12- Emotional Behaviours Flashcards
Panic Attack
rapid breathing marked by extreme symp NS arousal that makes someone worry they are suffocating
Mobius syndrome
unable to move facial muscles to smile
- still experience happiness
- hard to make friends
(smiling = slight increase happiness, frowning= decrease)
Emotional brain areas
Limbic System: forebrain areas surrounding thalamus
** frontal and temporal cortex
-disgust = insular cortex (primary taste cortex)
Behavioural Activation syst (BAS) - L frontal and temporal
-low to moderate autonomic arousal & approach (happiness/anger)
Behavioural Inhibition syst (BIS)- increase attention and arousal, decrease action (fear/disgust)
Prefrontal damage
impulsive decision making/unemotional
-cant decide b/c doesn’t know that one thing will feel bad, another good
Dilemmas
PRefrontal cortex, cingulate gyrus, amygdala
when we identify wt other person and feel their pain, we don’t want to harm them
(not logical)
Factors in Attack
- increase activity in corticomedial area of amygdala
- exposure to lead
- smoking during pregnancy, especially combined with complicated delivery
- genetics and troubled early environment
- low MAOlittleA monoamine oxidase activity and mistreatment in childhood = antisocial
Testosterone in attack
- males competing for mates ** young adult
- less acurate at identifying angry face
- increase amygdala response to angry face
Results of low serotonin
Rats: low serotonin turnover, increased aggression (most fighting)
Monkeys: female and male, low 5-HIAA (hydroxyindoleacetic acid- main metabolite for serotonin in CSF), fight more, die young
Humans: more violent crime
diet to increase serotonin = amino acid tryptophan, decrease other lg amino acids like phenylalanine (aspartame and maize)
Genetics: less active form of gene that controls tryptophan hydroxylase (converts tryptophan to serotonin) = increase aggrssion and violent suicide
serotonin released during aggressive behaviour (*low levels to start = abrupt change)
Amygdala
Integrates environmental and genetic influences to regulate anxiety
- cells in basolateral and central nuclei of Amygdala get info from pain fibers, vision, and hearing
- Output from amygdala to hypothalamus controls Autonomic Fear REsponses (increase BP)
- Damage impairs learning of new fear responses
- Any emotion triggers increase amygdala response
- responds to facial expressions of emotions especially when less obvious (cortico blindness and guessing experession)
Startle Reflex
response to loud noise
-midbrain (Pons)
Fast- auditory info to cochlear nucleus in medulla, to area in Pons, to tensing of muscles especially the neck
*more intense if already tense (PTSD)
What area of the brain is responsible for Approach/avoidance
prefrontal cortex
Toxoplasma gondii
Protozoan parasite
-reproduces in cates, exit eggs in feces, affects ground animals like rats and damages amygdala (animal behaves fearless and appraoches cat- so cat eats and parasite reproduces
Kluver-Bucy Syndrome in monkeys
Tame and placid
Alters social behaviour (shy and fearful or friendly and fearless)
pick up matches
Urbach-Wiethe Disease
skin lesions and accumulation of Calcium in Amygdala until it deteriorates
=impaired emotional processing if cues are subtle or ambiguous (less focused on emotional part of stories or images)
-look at nose/mouth to judge emotion rather than eyes
(fear shown in eyes, happiness in mouth)
Amygdala arousal
-Amygdala arousal depends on serotonin reuptake in the amygdala
CCK (Cholecystokinin) - one of amygdala’s main excitatory neuromodulators
= increase anxiety
GABA = decrease anxiety
Drugs that decrease anxiety
By blocking CCK or increasing GABA
Benzodiazepines: (Valium) diazepam, chlordiasepoxide, alprasolam
- binds to GABA receptor in 3/4 units surrounding chloride channel
- twists receptor so GABA binds more easily
- suppress startle increasing influences
- sleepiness, decrease memory, not for epileptic convulsions
GABA (A) Receptor
chloride channel, cite that binds GABA and modify sensitivity of GABA site
Diazepam-Binding Inhibitor
DBI
-chemical protein produced by brain, binds to same site and blocks effects of Benzodiazepines
Endozepines
Proteins released by glia that have opposite effect of bensodiazepines
-gene controlling (=anxiety disorders)
Alcohol
Alcohol
-promotes flow of chloride ions by binding strongly at special site found only on certain GABAlittleA receptors
-ROl5-4513 - drug
blocks effects of alcohol (motor coordination, decreased anxiety)
Microdyalisis
fluid-filled tube injected, for discovering which NTs are released
Behavioural medicine
emphasizes effects of diet/smoking/exercise/stress/ on health
Stress
nonspecific response of the body to any demand made upon it
events that are interpreted as threatening to an individual and elicit physio and behavioural responses
Activates SYmpathetic NS
HPA axis (hypothalamus, pituitary gland, adrenal cortex) - dominant for long term stress
-activation of hypothalamus induces anterior pituitary to secrete ACTH
ACTH (adrenocorticotropic hormone) - stimulates human adrenal cortex to secrete cortisol
Cortisol - prolonged alertness & increase memory, body fight infections/heal wounds
(3rd stage = exhaustion [decrease] -loss of immune syst energy)
= increase metabolic activity, increase blood sugar and nutrient levels
Immune System
Cells that protect the body against viruses/bacteria, intruders
-Autoimmune disease: body attacks normal cells (rheumatoid arthritis)
Leukocytes- WBC- B cells (mature in bone marrow, secrete antibodies) T cells (mature in thymus gland, attack intruders directly, help T and B cells multiply), natural killer cells (attack tumor cells/cells infected wt virus, and All intruders)
Cytokines - small proteins produced by leukocytes in response to infection (combat infection, communicate wt brain to elicit behav- fever, sleepiness, decrease energy/apetite/sex drive)
Antibodies- y-shaped proteins that attach to particular antigens
Antigens- surface proteins (B cells recognize ‘self’ antigens and attack foreign ones, remembers intruder and attacks more quickly after)
Psychoneuroimmunology
study of the ways experience alters the immune syst and how immune syst influences central NS
Stress
Stress (increase production of natural killers and secretion of cytokines)
-increase metabolic activity in hippocampus (cells more vulnerable = toxins more likely to damage and decrease adaptability of hippocampal neurons)
Long stress = increase risk of illness
-social support, breathing, meditation
Depression = sickness symptoms (increase cytokines)
Pure autonomic failure
output from autonomic NS to body fails almost completely
- no rxn to stress physiologically
- report same emotional responses with less feeling compared to before
(*James-Lange theory of emotion = less likely)