Unit 3 Flashcards
(49 cards)
Learned helplessness paradigm
- Great model for PTSD
- One group of rats can control their shocks, the other cannot - perception of being able to escape stress is a KEY PART of experiment - learning they can’t escape
Learned helplessness effects
- less responsive to shock
- less struggling when placed in water
- less aggressive
- decrease in social dominance
- decrease in defensive behaviors
- ALL OF THE ABOVE ARE DECREASED FLIGHT/FIGHT*
- less eating and drinking
- decrease in sexual behavior
- analgesia - less sensitive to pain
- learning impairments
- inappropriate maternal behavior
ALL OF THE FOLLOWING ARE INCREASE IN FEAR AND ANXIETY
- less interaction with others
- increase in axniety
- increases in fear-learning
END F&A
- Increase in ulcers
- Some drugs of abuse are more rewarding
What is learned helplessness associated with?
Deficits in escape behavior, which in turn is associated with flight or fight responds
What is both necessary and sufficient for learned helplessness?
The activation of the dorsal raphe nucleus
How do you block learned helplessness?
By destroying the DRN
DRN hypothesis of learned helplessness
Uncontrollable shock “overactivates” serotonin neurons in the dorsal raphe nucleus.
This “overactivation” of serotonin neurons in the dorsal raphe nucleus makes these neurons more sensitive to subsequent stimulation, and may also change the way the brain responds to serotonin.
These changes produce the behavioral changes associated with learned helplessness.
Transituationality
Once you learn something in 1 context, if you go into a similar setting, you’ll STILL feel helpless
DRN sensitization is produced by…
Dorsal raphe nucleus sensitization in learned helplessness is produced by reduced function of 5-HT1A autoreceptors on serotonin (5-HT) neurons.
What is 5-HT1A?
An inhibitory autoreceptor.
Function as a classic example of negative feedback, a homeostatic mechanism.
Where is the DRN?
Midbrain, brain stem, far back
Where does input come from if not the DRN?
- Locus coeruleus, norepinephrine nucleus
- Habenula, glutamate
- Corticotropin releasing factor
- Opiods
What is the medial pre-frontal cortex?
Collection of smaller subregions, thought to be important for executive control, inhibits lower brain regions, emotion regulation.
Activates GABA
Depression pre-frontal cortex treatment
Stimulate medial prefrontal cortex w/electrodes, invasive.
Anxiety stats
25-40 million Americans
19.5% woman, 8% men
65% of people w anxiety become depressed, 95% of depressed have at least 1 anxiety symptom
Types of anxiety
- Panic disorder
- Phobia-related disorders
- Generalized anxiety disorder
- Trauma and stress related - PTSD
- OCD
Bed nucleus damage…
…interferes with some fear/anxiety like paradigms
What hormone is tied to the bed nucleus?
Corticotropin-releasing hormone
What does corticotropin releasing hormone do in startle activity?
Enhances
Waddell, BNST
the BNST selectively mediates responses to
Walker, BNST
the BNST mediates responding as the threatening stimulus becomes LONGER in duration (phasic to sustained)
Goode and Maren, BNST
the BNST is involved in organizing fear responses to stimuli that poorly predict when danger will occur, no mater the duration, modality, or complexity of those stimuli. Unpredictability to the time component.
Anxiety treatment options, drugs
- Benzodiazepines like valium
- Barbituates
- Alcohol
Allosteric modulators
compounds that bind to a different part of the receptors and make the neurotransmitter better or worse at activating the receptor - other site than GABA site. Other allosteric sites offer binding, so when sites become bound, effects of GABA can either get stronger or weaker.
Serotonin and anxiety
Decrease anxiety by increasing serotonin
