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76 Cards in this Set

  • Front
  • Back
Endocrine Glands
ductless glands that secrete hormones
Hormones
chemicals that are transported by blood with effect on distant target cells
Peptide hormones
binds to receptors on the surface of cells
(strands of amino acids)
Steroid Hormones
can cross the cell membrane and bind to receptors within the cell.
Many steroid hormones can directly activate gene expression
Emotions as response patterns
behavioral: muscular movements appropriate to situation
autonomic: facilitate behavior by providing quick mobilization of energy
hormonal: reinforce autonomic responses; only for long-lasting things (stress)
Neural control of emotional responses
each type of emotional response controlled by separate neural systems
integration of all these structure seems to be controlled by the amygdala
Central Nucleus of the amygdala
-what it is
-lesion
-stimulate
-learning
-drugs
what: control center of the brain for emotional responses
lesion: absence of fear in animals and lower levels of stress hormones
stimulate: physiological and behavioral signs of fear
learning: conditioned emotional responses do not occur if leisoned
drugs: central nucleus has lots of opiate and GABA receptors- opiates and BZDs block learning and expression of conditioned emotional responses
Orbitofrontal Cortex
critical for perception of social situations and assessing personal consequences of what is happening presently
translates judgments into appropriate feelings and behaviors
damage reduces people's inhibitions and concerns
become indifferent to consequences of their actions
pain doesn't bother them- show no emotional response
Frontal Lobe (in regards to removing it)
when removed in chimpanzees, violent emotional reactions were eliminated
Prefrontal Lobotomy
relief from emotional anguish
no intellectual side affects
became irresponsible and childish- unable to make/carry out plans
all emotional reactions were eliminated
"common sense" theory
(of emotions as feelings)
Frightening Situation --> Emotion (Fear) --> Response (Increased heart rate)
James-Lange theory
(of emotions as feelings)
Frightening Situation --> Response --> Emotion
patterns of emotional responses and their outward expression give rise to feelings
Evidence:
-people with damage to the autonomic system show less intense feelings
-stimulated responses (make people make faces) alter activity of the autonomic nervous system
Stressor
a stimulus or situation that produces a stress response
Stress Response
a physiological or behavioral reaction caused by perception of aversive/threatening stimuli or situations
Epinephrine
adrenalin
cause energy to become available for muscles
adrenal gland hormone
made in the brain and can be used as neurotransmitter
norepinephrine
adrenal gland hormone
increase blood flow by making the heart pump harder
stressors can cause increase in it from brainstem neurons
release of it is controlled by the central nucleus of the amygdala
Glucocorticoids
break down proteins and convert them to glucose for energy, increase blood flow, and stimulate behavioral responsiveness
secretion is controlled by neurons in the paraventricular nucleus (PVN) of the hypothalamus
Consequences of long term exposure to glucocorticoids
increased blood pressure
inhibited growth
infertility
suppression of the immune system
brain damage (can cause cell death in hippocampus which can lead to memory loss)
Organizing Effects
(sexual development)
determine whether the brain and body will develop as a male or female during a sensitive stage of development
Activating Effects
(sexual development)
occur when a hormone triggers a particular response
Mullerian System
leads to female tract
Wolffian System
leads to male tract
Male Development
possess SRY gene on Y chromosome
SRY gene produces H-Y antigen which causes formation of testes
testes make Mullerian system inhibiting substance (defeminizes) and androgens (masculinizes)
Female Development
absence of SRY gene leads to development of ovaries
without androgens, wolffian system withers away
estrogen comes after reproductive tract has formed
Turner's Syndrome
XO
no ovaries or testes but looks female
Androgen Insensitivity Hormone
XY
but since testosterone is an androgen, look female
female reproductive cycle
in mammals, called estrous cycle
in primates, called menstrual cycle
menstrual cycle dependent on neuroendocrine control
arcuate nucleus
in the hypothalamus
releases luteinizing hormone releasing hormone (LHRH) for puberty
Gonadotrophic Hormones
Follice-Stimulating Hormone (FSH) and luteinizing hormone (LH)
released by anterior pituitary glands
cause the maturation of gametes (ova and sperm)
Menstrual Cycle
(how it works)
estradiol has positive feedback on LH and negative feedback on FSH
LH surge causes ovulation
at mid-cycle, estradiol has positive feedback on itself and progesterone
Brain differences in sexual orientation
Suprachiasmatic nucleus (SCN) is larger in homosexual men than in heterosexual men/women
Anterior commissure is larger in homosexual men/heterosexual women than in heterosexual men
3rd interstitial nucleus of the hypothalamus (INAH-3) is larger in heterosexual men than homosexual men/heterosexual women
Genetics in sexual orientation
twin studies show that there is a correlation of the same sexual orientation with siblings--high for identical/fraternal twins
What does EEG Measure?
brain waves
firing rate of neurons
variance in voltage over time
Slow potential activity of EEG comes from...
dendrites and soma
in layers 1-3 of the cortex
Lucid Dreaming
awareness of dreaming from within the dream
Sleep is...
active
complex
essential
highly regulated
involves different neuronal groups
composed of REM sleep and NREM sleep
Sleep- learning and memory
REM sleep and Stage 3/4 are vital to consolidation of new information
Sleep Apnea
excessive daytime sleeping
morbid obesity
snoring
witnessed apneas
morning headache & dry mouth
narrowed airway
Periodic Leg Movements
excessive daytime sleeping
restless legs syndrome
witnessed twitching
complaint of insomnia
complaint of shallow sleep
Narcolepsy
excessive daytime sleepiness
hallucinations
sleep attacks
cataplexy
sleep paralysis
complaint of insomnia
Phase Delay Syndrome
complaint of sleep onset insomnia
discrepant sleep schedules
normal sleep when schedule is ab libitum
age
Insomnia
increased sleep latency
early morning awakenings
decreased total sleep
non-restorative sleep
fatigue
concentration problems
memory problems
performance decrements
How do drugs get into the brain?
Most of them are lipid soluble
Important in Addiction
nucleus accumbens, VTA, substantia nigra
Cocaine
blocks the reuptake of Dopamine
effects: pleasure, enhance attention
Amphetamine
increases release of dopamine by inverting presynaptic pumps
Chronic use can induce psychosis with symptoms similar to schizophrenia such as paranoia, visual and auditory hallucinations.
Ecstasy
MDMA
stimulates the release of dopamine at low dose and serotonin at higher dose
Nicotine
agaonist of the achetyl-choline nicotinic receptors. Increases dopamine release in the nucleus accumbens
Caffeine
blocks adenosine (adenosine inhibits dopamine and acetylcholine release)
constricts blood vessels in the brain
Alcohol
inhibits flow of sodium across the membrane
decreases serotonin activity
facilitates GABA responses
blocks glutamate receptors
increases dopamine activity
Marijuana
binds cannabinoid receptors
leads to euphoria, lower IQ, reduced short term memory, paranoia
prevents nausea through blocking of serotonin type 3 synapse
Salvia
hallucinogenic drug
binds the kappa opioid receptor
short term effects
Effects: hallucinations, dissociation from self, as if traveling through time
Ketamine
blocks NMDA receptor
out of body experience, hallucinogenic
LSD
agonist of serotonin type 2 receptors
leads to hallucinations
Opiates
derived from the opium poppy
purified forms: heroin, morphin
binds opioid receptors in the brain
results in increased dopamine release
Rationalization
reinforces behavior
plays a factor in addiction
Hypovolemia
reduction in blood (extracellular) volume
detected by baroreceptor and blood flow receptors--both cause kidneys to release Renin
renin causes synthesis of angiotensin II in the blood
Angiotensin causes conservation of water and increased thirst
Paraventricular Nucleus (PVN)
area of hypothalamus in which activity tends to limit meal size and damage leads to excessively large meals
Angiotensin
responsible for conserving water and increasing thirst (retain water)
Effects of Angiotensin
secretion of aldosterone by adrenal glands (retention of sodium in kidneys and salt appetite)
secretion of vasopressin for water retention
contraction of blood vessels to increase blood pressure
stimulation of receptors in SFO in brain to cause drinking
Glycogen
stored in the liver
gets converted into glucose
Insulin
promotes storage of energy
promotes storage of glucose, fat, and protein in cells
lowers levels of fuel molecules in the blood
Glucagon
promotes use of energy
stimulates the liver to convert stored glycogen to glucose
more glucose in the blood allows use by brain and body
Set-point theory (of hunger regulation)
bodies have a specific energy level
hunger signals deficit in energy
this theory in dependent on negative feedback
Positive-Incentive Theory
ingestive behaviors are motivated by anticipated pleasurable effects
many factors influence the incentive for eating
Leptin
gene responsible for obesity (mutation)
when we eat, leptin is released into the blood from fat cells
leptin enters the hypothalamus and causes release of peptides to inhibit feeding
mutation obese has a defective leptin gene (doesn't produce leptin) which disrupts normal weight control
Neural mechanisms of hunger/satiety
arcuate nucleus of the hypothalamus has neurons that cause hunger and that cause satiety
these neurons release melanocortin to stimulate the paraventricular nucleus (PVN)
neurons that cause hunger release neuropeptide Y that inhibits the satiety neurons in the arcuate nucleus and PVN
Ventromedial Nucleus
helps us stop eating
lesions cause increased insulin levels, production of body fat and decreased fat breakdown
eating continue to provide energy for immediate needs
hyperphagia
bilateral lesions to ventromedial nucleus or paraventricular nucleus cause excessive eating
Paraventricular Nucleus (PVN)
helps us stop eating
inhibits lateral hypothalamus (which stimulates eating)
Lateral Hypothalamus
stimulates hunger
aphagia
bilateral lesions to lateral hypothalamus
complete cessation of feeding
lesions cause general decreases in responsiveness and movement (many not be specific to eating)
Factors influencing how much we eat
calories/volume can influence intake (if more calories, you consume less)
"Cafeteria" Diet- variety of food sources increased intake
sensory-specific satiety encourages consumption of a varied diet
Case of the Frozen Addict
rats not always a good substitute for human testing--need primates
making MPPP- designer drug
side product on MPTP- not directly harmful
MPTP mixes with MAO enzyme to produce MPP+
MPP+ kills dopaminergic neurons in the substantia nigra which is really harmful
Stages of sleep
Stage 1: beginning of sleep. irregular, jagged, low-voltage waves.
Stage 2: sleep spindles (short burst of 12-14 Hz waves) and K complexes (sharp high amplitude wave)
Stage 3/4: Slow wave sleep. heart rate/breathing rate decrease. slow, large amplitude waves
REM Sleep
EEG looks like wakefulness
dreams (but not all dreams)
important to consolidation of memory
more common towards the end of the night