problem 3 Flashcards
Biological motivators
- eating
- drinking
- sexual behavior
Social, psychological motivators
- Socializing with peers
- Experiencing love
- Sports
definition drive
A condition that energized an organisms behavior –> natural rewards
Hunger (drive) - seeks - food (goal)
intensive learning (Definition)
learning based on reinforcement
model (intensive motivation?/brain disease model?)
it suggest that motivation Is a reinforcement behavior.
An external stimulus, such as the sight of food is compared to the memory of its past reward value. At the same time, physiological signals of hunger and satiety modulate the potential value at the moment. these two types of information are integrated to produce the final incentive motivation for the external stimulus, which is manifested in behavior and conscious experience.
incentive motivation = regulated by dopamine.
Motivation states
A deficit causes the organism to seek out a goal
Mesolimbic dopamine pathway (reward circuit) - normal
- Set of nerve cells that originate in the ventral tegemental area (VTA) sends projections to target regions in the front of the brain (to the nucleus accumbens)
- VTA neurons communicate by dispatching (verzenden) the chemical messenger (neurotransmitter) dopamine from the terminals, of their long projections to receptors on the nucleus accumbens neurons.
VTA to the nucleus accumbens is critical for addictions
The VTA-accumbens pathway act as a rheostat (dimmer) of reward: it tells the other brain centers how rewarding an activity is. the more rewarding an activity is deemed (geacht), the more likely the organism is to remember it well and repeat it.
mesolimbic dopamine pathway - addiction
- Use of addictive drug –> dopamine neurons in VTA are activated (VTA sending signals to nucleus accumens)
- this activation causes neuron levels in the nucleus accumbens to rise.
first use of drug: dopamine releases
long association: (learning) –> dopamine is not being fired more, but its the anticipation of pleasure.
Incentive learning (how?)
- US (drug) –> UR (pleasure)
- NS (bar) –> no response
- NS + US –> UR
- CS –> CR
existing:
- CS (stimuli) + US (no drug) –> CS alone = withdrawal
Drug exposure
existing:
- CS (stimuli) + US (no drug) –> CS alone = withdrawal
- Drug exposure leads to development of adaptive neural changes that produce tolerance by counteracting the drug effect.
- With no drug to counteract them, the neural adaptations produce withdrawal effects opposite to the effects of the drug.
Tolerance - explained (short term)
- DA signaling leads to increase cAMP and calcium concentrations
- These increased concentrations activate CREB (cAMP response element-binding protein- transcription factor) which binds to DNA and activation specific genes.
- These genes bring about proteins involved with tolerance and dependence.
- Dynorphin is dispatched to VTA where it quits down DA release and dampens the reward circuit causing a user to need more drug to feel.
Craving + sensitization (explained) - also known as long term effect
- DA signaling leads to production of delta fosB
- DeltafosB represses (onderdrukt) dynorphin synthesis + activates specific genes (different from those switched on by CREB)
- activated genes give rise to proteins involved in sensitizing responses to drugs/reminders of past drug use
- CDK5 may promote structural changes that make Nacc neurons persistently (aanhoudend) sensitive to drugs and drug related cues.
How is it possible that different substances all elicit similar responses in the brains reward circuit?
All drugs of abuse, in addition to any other effects, cause the nucleus accumbens to receive a flood of dopamine and sometimes also dopamine mimicking signals. When a nerve cell in the VTA is ‘exited’, it sent an electrical message along its axon - which causes dopamine to be released from the axon tip into the tiny space - synaptic cleft. what separates the axon terminal from a neuron in the nucleus accumbens. from there dopamine latches onto its receptor on the accumbens neuron and transmits its signal into the cell.
to later shut down the signal, VTA neuron removes the dopamine from the synaptic cleft and repackages it to be used again when needed.
cocaine and other stimulants temporarily disable the transporter protein that returns the neurotransmitter to the VTA neuron terminals, thereby leaving excess dopamine to act on the nucleus accumbens.
heroin and other opiates on the other hand, bind to neurons in the VTA that normally shut down the dopamine-producing VTA neurons
Role of amygdala, hippocampus and frontal cortex in addiction
amygdala - helps to assess whether an experience is pleasurable or aversive - and whether it should be repeated or avoided.
hippocampus - participates in recording the memories of an experience, including where and when and with whom it occurred
frontal regions - of the cerebral cortex coordinate and process all this information and determine the ultimate behavior of the individual
these three structures communicate back and forth with the VTA and nucleus accumbens. they talk to the pathway by releasing glutamate
difference natural reinforcement and drugs
Activate the same circuit, but not to the same extent.
