Section 3 Lecture 4 Flashcards by Tedman McMahon

Which portion of the brain is the BG in?

Forebrain

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BG is involved in:

M control, cognitive fxn, and emotional or affective fxn

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Fxn of the BG in terms of what info travels through and to where:

To control excitatory drive to cortex

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What is the extrapyramidal system:

BG (does not operate independent of cortex, this is an old view)

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What is the striatum composed of?

Caudate and putamen

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What is the BG composed of?

Caudate, putamen and Globus pallidus

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T or F? The substantia nigran and the subthalamic nucleus are both part of the BG.

F. Neither are.

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Main fxn of SN:

dopamine released, altering the functional level of the striatum

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Damage to BG:

involuntary moves or slowness of movement (bradykinesia)

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BG diseases or disorders:

PD, ADHD, tourette’s, Restless Leg syndome, Tardive dyskinesia, Huntington’s, dystonias

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PD facts:

typical onset: 60+, more men than women, progressive, but slow, can live for 20+ yrs

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There is degeneration of this in PD:

substantia nigra

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Specific cell population affected in PD:

substantia nigra degeneration of neurons, loss of dop input to striatum, caudate and putamen

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Causes of PD:

unknown, genetic factors? Not a single gene mutation, would be genetic contribution or influence

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Post-infectious PD:

got it after a flu virus, some viral influence (in this case at least)

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Biochemical link to PD:

depression

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Cognitive affects of PD:

dementia, sometimes

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Motor symptoms of PD:

combo of + and - effects: tremor AT REST (esp hands and mouth), bradykinesia, akinesia

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cerebellar lesions lead to:

tremors when movements are activated

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Symptoms of PD:

motor, affective (depression), cognitive (dementia), tremor, brdykinesia, akinesia

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Absence of movement, especially self-initiated moves, i.e. lack of facial expression, swinging arms when walking):

Akinesia

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Are the motor symptoms connected to PD pos or negative?

both

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How to induce PD in animals:

MPTP

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BG is especially important in what type of moves?

self initiated movements

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The ability to walk and swing arms with legs (assoc moves) is lost with the disease:

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.

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.

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:

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.

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