Brain And Behavior 2: Executive Circuits And Memory/emotion Flashcards
How is sensory input filtered/sharpened?
Through reciprocal connections
Ex: cortex -> thalamus and thalamus -> cortex
pathological states in these reciprocal connections can cause “false signals or inappropriate suppression of sensations”.
Function of the parietal association cortex
Sensory guidance of motor behavior and spatial awareness
Temporal association cortex function
Recognition of sensory stimuli and storage of semantic knowledge (facts)
Frontal association cortex function
Organizing behavior and working memory
Limbic association cortex function
Complex functions related to emotion and episodic memory
Attention vs impulsivity
Both are opposites, but controlled by the nucleus accumbens and ventral tegmental areas in the limbic system
- increased release of dopamine -> increased pleasure and attention to that action
- decreased or no release of dopamine -> no increased pleasure and hypersensitivity to impulsive stimuli
*because of this, dopamine stimulant medications are used for ADHD patients since they are now able to block out irrelevant stimuli easier and focus on one stimuli since the dopamine medication makes them feel “pleasure” to that one stimuli by increasing dopamine release in the nucleus accumbens *
Types of declarative/explicit long term memory
Episodic memory
- events/ scenes
Semantic memory
- facts/semantics
both take place in hippocampus and associated cortical areas
Types of non declarative/implicit memory
Skills
Habits
Emotional memories
Conditioned reflexes
all are controlled by the cerebellum, basal ganglia, amygdala and associated cortical areas
Working memory
Describes what is being actively considered at the time or within a few seconds
Involves the hippocampus and prefrontal cortex
Modulated by dopamine and norepinephrine neurotransmitters
- dopamine antagonists result in decreased/delayed working memory (haloperidol)
- dopamine and NE agonists enhance working memory and improve attention
impaired working memory = ADHD and schizophrenia
ADHD pharmacological treatments
Dextroamphetamine or methylphenidate
- increase dopaminergic signaling via agonists of dopamine neurons
Transition of short-term -> long-term memory
Experiences enter the brain through senses and processed by respective cortexes
Processed information goes to the hippocampus and is assigned emotional importance via amygdala if possible
- more emotional response assigned = more permanent and/or easier to recall
Then is stored in the specific cortex again as long term memory
- this action is thought to occur during sleep (so getting good sleep = better long term memory)
Declarative memory
Thought to be physically contained in medial temporal and midline diencephalic structures and in the neocortex
Contains episodic and semantic memories
Nondeclarative memory
Skills and habits
Dependent on the neocortex and neostriatum
Cerebellum is highly important for nondeclarative memories associated with muscles specifically
Amygdala is highly important for emotional learning assigned to nondeclarative memories
Anterograde vs retrograde amnesias
Anterograde = can remember past but cant form new memories
- is believed to occur if the hippocampus or amygdala are lesioned
Retrograde = cant remember past memories but can make new memories
Feelings vs emotions
Emotion = set of physiological responses that occur more or less unconsciously when the brain encounters challenging situations
Feelings = conscious experience of these semantic and cognitive changes
How are emotional responses generated for external stimuli?
1) External stimuli are processed by their specific cortexes
2) the processed info (if emotionally salient) is then sent to the amygdala to attach emotional responses to the external stimuli
3) info is then sent out to the hypothalamus and brain stem to effector cells for actions to be tied to the external stimuli. Includes:
- pituitary and endocrine glands (increase cortisol if “stressed”)
- somatic motor nerves and skeletal muscles (freezes or flees)
- Autonomic nerves and smooth/cardiac muscles (increases or decreases HR/BP/BR)
note direct electrical stimuli to the hypothalamus induces “fight or flight responses subconciously
Aggression and serotonin levels
Indirectly proportional to each other.
Low serotonin metabolite levels (5-HIAA) are associated with increased aggressive behavior and greater suicidal ideologies, as well as increased odds of lethality in suicide attempts.
Acute tryptophan (precursor for serotonin) deficiencies = increased irritability and aggression
Theories surrounding the concept of feelings
Peripheral feedback theory
- feelings are generated as a sensory feedback in response to an emotional stimulation in the bodies actions.
Central theory
- feelings are generated directly by the hypothalamus after it has evaluated emotional qualities of an external stimulus.
Papez circuit
- same thing as central but details more of the actual circuit used to conduct this
neural correlates in response to feelings supports hypothesis that feelings are correlated with activity in brain regions that monitor the body’s overall state.
Hypothalamic-Pituitary- Adrenal axis (HPA)
Mediates the stress response in humans
- hypothalamus tells the pituitary to release ACTH into the circulation which then acts on adrenal glands to release cortisol into the blood stream which then mediates peripheral and CNS effects of “stress”
ACTH -> cortisol -> feelings of stressed out
patients with primary endocrine disorders (addisons, Cushings, hypo/hyperthyroid, etc) can present with psychiatric symptoms
Effects of cortisol on the amygdala and hippocampus
Amygdala = prolonged stimulation - prolonged stress response
- improper emotional connection with external stimuli
Hippocampus = impairs stimulation
- impairs memory formation
- decreases neurogenesis and increases atrophy of the hippocampus
- disrupted long-term potentiation of neuronal pathways
- cant form long term memories
- increases depressive ideologies
HPA axis in depression
Dexamethasone suppression test (DST)
HPA activity is increased in roughly 40-60% of all depressed patients
- increased cortisol levels are observes in almost all of these 40-60%
- also depressed individuals are associated with increased inflammation (feels fatigued and sick)
The laboratory test of use of dexamethasone to determine HPA axis activity and cortisol dysregulation can be used to help diagnosis depression
- normal patients = lower cortisol levels and suppression of the HPA axis
- depressed patients = no changes still dysregulated
- note that while DST is useful, it is limited since it often produces false positives as well as isnt specific to depression (others tests/ contains yield positive results for DST) *
Cortisol and the immune system
Inverse relationship.
Increased cortisol levels suppress innate immunity
Also increased cytokine signals are received by the CNS causing feelings of fatigue
Primary or secondary psychiatric disorders means what?
Primary = idiopathic or psychiatric cause
Secondary = organic cause due to endocrine hormone issues (hypothyroidism, cushings, Addisons, etc.)
Learning vs memory
Learning = new information acquired by the nervous system which can be observed in the individual through behavioral changes
Memory = encoding, storage and retrieval of learned informations
* directly contributes to personality, habits and disposition unconsciously*
Short term vs working memory
Working memory = what is being actively considered at the current time
- manipulates information to achieve an immediate goal
- (i.e: looking up a phone number and remembering it while actively dialing it)
- used for multitasking/calculations and reading
- there are no planning invitation or high level cognitive skills at work here (executive function)
Short-term memory = temporary, short term maintenance of information
- lasts a few minutes to days
- not quite long term
- often recalled for working memory
