIDUS (GP) •Has 2 parts, a lateral, external (or outer) segment and a medial, internal (or inner) segment : GP(external) and GP(internal • GP(internal) contains the output neurons of the basal ganglia circuit. They project to ipsilateral motor thalamus, VA and VL • One of the pathways that conveys information from GP(internal) to motor thalamus is the ansa lenticularis.
- 11. THE GLOBUS PALLIDUS •Located just inside the putamen, with an outer part and an inner part. • Receives inputs from the caudate and putamen and provides outputs to the substantia nigra (below). THE NUCLEUS ACCUMBENS • Nucleus just below the globus pallidus • Receives signals from the prefrontal cortex and sends other signals back there via the globus pallidus.
- 12. THE SUBSTANTIA NIGRA("black substance") • Located in the upper portions of the midbrain, below the thalamus • Gets its colour from neuromelanin, a close relative of the skin pigment. • Made up of two parts: - The pars compacta uses dopamine neurons to send signals up to the striatum - The pars reticulata is mostly GABA neurons. Mainly controls eye movements.
- 14. COMPONENTS OF THEBASAL GANGLIA 1. Input Nuclei • Striatum : Caudate and Putamen - Receives information from almost all regions of the cortex, except primary visual and primary auditory cortices. - Projections from the cortex to striatum - corticostriatal pathway - Projects to other parts of the basal ganglia, specifically the globus pallidus or substantia nigra
- 15. 2. Output Nuclei: • Globus Pallidus Interna • Substantia Nigra Pars Reticulata - Main sources of output from the basal ganglia. - In contrast to upper motor neurons, they do not project directly to local circuit or lower motor neurons.
- 16. 3. Intermediate Nuclei •Globus Pallidus Externa (Gpe) • Subthalamic Nucleus (STN) • Substantia Nigra Pars Compacta (SNpc) • Cholinergic interneurons in the striatum -Relay information between nuclei of the basal ganglia
- 17. • The basalganglia affect function mediated by the ipsilateral motor cortex. • Since motor cortex controls the movements of the contralateral body.... • The Basal ganglia circuits affect movements of the contralateral body.
- 18. THE BASAL GANGLIAPATHWAYS BG influences movement by regulating upper motor neurons-necessary for normal initiation of voluntary movement • There are two important pathways through which striatal information reaches GP(internal) – • The direct pathway and the indirect pathway • Both pathways have opposite effects on motor activity
- 19. • Both pathwaysbegin in the cortex and both pathways converge on the globus pallidus interna, the main outflow of the basal ganglia
- 20. MOTOR PATHWAY • DirectPathway - Dopamine stimulates the direct pathway and inhibits the indirect pathway for an overall excitatory effect. - Overall Excitatory by dis-inhibiting the upper motor neurons in the cortex (promotes movement) • Indirect Pathway –Inhibits unwanted movement –Serves to modulate the dis-inihibitory actions of the direct pathway
- 21. NEUROTRANSMITTERS • Basal Ganglia(Caudate, Putamen, and GP) – Medium Spiny neurons = GABAergic • GABA = Inhibitory • Cortex, Thalamus, STN Glutamate = excitatory Glutamatergic neurons –Glut=excitatory
- 22. DIRECT PATHWAY • Thecorticalprojections to the striatum use the excitatory transmitter glutamate. • these cortical projections excite striatal neurons. • This striatal cell uses the inhibitory transmitter GABA • This inhibits the GP(internal). The cells in GP(internal) that project to VA/VL also use GABA.
- 23. • The corticalsignal results in MORE inhibition from striatum to GP(internal) • More inhibition of GP(internal) means LESS inhibition of motor thalamus (VA/VL) • Since the motor thalamus receives LESS inhibition, the VA/VL cells will INCREASE their firing • (VA/VL cells are receiving other excitatory inputs [one source is cerebellar]). This decrease in inhibition is called dis-inhibition. • This results in INCREASED FIRING OF VA/VL NEURONS AND IN TURN MOTOR CORTEX.
- 24. Direct Pathway (aka theExpress Route) CORTEX PUTAMEN (GPe) (STN) GP interna VA/VL THALAMUS Glutamate (+) Glutamate (+) GABA (-) GABA (-)
- 25. INDIRECT PATHWAY • Thestriatal neurons project to GP(external) • GP(external) project to the subthalamic nucleus • Cells in the subthalamic nucleus then project to GP(internal), which in turn projects to VA/VL. • Then to to motor cortex.
- 26. Indirect Pathway (aka, scenicroute) CORTEX PUTAMEN GP externa STN GP interna VA/VL THALAMUS Glutamate (+) GABA (-) Glutamate (+) GABA (-) GABA (-) Glutamate (+)
- 27. • The increasedactivity of the GABAergic striatal neurons decreases activity in GP(external). • The GABAergic cells in GP(external) inhibit cells in the STN, resulting in less inhibition of the cells • Thus, STN neurons are dis-inhibited and increase their activity resulting in more excitation to cells in GP(internal). • There is an increase in activity of the GABAergic cells in GP(internal) that project to VA/VL or an • INCREASE in INHIBITION of the thalamic neurons
- 28. CORTEX PUTAMEN (GPe) (STN) GP interna VA/VL THALAMUS Glutamate(+) Glu(+) GABA (-) GABA (-) Direct and Indirect Motor Loops (--) CORTEX PUTAMEN GP externa STN GP interna VA/VL THALAMUS Glutamate (+) GABA (-) GABA (-) GABA (-) Glutamate (+) DA (+) Glu(+)
- 29. PATHWAY MODULATORS 1.DOPAMINE • producedby cells in the pars compacta of the substantia nigra (SNc). • Has an EXCITATORY effect upon cells in the striatum that are part of the Direct Pathway via D1 receptors. • Has an INHIBITORY effect upon striatal cells associated with the Indirect Pathway via D2 receptors. DOPAMINE EXCITES THE DIRECT AND INHIBITS THE INDIRECT
- 30. CHOLINERGIC (ACh) INTERNEURONS •They synapse on the GABAergic striatal neurons that project to GP(internal) AND on the striatal neurons that project toGP(external). • The cholinergic actions INHIBIT striatal cells of the Direct pathway and EXCITE striatal cells of the Indirect pathway. • Thus the effects of ACh are OPPOSITE the effects of dopamine on the direct and indirect pathways • ACh INHIBITS THE DIRECT AND EXCITES THE INDIRECT PATHWAY
- 32. LESIONS OF THEBASAL GANGLIA Movement Disorders • Hyperkinetic –Hemiballismus –Huntington’s Disease • Hypokinetic –Parkinson’s Disease –Drug Induced (Neuroleptics, MPTP)
- 33. Hemiballismus • Injury usuallyto STN by infarct, tumor, surgery • Decreased inhibition (Indirect Pathway) • Lesion in STN reduced inhibitory outflow of basal ganglia in indirect pathway • Symptoms: - violent, involuntary movement of limbs - Characterized by uncontrolled flinging • TX: Dopamine Antagonist
- 34. CORTEX PUTAMEN GP externa STN GP interna VA/VLTHALAMUS Glutamate (+) GABA (-) GABA (-) GABA (-) Glutamate (+) Glutamate (+) Hemiballismus +
- 35. Huntington’s Disease CORTEX PUTAMEN GP externa STN GPinterna VA/VL THALAMUS Glutamate (+) GABA (-) Glutamate (+) GABA (-) GABA (-) Glutamate (+) +
- 36.
- 37. Huntington’s Disease • AGenetic disorder • Loss of striatal neurons; cell death in the caudate nucleus • Early Symptoms: –Change in personality, intellect –loss of memory –odd jerking movements called chorea ("dance"). Late findings: –Akinesia Vegetative
- 38. Parkinson’s Disease • Lossof DA neurons in substantia nigra • Loss of DA : Loss excitatory effect on direct pathway, loss inhibition of indirect pathway • Overactive GPi and overactive STN increased inhibition of motor thalamus • Symptoms: Tremor (shaking), rigid muscles, difficulty making quick, smooth movements, and difficulty standing and walking.
- 39. • Progresses toother parts of the basal ganglia and to the nerves that control the muscles, involving other neurotransmitters. • Possible causes or contributing factors include - environmental toxins - head trauma - genetics.
- 40. CORTEX PUTAMEN (GPe) (STN) GP interna VA/VL THALAMUS Glutamate(+) Glu(+) GABA (-) GABA (-) Parkinson’s Disease (--) CORTEX PUTAMEN GP externa STN GP interna VA/VL THALAMUS Glutamate (+) GABA (-) GABA (-) GABA (-) Glutamate (+) DA (+) Glu(+)
Editor's Notes
- #24 Overall Excitatory by disinhibiting the upper motor neurons in the cortex (promotes movement)
- #33 Injury to STN by infarct, tumor, surgery Con of D2-antagonist: risk Parkinsonian state
- #36 Autosomal Dominant, Chromosome 4 Huntingtin protein Loss of striatal neurons Early Change in personality, intellect Chorea/athetosis Late findings Akinesia Vegetative