Section 3 Lecture 4 Flashcards
Which portion of the brain is the BG in?
Forebrain
BG is involved in:
M control, cognitive fxn, and emotional or affective fxn
Fxn of the BG in terms of what info travels through and to where:
To control excitatory drive to cortex
What is the extrapyramidal system:
BG (does not operate independent of cortex, this is an old view)
What is the striatum composed of?
Caudate and putamen
What is the BG composed of?
Caudate, putamen and Globus pallidus
T or F? The substantia nigran and the subthalamic nucleus are both part of the BG.
F. Neither are.
Main fxn of SN:
dopamine released, altering the functional level of the striatum
Damage to BG:
involuntary moves or slowness of movement (bradykinesia)
BG diseases or disorders:
PD, ADHD, tourette’s, Restless Leg syndome, Tardive dyskinesia, Huntington’s, dystonias
PD facts:
typical onset: 60+, more men than women, progressive, but slow, can live for 20+ yrs
There is degeneration of this in PD:
substantia nigra
Specific cell population affected in PD:
substantia nigra degeneration of neurons, loss of dop input to striatum, caudate and putamen
Causes of PD:
unknown, genetic factors? Not a single gene mutation, would be genetic contribution or influence
Post-infectious PD:
got it after a flu virus, some viral influence (in this case at least)
Biochemical link to PD:
depression
Cognitive affects of PD:
dementia, sometimes
Motor symptoms of PD:
combo of + and - effects: tremor AT REST (esp hands and mouth), bradykinesia, akinesia
cerebellar lesions lead to:
tremors when movements are activated
Symptoms of PD:
motor, affective (depression), cognitive (dementia), tremor, brdykinesia, akinesia
Absence of movement, especially self-initiated moves, i.e. lack of facial expression, swinging arms when walking):
Akinesia
Are the motor symptoms connected to PD pos or negative?
both
How to induce PD in animals:
MPTP
BG is especially important in what type of moves?
self initiated movements
The ability to walk and swing arms with legs (assoc moves) is lost with the disease:
PD
T or F? Excitation and inh are intrinsic properties of dopamine.
F. They are not
Is PD slow or fast progressing?
slow prog
What is DBS and explain how it works.
deep brain stimulation: electrodes, subthalamus n., like a pacemaker
What led to the discovery of MPTP and what does it damage?
attempts to make heroin,MPTP damages SN
Effects of MPTP:
destroys neurons in substantia nigra
T or F? Most neurogenic disease aren’t found in animals.
T
Death of neurons in the sub nigra lead to what?
gradual loss of dopamergic input to caudate and putamen
Cause of PD:
not known
Tx for PD:
l-dopa, tissue/stem cell implants, lesion in pwy, or DBS
Why can’t we give dopamine to tx PD?
bc it wont pass BB barrier, give a precursor
Experimental procedure to tx PD:
Implant cells that will synthesize dopamine,
Goal in the tx of PD:
block or reduces abnormal drive to MC, disrupt abnormal activity in the BG
What happens w the removal of dopamine?
too much excitation in one place, too little in another.
Recent development that will help our understanding of PD:
we now have animal models of PD
PD involves the synapse bw:
SN to striatum
Transporter protein takes up:
serotonin, dopamine
Stimulant drugs act by:
changing dop levels, reuptake of dop at synapse is terminated by a “transporter” i.e. coin works on dop transporter
T or F? Dopamine is involved only in the M system.
F. other cell groups synthesize and release dop
Lack of sufficient dopamine reuptake can be related to:
transmitter concentrations, receptors, or transporters
How do the serotonin levels in depressed people compare with those of non-depressed people?
the same, receptor function may be inhibited
Subtypes of dopamine receptors:
D1-D5
Which subtypes of dopamine receptors are found in the hypothalamus?
D3 and D5
Which subtypes of dopamine receptors are found in the corpus striatum?
D1 and D2
What is neurological basis of shizophrenia:
too much dopaminergic action in the frontal lobe (hypothesis)
Dopamine receptor blockers:
neuroleptics, used to be tx for schizo, i.e. Chlorpromazine (Thorazine) and Haloperidol (Haldol)
Long term use of neuroleptic drugs for schizo can lead to:
motor disorders: tardive dyskinesia (invol mouth, face and hand moves) or tardive dystonia (abnormal m. tone or postures)
Which lobes of the brain are implicated in schizo?
frontal
Newer drugs for schizophrenia:
atypical antipsychotics, act on dop receptors in cerebral cortex (frotal lobe) and not subsets in the BG (tx cortical and does not interfere with M systems use of dopamine) Also used to tx bipolar disorder
Symptoms of atypical antipsychotics:
weight gain and diabetes
List of atypical antipsychotic Dx:
Risperdal (Risperidone), Olanzapine (Zyprexa), Quetiapine (Seroquel), Ziprasidone (Geodon), Aripiprazole (Abilify), Paliperidone (Invega), Lurasidone (Latuda)
T or F? ADHD is a M system disorder.
F.
What NT is implicated in ADHD?
dop, fxnal dopamine deficiency (hypothesis)
T or F? ADHD is a lifelong disorder
F, mainly. “symptoms MAY continue into adulthood”
Fxn of ritalin (methylphenidate) or adderall:
increase dopamine levels (adderral increases NE as well)
What is the biomarker for ADHD?
There isn’t one
Rital fxns by:
acting on the dop transporter
Adderall fxns by:
inc the release of dop and NE
Tourette’s is a movement disorder assoc w this part of the brain:
BG
T or F? The tics that come with Tourett’es an be suppressed and controlled.
F. Can’t control but can suppress
T or F? Tourette’s is a single gene disorder
F. Hereditary, but not a single gene
Is Tourettes’ more prevelant in men or women?
Men 3:1
What is the neurological basis of Tourette’s?
Too much functional dopamine (hypothesis)
Tx or Tourette’s
dopamine receptor blockers, ie Haldol (still?)
Typical age of onset of Tourette’s:
childhood, often w ADHD
T or F? Restless Leg Syndrome has M symptoms only.
F. Sensory and motor symptoms
RLS is a disorder of what part of the brain?
BG (hypothesis)
Tx for RLS:
increase synthesis of dopamine (L-dopa carbidopa = Sinemet) or mimic the action of dopamine (ropinirole, pramipexole, and rotigotine)
Symptoms of RLS are more pronounced:
at night
Who are affected by RLS more, men or women?
Women
What portion of the brain is involved with Huntington’s?
BG disease:
T or F? Huntington’s a dopamine disorder.
F
What is going wrong in the brains of pts with Huntington’s?
Death of cells in caudate and putamen (the striatum)
Does Huntington’s have a genetic basis?
Yes, 1 in 10,0000
How is Huntington’s passed geneticlally:
Autosomal dominant
