Bridges Basal Ganglia Flashcards
two parts of substantia nigra
pars compacta and pars reticulata
part of substantia nigra…sends dopaminergic fibers to neostriatum (this part damaged in Parkinson’s disease)
pars compacta
area that sends dopaminergic input to neostriatum (in addition to pars compacta of substantia nigra)
ventral tegmental
area of neostriatum that receives dopaminergic projections from the ventral tegmental area
ventral striatum/nucleus accumbens
pars reticulata (part of SN) resembles what structure cytologically?
globus pallidus
when we are faced with many alternative actions…basal ganglia do not trigger movement but release the chosen action and reject the other unwanted possibilities
action selection hypothesis
basal ganglia receive input from this structure…why it is suggested involved in habit formation and motor activity
posterior parietal cortex
input to basal ganglia
cerebral cortex
output of BG to cerebral cortex; this output is via what?
prefrontal, orbitofrontal, cingulate, premotor, supplementary motor, primary motor; thalamus
does the BG or cerebellum have projections to brainstem nuclei?
cerebellum
does the BG or cerebellum receive direct information from the spinal cord?
cerebellum
NT for inhibitory input from ventral striatum to output nuclei
GABA
NT for cortex to neostriatum
glutamate
NT for input from subthalamic nucleus to output nuclei
glutamate
NT used in input from neostriatum to GP externa, and from GP externa to subthalamic nucleus
GABA
NT for SN (pars compacta) and ventral tegmentum to input nuclei
dopamine
dopamine receptor that is inhibitory…acts in indirect pathways (inhibits the indirect pathway…why dopamine always enhances facilitation of cerebral cortex)
D2
dopamine receptor that is excitatory
D1
NT from output nuclei to thalamus
GABA
NT from thalamus to cortex
glutamate
activation of direct or indirect pathway will increase the facilitation of cortical neurons concerned with motor function (more input from thalamus helping neurons in motor cortex)?
direct
activation of direct or indirect will decrease thalamus facilitation of motor cortical neurons?
indirect
abnormal involuntary movements
dyskinesia
slow writhing movements of extremities or head and trunk (dystonia)
athetosis
random controlled movement patterns that occur continuously (sometimes flicking mvmnts involving extremities and facial muscles)
chorea
type of chorea…normal progression of movements cannot occur; person performs one movement pattern for few seconds, switch suddenly to another movement pattern (typically involved with childhood)
St Vitus’ Dance
chorea occurs from widespread damage to what structures? what neurons seem to be affected more?
caudate nucleus and putamen; Gaba-ergic
uncontrollable succession of violent, flailing, movements of large areas of body; what structure is normally damaged?
hemiballismus; subthalamic nucleus
more commonly involved in cognitive deficits/dementia with movement disorders; what specific structures are most likely?
limbic loop; ventral pallidum, ventral striatum, dopaminergic ventral tegmentum
typical presentation of a patient with Parkinson’s disease
unilateral resting tremor, reduced arm swing, slowed hand movement, change in gait/dexterity/energy level
surviving neurons from Parkinson’s disease contain these eosinophilic structures; what do these contain?
Lewy bodies; alpha-synuclein
what is major pathological finding in Parkinson’s disease? where does this occur?
dopaminergic neurons; SNc
this drug binds dopamine receptors…can cause similar Parkinson-like disorder
antischizophrenic
the tremor of Parkinson’s disease may involve this; oscillating state of activity of neurons that control extensor and flexor muscles (normally damped by basal ganglia)
subthalamic nucleus
deep brain electrical stimulation is designed to treat Parkinson’s by stimulating this area, and decreasing activity of this area
thalamus, subthalamic nucleus
possible treatment for Parkinson’s…based on the increased activity of GP interna
pallidotomy
another surgical intervention for Parkinson’s disease that has a good effect on the tremor (but not on any of the other symptoms)
thalamotomy
Syndenham’s chorea/St Vitus’ Dance can follow these childhood diseases
streptococcal infection or acute rheumatic fever
option for symptomatic treatment for Huntington’s disease (but there is no treatment)
haloperidol
gene for Huntington’s Disease located on what chromosome? what protein does this encode for?
4; huntingtin
Huntington’s Disease is example of this mutation, who’s length directly correlates to age of onset; what codon is involved?
trinucleotide repeat; CAG
repetitively tapping forehead around eyebrow causes uncontrollable blinking of the eye
glabellar reflex/Myerson’s sign
ventral fusion of caudate and putamen that merges into nucleus accumbens and striatal portions of olfactory tubercle
ventral striatum
caudate + putamen + globus pallidus
corpus striatum
caudate + putamen
neostriatum (dorsal striatum)
putamen + globus pallidus
lenticular (lentiform) nucleus
region of neostriatum that receives dopaminergic neurons from ventral tegmental area
nucleus accumbens (of ventral striatum)
input nuclei of basal ganglia
caudate nucleus and putamen (neostriatum), ventral striatum (nucleus accumbens)
output nuclei of basal ganglia
SNr and GP internal, ventral pallidum (extension of GP below anterior commissure)
intrinsic nuclei of basal ganglia
SNc, GP external, subthalamic nucleus
NT from thalamus, cortex, and subthalamic nucleus that is excitatory
glutamate
major input to basal ganglia (excitatory)
corticostriatal projection
skeletomotor loop mainly concerns this basal ganglia…used in control of musculature, acquisition of motor skills
putamen
where is output of skeletomotor loop (putamen) directed back to (via GP and thalamus)?
supplementary motor, premotor, motor cortex
nucleus involved in oculomotor and spatial memory loop…receives input from remainder of frontal and parietal lobes (*controls extraocular muscles and aspects of orientation memory*)
caudate
this may be involved in action selection
prefrontal/executive loop
where do hippocampal formation, amygdala, and anterior cingulate gyrus project in limbic loop?
ventral striatum
OCD and schizophrenia have been associated with this basal ganglia loop
limbic
this may involved hyperactivity in cognitive circuitry regulating prefrontal speech areas
Tourette’s syndrome
striosomes (patch of neurons in neostriatum) have this kind of receptors
opiate
what is input to striosomes? where do they project?
limbic cortical area; SNc
what is most common presenting sign of Parkinson’s?
rhythmical tremor (that disappears during voluntary activity)
gene for familial Parkinson’s that is located on chromosome 4 encodes for this…necessary for ER to Golgi trafficking (concentrated in presynaptic terminals)
a-synuclein
symptoms of Parkinson’s appear after this percentage of dopaminergic innervation of neostriatum has been lost
85%
precursor for dopamine that can cross BBB…given as treatment for Parkinson’s (w/ peripheral DOPA decarboxylase)
L-DOPA
fetal dopaminergic cells can be taken from this area as possible treatment for Parkinson’s
mesencephalon
growth factors that could be injected to save/rescue patient’s own dopaminergic neurons
GDNF and PDGF
abnormal posture held for a long time (terminal stage of Huntington’s disease)
dystonia
earliest Huntington’s effects stem from loss here
striatal neurons of indirect pathway (GABA projecting to external GP, also cholinergic within)
loss of GABA neurons in Huntinton’s disease early on is similar to lesion of this
subthalamic nucleus
changes in personality/non-motor aspects in Huntington’s disease is associated with this
caudate nucleus
in Parkinson’s….lack of dopaminergic input causes reduced activity of neurons with these receptors; and increased activity of neostriatal neurons with these receptors
D1; D2 (overall enhanced inhibition of thalamus)
blood supply to head of caudate
medial striate
blood supply to posterior limb IC
anterior choroidal
