Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
64 Cards in this Set
- Front
- Back
What is the thalamus?
|
a relay center for incoming sensory information and outgoing motor information; acts as a filter to fine-tune incoming and outgoing information
|
|
What does the hypothalamus do?
|
receives neurochemical signals from the brain and neuroendocrine signals from the body to regulate homeostasis and drive behavior towards homeostasis
|
|
What does the amygdala do?
|
receives information from all modalities and processes information regarding unconditioned fear and reward and conditioned fear and reward
|
|
What is the hippocampus involved in?
|
memory consolidation and recall.
|
|
What does the cortex do?
|
associates information from many brain regions and is involved in executive functions
|
|
The striatum is a motor interface. What does that mean?
|
it connects many nonmotor structures with the primary motor cortex via the basal ganglia.
|
|
What is in the Dorsal striatum?
|
caudate and putamen
|
|
What is in the Ventral striatum?
|
nucleus accumbens
|
|
What is the nucleus accumbens?
|
a small structure in the diencephalon that is highly involved in turning motivation into action
|
|
What does the nucleus accumbens do?
|
-receives information from all other
limbic regions (decisions from PFC, memory from hippocampus, emotion from amygdala, and motivation from hypothalamus, also input from midbrain monoamine systems) -Considered the start of the motor output of the limbic system; “limbic-motor interface”. -The nucleus accumbens sends information to the motor component of the limbic system to produce a behavioral output (approach vs. avoid) |
|
What is considered the brains reward center?
|
nucleus accumbus
|
|
What happens when there is damage to the accumbens?
|
-Reduction in eating, drinking, sex,
drug-taking -Reduction in intracranial selfstimulation (electrical stimulation of the brain’s reward pathways) |
|
What disorder would have low nucleus accumbens activity?
|
depression
|
|
What disorder would have high nucleus accumbens activity?
|
addiction
|
|
In addition to turning motivation into action, the nucleus accumbens is also involved in...
|
attention
|
|
Nucleus accumbens responds to...
|
new or important items in the environment and then motivates the animal to act accordingly (approach or avoid)
|
|
The nucleus accumbens is rich in...
|
dopamine receptors and receives
dopamine signals from the ventral tegmental area (VTA). |
|
Where is the ventral tegmental area (VTA) located?
|
in the tegmentum
|
|
How does nucleus accumbens work?
|
Good stuff -> NAC activated ->
approach the good stuff Bad stuff -> NAC activated -> avoid the bad stuff |
|
What does blocking dopamine receptors in the nucleus accumbens do?
|
makes animals work MORE for electrical stimulation
-stimulation not as rewarding so need more stimulation-> more lever pressing |
|
What does enhancing dopamine transmission (giving amphetamine) do?
|
-makes an animal work LESS for electrical stimulation
-stimulation is more rewarding so need less stimulation -> less lever pressing |
|
What does Wellbutrin do?
|
a dopamine reuptake inhibitor (like cocaine but not as strong) that effectively treats some forms of depression
|
|
What does Wellbutrin=Zyban do?
|
“no smoking pill”
-The idea is to elevate dopamine first so that the ability of nicotine to elevate dopamine is not detected -> no rise in dopamine by nicotine -> no motivation to smoke or attention to smoking -> stop smoking |
|
Dopamine levels rise in the nucleus accumbens in response to...
|
appetitive AND aversive situations
|
|
Dopamine goes up in the nucleus accumbens when...
|
-Having sex, eating food, drinking water, being shocked etc.
-Taking drugs of abuse -All addictive drugs increase dopamine in the nucleus accumbens! |
|
What do drugs of abuse do to the accumbens?
|
sensitize dopamine
|
|
What is the dopamine hypothesis of addiction?
|
The ability of drugs of abuse to elevate and to sensitize this elevation in nucleus accumbens levels of dopamine is responsible in part for the increased attention to and/or motivation for the effects
of the drug and the motivation to keep taking the drug (addiction) |
|
What leads to addiction?
|
-Chronic stimulant use decreases the number of dopamine transporters in your nucleus accumbens
-Less transporters -> less reuptake -> more dopamine in synapse -> higher motivation for drug + greater attention to drug -> addiction |
|
What is considered the critical
pathology in addiction and other disorders? |
A dysregulation of the circuit involving the VTA, nucleus accumbens, prefrontal cortex and amygdala
|
|
What is the basal ganglia?
|
similar to the limbic system in that it is
also a circuit of inter-connected brain regions |
|
What is the key role of the basal ganglia?
|
-the initiation, coordination and control of motor movements
-procedural memory (the memory of performing an act; e.g. riding a bike, writing) -“habit” circuit of the brain and can be, but is not necessarily, driven by emotionally or motivationally relevant items |
|
Where is the limbic system and the basal ganglia located?
|
diencephalon and mesencephalon, where they curve around the thalamus
|
|
The limbic system and the basal ganglia receive inputs from...
|
from structures in both the diencephalon and the midbrain
|
|
Both the limbic system and the basal ganglia are surrounded by...
|
cortex enabling these circuits to receive primary, secondary and associative sensory information and to send motor information to the primary and secondary motor cortices
|
|
Where does dopamine originate in the basil ganglia?
|
substantia nigra (black substance; SN)
|
|
Where is the substania nigra (SN) located?
|
the tegmentum
|
|
The substania nigra (SN) is so called because...
|
it is high in the dark pigment, melanin
|
|
The SN sends neurons to
a region called the... |
caudate-putamen (in primates) or the dorsal striatum (in lower mammals not divided)
|
|
The nigro-striatal dopamine system is so-called because...
|
it originates in the substantia nigra (nigro) and projects to the dorsal striatum (striatal)
|
|
Why is the nigro-striatal dopamine system important?
|
for the consolidation and recall of procedural memory (learned motor
patterns and habits) |
|
What do stimulant drugs do to dopamine levels in stratium?
|
increase!
|
|
Hyper-activation of the nigro-striatal dopamine pathway does what with each stimulant experience?
|
sensitizes (gets bigger)
|
|
How do habits form?
|
The sensitization of dopamine transmission in the striatum accounts for the sensitization of motor behaviors with repeated drug use -> habit formation
|
|
Hyper-activation of the nigro-striatal dopamine pathway leads to what?
|
motor hyperactivity -> ADHD
|
|
Hyper-activation of the nigro-striatal dopamine pathway causes....
|
fidgeting, leg bouncing, finger tapping, picking (at skin, clothing etc)
|
|
When not on drug, stimulant addicts...
|
exhibit many of the motor symptoms of ADHD
|
|
When on drug, stimulant addicts....
|
can “get stuck” in behavioral patterns (re-arranging, skin-picking, etc; almost autistic-like)
(sensitization of dopamine?) |
|
Certain types of schizophrenia are associated with...
|
hyperactivity and involuntary motor movements
|
|
What is the treatment for schizophrenia?
|
block dopamine receptors to prevent excessive dopamine from hyper-activating the striatum
|
|
What receptors do anti-psychotic drugs block?
|
D2 dopamine receptors
|
|
Tourette’s Syndrome is characterized by...
|
motor and verbal tics (involuntary movements
|
|
What is treatment for tourette's syndrome?
|
block D2 dopamine receptors
(in fact, treat with antipsychotic drugs) |
|
Hypo-activation of the nigro-striatal dopamine pathway causes...
|
a variety of motor disturbances
-Type of motor disturbance depends on whether the SN or the striatum is affected |
|
What is Huntington’s Disease?
|
genetic disorder characterized by
ballismus, hyperactivity, inability to control motor movements produced by a loss of striatal interneurons |
|
What are striatal interneurons?
|
GABA neurons that go to rest of basal ganglia
|
|
What does reduction in GABA output from the striatum cause?
|
enhancement of excitation (glutamate) of the motor cortices -> ballistic movements -> Huntington’s Disease
|
|
What is Parkinson’s Disease?
|
characterized by inability to initiate
or terminate a movement, resting tremors, shuffling, loss of fine-motor control |
|
What causes Parkinson's disease?
|
selective loss of SN dopamine neurons
-low dopamine in striatum -> motor problems |
|
What does a reduction in nigro-striatal dopamine pathway cause?
|
reduction in excitation (glutamate) of the motor cortices -> reduction in motor control -> Parkinson’s
Disease |
|
There are 2 pathways in the basal ganglia out of the....
|
striatum
|
|
Loss of striatum=
Loss of SN= |
Huntington’s=hyper-movement
Parkinson’s=hypo-movement |
|
What happens if someone overdoses with anti-psychotics?
|
Anti-psychotic drugs block the effects of dopamine in the striatum -> shutting down effect of dopamine in striatum -> turn a schizophrenic into a patient with Parkinson’s-like symptom
|
|
What does MTPT do?
|
-supposed to be a synthetic
heroin -> teenagers and young adults showing up in the ER with “Parkinson’s” -MPTP turned out to be a neurotoxin for dopamine neurons (killing of both the VTA and SN) |
|
How to elevate SN dopamine signals to treat parkinsons....
|
-L-DOPA crosses the blood-brain barrier and becomes converted into
dopamine in the brain. Currently a major therapy but lasts only as long as you have dopamine neurons to convert it. -Give stimulants like amphetamine that release dopamine (only works so long as there are enough dopamine neurons) -Activate dopamine receptors directly with drugs that cross the blood-brain barrier (apomorphine; current therapy) |