3-19 Basal Ganglia Flashcards
What are the 4 major parts of the of the basal ganglia?
Striatum
Globus pallidus
Subthalamic nucleus
Substantia nigra
What makes up the striatum?
caudate nucleus
nucleus accumbens
putamen
What makes up the lentiform nucleus?
Putamen
Globus pallidus - internal and external
What makes up the globus pallidus?
Globus pallidus internal
Globus pallidus external
What parts make up the substantia nigra?
pars compacta
pars reticulata
What is the subthalamic nucleus a part of, other than the basal ganglia?
Diencephalon
Where is the substantia nigra in the brain?
Mesencephalic nucleus in midbrain
What is the nucleus accumbens?
Part of basal ganglia
Where caudate nucleus and putamen meet, closer to posterior aspect of brainstem
What is the source of dopamine in the basal ganglia?
pars compacta
What kind of neurons leave pars reticulata?
mostly gaba-ergic
How is the location of the basal ganglia in the brain helpful to it’s function?
BG is a recursive circuit that is important in connecting different parts of the brain to allow for continuity of repetitive behavior
Located near thalamus and internal capsule so that it can connect with motor outputs ‘smooth out’ motions
What cerebral structure is the basal ganglia at the center of?
Telencephalon
What helps to make movements smooth, linked, and repeating?
An “accessory motor circuit”, involving the basal ganglia
What is the basic idea behind direct excitation?
Depolarization -> AP -> NT release
What is the basic idea behind indirect excitation? What is another name for this concept?
AKA - disinhibtion
Constant hyperpolarization prevents APs in an otherwise active circuit
Removing the inhibitory action allows the system to “go”
- like easing off the brakes, or letting the puppy have more leash
What is the direct pathway? What are the major players, and what kinds of NTs do they release?
- Motor Cortex
- signal muscles to move
- phasic
- glu/excitatory neurons to striatum - Striatum (caudate + putamen)
- GABA-ergic
- phasic
- fires on GPi and SN pars reticulata - GPi and SN pars reticulata
- TONIC
- GABA-ergic to thalamus
- inhibits thalamus - Thalamus - VA/VL nuclei
- TONIC
- glu/exctitatory neurons to motor cortex
What roles does the substantia nigra pars compacta play in the direct basal ganglia pathway?
Releases dopamine onto striatum
- Striatum receives it with D1 receptors
- D1 receptors = excitatory
Helps create smooth, linked movements by decreasing GPi’s inhibitory effects on the thalamus
What is the indirect BG pathway? What are the major players, and what are their roles?
- Motor Cortex
- excitatory signal to striatum - Striatum
- inhibitory signal to GPe - GPe
- inhibitory signal to subthalamic nucleus - Subthalamic nucleus
- glu to GPi - GPi
- glu to thalamus - Thalamus
- glu to motor cortex
What are the 2 major pathways by which dopamine turns the basal ganglia on?
Nigrostriatal pathway
Mesolimbic oathway
What does the nigrostriatal pathway consist of?
Projections from the Substantia Nigra pars compacta to the caudate or putamen
Motor-related
What does the mesolimbic pathway consist of?
Projections form Ventral Tegmental Area to the nucleus accumbens
Limbic - generally reflects goal-oriented behavior, as nucleus accumbens is associated with goal-oriented behavior and addiction.
What can happen to the nucleus accumbens when dopamine is released around it?
“Chia pet effect”
NA will grow more dendrites to suck up all the delicious dopamine, and will reward goal-oriented behavior and/or addiction.
What are the 3 major pathways that reach the thalamus from the cortex?
Ansa lenticularis - lens hook
Lenticular fasciculus - lens-like bundle
Thalamic fasciculus
What is another name for the thalamic fasciculus? What info does it carry?
AKA Forel’s field
Also carries cerebellar info
What does Parkinson’s Disease involve, pathologically? At what point do clinical symptoms manifest?
Progressive loss of dopamine neurons
60% of neurons die before symptom onset
What is the motor triad phenotype of Parkinson’s Disease?
Resting tremor
Rigidity (lead pipe/cogwheel) - mm is stiff and spastic until overwhelmed with force
Bradykinesia/akinesia - inability to make smooth and linked movements
What can long term dopamine treatment lead to?
Dyskinesia
- movement when you’re not trying to move
What are some non-motor components of Parkinson’s Disease?
100% of men with REM behavior disorder will develop Parkinson’s Disease
Impulse control deficiencies present later
Cognitive effects dependent on laterality
What is the genetic cause of Huntington’s disease?
genetic mutation of polyglutamine (CAG) repeats causes neuronal death
Spontaneous mutation
- can show symptoms later in life
- will show up earlier in each successive generation
What is the pathology of Huntington’s disease?
Targets the striatum
Chorea (random, involuntary, flicking mvmt.)
Considered a disorder of “hyperkinesia”
- loss of neurons in striatum, which leads to loss of disinhibition
Indirect pathway is diminished relative to direct pathway
Often begins with depression
- indicates BG is tied up intimately with limbic lobe
Are Huntington’s and PD strictly diseases of motor control?
No
What is the cognitive/prefrontal loop?
Regulates initiation and termination of cognitive processes
What are the 4 parts of the cognitive/prefrontal loop?
Dorsolateral prefrontal cortex
Caudate
GPi
Mediodorsal thal, VA/VL thal
What makes up the limbic loop portion of the BG?
amygdala, hippocampus, orbitofrontal cortex, anterior cingulate
Ventral striatum (includes nucleus accumbens)
Ventral pallidum
Mediodorsal thal
What is dysfunction of the limbic loop indicated in?
Tourette’s syndrome
OCD
Addiction - not unusual for addicts to develop Parkinsonian symptoms
The BG has what kind of effects, in general?
Motor - smooth, linked, repetitive behaviors
Non-motor - behavior, motivation, and adaptive behaviors
What is the effect of a lesion of the GP?
inability to maintain postural support
