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Terms in this set (80)
a stimulus that the brain interprets as intrinsically positive, or as something to be approached.
stimulus that increases the probability that behaviors paired with it will be repeated. Not only for rewarding stimuli, a negative stimulus can increase avoidance
thought to underlie the perception of reward and positive reinforcement. Complements pathways that are involved in the fear response 2
2 ways reward circuits have been characterized
1) natural reinforcers such as food and water
2) drugs of abuse
Difference between natural reinforcers and drugs
Natural reinforces activate sensory pathways and internal cues to activate the reward pathway. Addictive drugs stimulate the same pathways using chemical means, bypassing evolutionarily useful behaviors.
Problem with drugs
1. Lead to extreme euphoric states
2. Extreme changes in reinforcement behaviors that lead to compulsive use.
3. The design of the human brain that has helped us to promote survival has also made us vulnerable to addiction
Compulsive drug seeking and consumption despite serious negative consequences
Two types of drug reinforcement
1. Initial drug use is reinforcing because it produces pleasurable states
2. Once repeated, drug use has impaired the function of reward circuitry, so the drug use alleviates the adverse effects of withdrawal
Measuring reinforcement is lab animals
1. operant conditioning
2. fixed, continuous, or variable ratio schedules
3. Passive avoidance- drug associated with an averse location
diminished response to a drug after repeated exposure to that drug. When tolerance develops, increasingly larger doses of a given drug must be administered to obtain the same magnitude of biological response.
enhancement of a particular drugs effects following repeated administration of the same dose of the drug. Paranoia is commonly an example of this
Drug associated changes in reward pathways
1) Upregulation of cAMP systems and CREB
2) Changes in dopamine transporter numners
3) Changes in the expression of dopamine and glutamate receptors
4) increased release of CRF
Dendridic changes and drugs
There is an increase of dendrite spines after cocaine and amphetamine use that is only reversible after a very long time.
Factors leading to relapse
2. Cues in the environment that are associated with previous drug-taking.
Rehab is more to prevent relapse than it is to make you want to stop- most people want to stop
transient responses to environmental and internal stimuli
(if the occur without stimuli, that is considered abnormal)
predominant emotional state over time
necessity of emotions
Not just subjective feelings- critical to survival
activate behavioral and physiologic mechanisms that represent adaptive responses to external and internal stimuli. We often need these to sustain life.
such as fear and anxiety- these lead to avoidance, escape, and protective responses. Could save your life!
result from presence of rewarding stimuli that indicate safety, comfort, and the presence of food. Often lead to approach behavior and increased socialization
Primary functions of emotions in the brain
1. APPRAISE the significance of a stimulus and, if necessary, activate the output systems that prepare the organism to respond.
2. SUPPRESS ongoing behaviors that are not relevant to the stimulus (you can only deal with 1, multitasking isn't real)
3. ACTIVATE neuroendocrine and autonomic nervous systems(glucocorticoids, etc)
4. ENCODE the new experience in memory to provide appropriate warnings in the future (emotional memories are strong, fast, salient)
A number of interrelated structures including the hippocampus, septum, amygdala, olfactory bulb, hypothalamus, and cingulate cortex.
Primary neurotransmitter in the limbic system
Primarily glutamatergic to allow for faster processing
Modulatory neurotransmitters in the limbic system
monoamine systems modulate (DA,NE,5-ht)
How to measure fear
Pavlovian conditioning- pair tone with shock
Fear potentiated startle- natural startle response to a loud tone is elevated if the organism is in a fear environment
a state characterized by arousal, physiologic preparedness, and negative subjective state. Anxiety is different from fear in that it is triggered in the absence of immediately threatening stimuli.
How to measure anxiety
1. Elevated plus maze
2. Open field test
Activation of amygdala
1) Suppresses ongoing behavior so that other behaviors that are critical for survival can be activated
2) regulates arousal and attention
3) Activates the neuroendocrine systems
-Mostly regulated by the light/dark cycle
-Also activated by stress in the environment
-Releases hormones involved in the stress response.
-Can be activated by the amygdala
multiple attacks of intense anxiety that are accompanied by somatic symptoms such as dizziness and tachycardia. Feels like a heart attack. Usually occurs in people in their 20's and 30's
Generalized Anxiety Disorder
Unrealistic and excessive worry sustained for 6 months.
Occurs after serious trauma and is characterized by cue-induced flashbacks of the traumatic experience, increased startle and nightmares.
Intense fear of specific stimuli such as spiders or airplane travel
Persistent fear of social situations
Treatment of Anxiety Disorders
side effects: sedative, tolerance, dependence
GABAa and mood
This receptor potentially reduces excitatory transmission through the amygdala
Characterized by sad mood or loss of interest in usual pursuits, accompanied by abnormalities of sleep, appetite, energy, sex drive, motivation, hopelessness, and suicidal ideas.
Characterized by episodes of mania, with or without distinct episode of depression
Neuchemistry of Major depression
1. altered 5-HT and NE systems
2. Elevated CRF levels
3. Down regulation of neurotrophic factors such as BDNF
4. Neuropeptides such as substance P.
How do antidepressants work
primarily target serotonin (5-HT) and norepinephrine (NE) uptake sites or block NE or 5-HT metabolism. Generally takes a while to kick in, 2-3 weeks to fully work.
These cause up regulation of cAMP and CREB- promoting cell survival
Prolonged stress causes atrophy and dendridic death
critical for circadian rhythmicity and sleep- lesions of this region create a state of chronic insomnia. Cats with lesions here can't sleep and eventually die.
regulates circadian rhytmicity in mammals
slight modifications of the same gene
Clock genes in humans
Period (per) and timeless (tim). Their protein products are produced during the day and dimerize as they accumulate. These dimers eventually negatively regulate their own translation. They are degraded by phosphorylation
Tonic activity of histamine neurons in the Tuberomamilary region suppresses sleep, sustaining wakefulness. GABA neurons in the POAH suppress these neurons causing sleep. TM activity and POAH activity is always opposite.
needed to go into non-rem sleep. It is a positive modulator of the GABA from the POAH. without it you get an abnormal rem pattern
controlled by activation of cholinergic neurons in the pontine tegmentum (PPT). These are called REM-on cells. These cells are inhibited by 5-HT from the rap he and NE from the locus ceruleus (LC)
Arousal/termination of REM can be intimated by activating NE and 5-HT cells. These cells are activated by circadian rhythm, fear, or intense emotion
Difficulty initiating or maintaining sleep
Often associated with mood disorder, pain, or other medical conditions
Abnormal transition between REM and NonREM and intrusive REM during the day. This is a heritable disorder. It is caused by a mutation in the orexin receptors in the lateral hypothalamus
Proper allocation of resources to relevant stimuli. Important stimuli receive a larger share of resources including conscious awareness and neuronal representation than do other stimuli.
Two major processes involved in directing attention
1. maintenance of neuronal activity related to a particular stimulus or group of stimuli
2. Filtering of stimuli that compete
happens on a millisecond level
used to assess attention. Participants are required to name the ink color of a printed color word
inability to maintain attention combined with hyperactivity or impulsivity
Most common treatment is amphetamine like drugs
Purpose of PET
to obtain quantitative information on ligand bind in vivo
Mechanism of PET
Inject a small amount of radio tracer with a well characterized binding potential. Then measure how much binding is present. This can show receptor density/localization or how much radio tracer is displaced by a synaptic event
using PET to determine a release
Look at basline levels of D2 binding. Then give amphetamine, saturating the terminals with excess dopamine, see how the receptor saturation changes. This gives a very accurate measure of dopamine release in humans.
If there is reduced TH in the brain, the pools of dopamine would go down. Amphetamine wouldn't fix this because the person doesn't have dopamine to start with, there will be less displacement of the radioligand in this instance.
Cocaine use, a PET study
in drug dependence, people will have less initially bound radioligand than healthy controls. Thus is due to receptor down regulation.
the integration of optics and genetics to control precisely defined events within specific cells of living tissue
It involves introduction of fast light-activated channels and enzymes that allow temporally precise manipulation of electricl and biochemical events while maintaining cell-type resolution through targeting mechanisms
• Channelrhodopsins (ChR2, CHr1, VChR1, SFOs) are used to excited neurons to produce excitation
• Halorhodopsin- (NpHR)enhanced halorrhodopsins have been employed to inhibit neurons.
Benefits of Optogenetics
Can be used in an awake, behaving animal
Allows you real time control of how many channels are open by how long you pulse the light
can select which cells to inhibit
this is the only real method of producing inhibition
Generally applies to behavioral processes such as attention, perception, working memory, goal-directed action, and problem solving
localized to the cerebral cortex
organization of the cortex is kinda fuzzy, more like a chain reaction of different areas
"It is cortex devoted to action of one kind or another, whether the action is skeletal movement, ocular movement, the expression of emotion, speech, or visceral control; it can even be the kind of internal, mental, action that we call logical reasoning. Frontal cortex is 'doer' cortex"
main purpose is to organize behavior in the temporal domain. Bridge between remembering an planning
induce dramatic personality changes with patients becoming impulsive and irritable. Exhibit reckless high-risk behavior, severely disordered attention and are easily distracted
damage can result in loss of motility, emotion, and attention. Such individuals have loss of spontaneity and are often apathetic or unable to concentrate
inability to formulate and carry out plans and sequence, which can extend to the representation and construction of language
Temporal cognitive function
attention, working memory, preparatory set, and response inhibition
looks toward the past to retrieve relevant info
planning actions for the future, priming of motor structures.
neurochemistry of cognition
all efferents and most afferents are glutamatergic
glutamate agonists mess you up!
many glutamate antagonists are drugs of abuse. This can also cause disinhibtion of some GABA interneurons
Dopmaine and cognition
necessary for working memory and problem solving abilities. Can be seen to spike during a working memory task in rodents
a state where an individual loses touch with reality. May involve hallucinations, delusions, illusions, or formal thought disorder
perceptions unconnected to external stimuli
sustained false beleifs
distorted perceptions of environmental stimuli
formal thought disorder
disruption in the logical flow of ideas.
affects 1% of the population
most common cause of chronic psychosis
biggest bed filler in hospitals
associated with PFC disfunction
activate a single gene and produces 1000000+ proteins- amplifications. This is also function specific because distinct receptors must be activated for them to be activated. Very unique to the brain
inhibits the uptake of monoamines, especially dopamine
increases the release of monoamines, especially dopamine
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