exam 4

QUIZLET IMPORT — PSYC 2200 DECK 2: Reading 12.2 + Past-Exam Patterns + Who Did What

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Copy everything BELOW the dashed line.

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READING 12.2 — Reconsolidation

When an established memory is RETRIEVED it becomes temporarily unstable (postretrieval lability) and can be restructured before it is stored again. This means most long-term memories are maintained by a DYNAMIC process rather than being stored permanently — retrieval is an opportunity to update, but it also makes it virtually impossible to keep an episodic memory in the exact form it was first consolidated. Memories not retrieved for a long time may decay or drift from the original. Past exam wording: 'Reconsolidation occurs after a long-term memory has been RECALLED.'

READING 12.2 — Jennifer Thompson-Cannino and Ronald Cotton

The eyewitness case that demonstrates reconsolidation in humans. Thompson-Cannino deliberately studied her rapist's face during the 1984 attack, helped build a composite sketch, and confidently picked Ronald Cotton from a photo lineup and then a physical lineup; when told her two choices matched, she was 100% confident. Cotton was convicted twice and served 11 years before DNA evidence matched Bobby Poole, the inmate Cotton had suspected. Neurobiological reading: reactivating her memory network for the face made it vulnerable, and as she studied lineup photos that did not contain the true perpetrator her circuits incorporated the closest-looking face, reconsolidating the memory around the wrong man. She and Cotton are now friends and co-wrote 'Picking Cotton.'

READING 12.2 — How researchers study reconsolidation in animals

Train the animal with a simple, unambiguous form of learning — classical conditioning — so an acquired memory is clearly demonstrated. Present the unconditioned stimulus to prompt RETRIEVAL of that memory. At that moment, administer a drug that blocks PROTEIN SYNTHESIS, since new protein is needed for memory-based synaptic plasticity. Giving a protein synthesis inhibitor AFTER a previously consolidated memory has been retrieved disrupts the original version of the memory — evidence that retrieval reopens the memory to modification.

READING 12.2 — Misinformation and implanted memories

Human evidence for reconsolidation: college students can easily be prompted into believing that a fabricated childhood event (the classic example is being lost in a mall), introduced by experimenters working with the students' parents, actually happened. Misinformation is incorporated into earlier memories with very little effort. Loftus is the associated name.

READING 12.2 — Spontaneous confabulation ('honest lying')

Seen in patients with ORBITOFRONTAL CORTEX damage: they effortlessly make up stories to fill gaps in their memories. The false memories usually contain bits of TRUE information, so the patient fully believes the fabricated segments are honest reflections of reality — hence 'honest lying.' The analogy given is the visual system filling in the blind spot with a probable image. Early accounts came from chronic alcoholic patients with KORSAKOFF'S SYNDROME (an atypical loss of short-term memory; caused by THIAMINE deficiency), whose autopsied brains show lesions in the DORSOMEDIAL THALAMIC NUCLEUS — so that area is also cautiously implicated in confabulation.

READING 12.2 — Stress and forgetting: the hot-car cases and David Diamond

Diamond (Univ. of South Florida) argued that cases where a parent forgets a baby in a hot car have less to do with parenting quality and more to do with the stressful circumstances of that particular day. His line: memory is a machine and it is not flawless; the conscious mind prioritizes by importance but at the cellular level memory does not — if you can forget your phone you can potentially forget your child. Mechanism: under stress, BASAL GANGLIA procedural memory gets you from A to B just fine on autopilot, while the HIPPOCAMPUS and PREFRONTAL CORTEX fail to register what was encountered along the way. In the case described, a pile-up of routine changes (different car, car seat not visible in the mirror, sleepless night, unusually quiet baby, phone calls) created a 'perfect stress storm.' About 40% of these cases result in no charge; 60% result in a felony charge.

READING 12.2 — Diamond's cat-exposure stress model (Fig 12.26)

Rats were given unavoidable exposure to a cat, a natural predator. Compared with rats simply placed in an unfamiliar cage with no cat and with control rats in their home cage, the STRESSED rats showed LESS evidence of a low-threshold version of LTP and made MORE ERRORS on a hippocampus-dependent spatial task (water maze / radial arm maze). A related Diamond study found predator stress lowered NEURAL CELL ADHESION MOLECULES, a glycoprotein critical for neuronal development and synaptic plasticity, alongside compromised spatial memory. Important qualifier: the impairment is NOT permanent — when rats are removed from the stressful environment and housed in a familiar one, memory recovers.

READING 12.2 — Stress ENHANCING memory, and PTSD

In life-and-death situations stress fixes explicit memories in the network — adaptive, since it pays to remember threats (avoid the dog that bit you). The AMYGDALA interacts with stress hormones and stress-related neurochemicals to facilitate consolidation of threatening memories. When the memory is strong enough it can produce PTSD: intrusive memories of the trauma plus avoidance of triggers, leaving chronic hyperarousal. Not everyone traumatized develops it, so biological predisposition interacts with the event. Marker: heightened autonomic response, e.g. heart rate reactivity to a related stimulus (veterans reacting to noises like gunfire).

READING 12.2 — PTSD brain findings (Fig 12.27)

HYPERactivation of the AMYGDALA (conditioned fear), the INSULA (body awareness), and the ANTERIOR CINGULATE CORTEX (error detection and fear learning). DIMINISHED activity in the VENTROMEDIAL PREFRONTAL CORTEX. The HIPPOCAMPUS — which interprets contexts as safe or dangerous — is altered but the direction is unpredictable, with both hypo- and hyperreactivity observed. Reduced volumes of both the hippocampus and vmPFC relative to controls. Counterintuitive point worth remembering: PTSD is NOT reliably associated with high cortisol — in some cases a cortisol DEFICIT has been implicated.

READING 12.2 — Mitra et al.: persistent stress memories (Fig 12.28)

Rats exposed to acute stress (two hours of immobilization) showed increased spine density on AMYGDALA neurons and persistent avoidance of the open arm in the ELEVATED PLUS MAZE — more anxiety. Key detail: the effects BUILT OVER TIME. No differences one day after the stress, but clear effects 10 days later, suggesting the rats had difficulty shifting from a stress mode back to a safety mode after the stressor was removed.

READING 12.2 — Moderate stress and McGaugh's norepinephrine work

NOREPINEPHRINE, released during stress, contributes to the consolidation of emotionally arousing memories. James McGaugh (UC Irvine) found that injecting rats with EPINEPHRINE ANTAGONISTS IMPAIRS memory in the Morris water maze, while infusing BETA-ADRENERGIC RECEPTOR AGONISTS ENHANCES consolidation. Conclusion: moderately emotionally aroused rats outperform relaxed ones. So severe stress impairs memory but moderate arousal facilitates it — a delicate balance between the stress and memory systems.

READING 12.2 — Highly superior autobiographical memory (HSAM)

Jill Price wrote to James McGaugh describing an uncontrollable, exhausting ability to recall any date since 1974 — what day it fell on, what she was doing, what happened. McGaugh and Larry Cahill tested her and confirmed it. Crucially it is ONLY autobiographical: given long lists of words she showed NO superior ability and became frustrated. Contrast with Luria's case 'S,' a professional MNEMONIST who used memory aids for lists but had ordinary autobiographical memory. Ten more HSAM cases were identified; their memories became enhanced around age 10, they did not score above average on standard lab memory tests, and they showed obsessive-compulsive tendencies expressed as meticulously organized collections (the actress Marilu Henner and her shoes).

READING 12.2 — HSAM brain findings

Enlarged CAUDATE and PUTAMEN — the striatal areas associated with COMPULSIVE disorders, which supports the link between HSAM and compulsive behavior. Certain areas of WHITE MATTER connecting brain regions were also larger. More directly memory-related, the INSULA and PARAHIPPOCAMPAL CORTEX were larger than in age-matched non-HSAM participants (LePort et al., 2012).

READING 12.2 — Method of Loci

An ancient Greek memory-training technique: use a familiar location such as your house and mentally attach items from a memory list to specific sites in it, then recall the list by mentally walking through the location. The reading's framing: before anything is committed to memory the brain must properly attend to it, which is why attention comes next.

READING 12.2 CONTEXT MATTERS — Jovanovic et al. (2009), safety signals and PTSD

Question: does impaired fear INHIBITION contribute to PTSD? Method — conditional discrimination. UCS = an annoying air blast to the larynx; response measured as a fast eye-blink startle (like the rabbit work). A loud noise probe served as a second UCS for baseline. Conditioned stimuli were colored lights: A green, B purple, C orange, X blue. Training: A+X was followed by the air blast six times; B+X was never followed by it, so B becomes a SAFETY SIGNAL. Groups: 28 healthy males, 27 with PTSD, split into high-symptom and low-symptom. RESULT: everyone startled more to A+X (the threat cue); controls and LOW-symptom PTSD participants SUPPRESSED startle when the safety signal B was present, but HIGH-symptom PTSD participants could not discriminate safety from threat. Conclusion: being able to distinguish safe from threatening environments builds resilience — but it is not sufficient, since the low-symptom group could inhibit and still had symptoms. Possible future BEHAVIORAL marker (not a biomarker) for PTSD vulnerability.

PAST EXAM — Alpha-fetoprotein: what happens without it?

Alpha-fetoprotein binds circulating estrogen in developing FEMALES and keeps it out of the brain. It is found in HIGHER levels in young FEMALES. If a female rat fetus developed with NO alpha-fetoprotein, her hypothalamus would develop in a PARTLY MASCULINIZED manner, because circulating estrogen would reach the brain. This has appeared on nearly every past Exam 4.

PAST EXAM — Aromatization

The process that converts TESTOSTERONE into ESTRADIOL, carried out by the enzyme aromatase. It is why estrogen is the hormone that actually masculinizes the developing brain.

PAST EXAM — Estrogen given to a newborn female rat

Causes her to exhibit MALE sexual/social preferences in adulthood — she is behaviorally masculinized. (Answer choice on multiple past exams.) Related item: prenatal exposure to TESTOSTERONE and to DES both masculinize developing girls, so the correct answer on Spring 2018 was 'two of these.'

PAST EXAM — Who develops as intersex?

A genetic FEMALE exposed to MORE TESTOSTERONE than normal during early development. (A genetic male exposed to extra estradiol does not, because the male brain is already being masculinized via aromatized estrogen; a genetic male with extra testosterone just develops as male.)

PAST EXAM — SRY, Mullerian and Wolffian ducts

The SRY GENE causes the primitive gonads to develop into masculine structures. MULLERIAN ducts are present in ALL EMBRYOS early in development, not just females. Normal FEMALE development proceeds with MAINTENANCE OF THE MULLERIAN DUCTS (not activation of SRY, not testes, not Wolffian maintenance). Elaboration and maturation of the Mullerian ducts leads to female internal reproductive anatomy.

PAST EXAM — Gametes: which sex produces them all early?

FEMALES. Female mammals produce all of their gametes BEFORE BIRTH. Sperm production begins during PUBERTY and continues; egg production begins during GESTATION. This exact contrast has appeared on four different past exams.

PAST EXAM — Congenital adrenal hyperplasia: who is most affected?

NEWBORN FEMALES — CAH has the greatest effect on the sexual appearance of newborn females, because excess adrenal androgens masculinize external anatomy prenatally.

PAST EXAM — Androgen insensitivity: what is the person genetically?

Genetically MALE, but develops looking more like a female. The way they are most like a normal male is GENETICALLY — not in appearance, gender identity, or rearing.

PAST EXAM — Steroid hormones are built from what?

CHOLESTEROL. Not amines, not peptides, not amino acids.

PAST EXAM — Where does each hormone come from?

LUTEINIZING HORMONE is released by the ANTERIOR PITUITARY. PROGESTERONE is secreted by the CORPUS LUTEUM (so on a list of hypothalamus/adrenal/uterus/corpus callosum the answer is 'none of these'). CHORIONIC GONADOTROPIN is secreted by the UTERUS and acts to MAINTAIN THE CORPUS LUTEUM. The stimulus that increases FSH production is GnRH from the hypothalamus. The event just BEFORE ovulation is an INCREASE IN LH.

PAST EXAM — What causes ovulation in an induced ovulator?

ODORS. (Not photoperiod, not day-night cycle, not diet, not social density — those are the SPONTANEOUS ovulator cues.) This has been asked twice with the same distractors.

PAST EXAM — LeVay's size difference was in a nucleus in what region?

The HYPOTHALAMUS — INAH 3, larger in heterosexual than homosexual men.

PAST EXAM — Twin/sibling data on sexual orientation: the safe conclusion

Sexual orientation is determined by BOTH GENES AND OTHER FACTORS. Never pick 'completely determined by genes,' 'no role for genes,' or a sex-specific version. Related: the textbook says most homosexual men have testosterone levels WITHIN THE SAME RANGE as heterosexual men, and sexual orientation has been linked to prenatal stress, the mother's immune system, and genetics — but NOT to adult hormone levels.

PAST EXAM — Sex differences vs. gender differences

Sex differences are to ANATOMY as gender differences are to BEHAVIORS.

PAST EXAM — Papez circuit: which structure is NOT part of it?

The original limbic loop is CINGULATE CORTEX → HIPPOCAMPUS → HYPOTHALAMUS/MAMMILLARY BODIES → THALAMUS → back to cortex. Structures that have been the correct 'not part of it' answer: PREFRONTAL CORTEX and the INSULA. Know the four members so you can spot the intruder.

PAST EXAM — James-Lange, one-line version

An emotion is an INTERPRETATION OF THE BODILY RESPONSE to a stimulus — arousal and action lead to the feeling. Emotional intensity is a function of physiological responses. Findings from PURE AUTONOMIC FAILURE suggest autonomic output is IMPORTANT for experiencing emotion, which SUPPORTS James-Lange.

PAST EXAM — Cannon-Bard, one-line version, and why it is top-down

A stimulus evokes BOTH an emotion and a response, simultaneously. It counts as a TOP-DOWN theory because it EMPHASIZES THE CORTEX (and thalamus) in managing emotional responses rather than the periphery.

PAST EXAM — The two-factor theory of emotion

Developed by SCHACHTER-SINGER. The two factors are PHYSIOLOGICAL RESPONSES and SITUATIONAL CONTEXT — you feel arousal and then label it using the context. Not on your lecture list but it is on the past exams and in the text.

PAST EXAM — Somatic marker hypothesis

Damasio's idea, and the textbook's framing of the vmPFC: bodily/visceral signals GUIDE GUT FEELINGS and therefore decision-making. The cortical area that generates gut feelings is the VENTROMEDIAL PREFRONTAL CORTEX. On the Iowa Gambling Task, a person with vmPFC lesions will choose REPEATEDLY FROM THE RISKY DECKS, ignoring outcomes, and incur large losses.

PAST EXAM — Insula: anterior vs. posterior, in exam wording

The FIRST place in the cerebral cortex to get information about VISCERAL sensations is the POSTERIOR INSULA — basic visceral sensations are associated with the posterior insula. The ANTERIOR INSULA BINDS TOGETHER basic visceral sensations into COMPLEX sensations. Both phrasings have appeared verbatim.

PAST EXAM — Limbic motor cortex

Lies within the CINGULATE CORTEX. Asked twice with the same distractors (vmPFC, entorhinal cortex, anterior insula).

PAST EXAM — Reappraisal, textbook definition

The CHANGING OF EMOTIONAL REACTIONS BASED ON CONTEXT. Not 'deciding solely from visceral signals,' not classical conditioning.

PAST EXAM — Amygdala: inputs, prescreening, and the two nuclei

The amygdala PRE-SCANS our sensory input for potential problems. It receives input from the outside world via the THALAMUS AND CORTEX. It uses the BASOLATERAL NUCLEUS to gather information and prioritize behavioral responses — the basolateral amygdala learns and tracks THE SIGNIFICANCE OF STIMULI IN THE OUTSIDE WORLD. LeDoux used the conditioned emotional response to localize emotional learning to the AMYGDALA. People with amygdala damage most likely have DIFFICULTY KNOWING WHO TO TRUST.

PAST EXAM — Which lesion does NOT reduce aggressive displays between male rats?

The ORBITOFRONTAL CORTEX. Lesions of the lateral septum, the bed nucleus of the stria terminalis, and the medial amygdala DO reduce aggressive displays.

PAST EXAM — The court case where hormone levels were argued to influence aggression

It was based on PREMENSTRUAL SYNDROME.

PAST EXAM — Moniz, Freeman, and the leucotome

Names associated with LOBOTOMIES. A leucotome is the instrument. Penfield attempted to cure EPILEPSY by stimulating parts of the cerebral cortex and removing small pieces.

PAST EXAM — Objective measures of emotion

A scientist wanting an OBJECTIVE measure would use MEASURES OF AUTONOMIC NERVOUS SYSTEM REACTIONS — not self-report and not observer ratings. Universal recognition of emotions across humans points to emotions HAVING A BIOLOGICAL BASIS.

PAST EXAM — Anxiolytics

Relieve anxiety and agitation and affect levels of GABA. (Distinguish from SSRIs, serotonin autoreceptors, and reboxetine, which is an NRI.)

PAST EXAM — Mass action vs. equipotentiality, in exam wording

MASS ACTION: learning deficits are a FUNCTION OF THE AMOUNT of brain tissue removed — 'the more cortex the better.' EQUIPOTENTIALITY: ALL PARTS OF THE CORTEX CONTRIBUTE EQUALLY to complex behaviors such as learning; for complex function all brain regions are equal. Lashley searched the CEREBRAL CORTEX for memory traces. Maze learning is described by the rules of SKINNERIAN conditioning.

PAST EXAM — Thompson's learning site, and the red nucleus dissociation

Thompson found the site of classical conditioning with an air puff and a tone in a sub-region of the CEREBELLUM (the lateral interpositus nucleus). The RED NUCLEUS is necessary for PERFORMING a conditioned response — NOT for learning it. That distinction is the whole point of the cryoprobe experiments and it has been a multiple-choice answer.

PAST EXAM — Pavlov in exam wording

In Pavlovian conditioning an animal learns to associate a STIMULUS with a STIMULUS. During classical conditioning, a CS is associated with a UCS. In Pavlov's experiment the BELL is the CONDITIONED STIMULUS and the MEAT is the UNCONDITIONED STIMULUS.

PAST EXAM — Thorndike, Skinner, contingency, and operants

The LAW OF EFFECT was proposed by THORNDIKE, and the name Thorndike is most closely related to SKINNER. CONTINGENCY is most closely associated with SKINNER. Skinner postulated that animals continually emit random behaviors known as OPERANTS. Operant conditioning states that a random behavior is more likely to increase when it LEADS TO REWARD.

PAST EXAM — Non-associative learning

HABITUATION and SENSITIZATION. (Episodic, semantic, declarative, and list learning are all associative/declarative and are the standard distractors.) Habituation and sensitization differ depending on whether the RESPONSE GROWS WEAKER OR STRONGER. Sensitization is becoming OVER-responsive to a mild stimulus after receiving an intense one.

PAST EXAM — Aplysia: the mechanisms in exam wording

HABITUATION: synapses decrease activity by ALTERING QUANTAL RELEASE. SENSITIZATION: presynaptic stimulation with SEROTONIN causes a change in POTASSIUM CHANNELS. Why Aplysia is useful: it can YIELD CANDIDATE MECHANISMS for learning and memory (not because its nervous system resembles a primate's, and not because it has a long memory span).

PAST EXAM — Hebb in exam wording

A HEBBIAN SYNAPSE increases in effectiveness because of SIMULTANEOUS ACTIVITY in the presynaptic and postsynaptic neurons. The HEBBIAN rule states that if a presynaptic cell consistently participates in driving a postsynaptic cell, the connections between them are STRENGTHENED. Hebbian systems display ASSOCIATIVITY AND SPECIFICITY — and the trio SPECIFICITY, COOPERATIVITY, AND ASSOCIATIVITY is a feature of LTP.

PAST EXAM — NMDA receptors in exam wording

The neurotransmitter acting as a LIGAND at NMDA receptors is GLUTAMATE. Under most conditions NMDA receptors do NOT respond to their neurotransmitter because MAGNESIUM IONS BLOCK the passage of calcium through the channel. LTP works through the detection of CONVERGENT information by NMDA RECEPTORS. AMPA is most closely related to NMDA. LTP is produced by A BURST OF MANY STIMULI IN A FEW SECONDS.

PAST EXAM — Memory terms worth knowing cold

RETROGRADE amnesia affects EPISODIC MEMORIES MADE BEFORE a certain time point; anterograde affects forming new ones. PROCEDURAL memory is the development of motor skills; IMPLICIT memory is the influence of recent experience on behavior. H.M. could RETAIN NEW SKILLS BUT NOT REMEMBER HAVING LEARNED THEM. A RADIAL MAZE is used to study the HIPPOCAMPUS. GRID cells are in the ENTORHINAL CORTEX; PLACE cells are in the HIPPOCAMPUS. SHARP WAVES in the HIPPOCAMPUS are involved in MEMORY CONSOLIDATION AND RETRIEVAL. The MULTIPLE TRACE, DUAL PROCESS, and RELATIONAL theories all describe possible roles for the HIPPOCAMPUS.

PAST EXAM — CaM KII, neurogenesis, epigenetics, spike timing

CaM KII may be an important substrate for MEMORY FORMATION. The finding of NEUROGENESIS in the HIPPOCAMPUS suggests new means for storing memories. EPIGENETICS is most closely related to DNA METHYLATION. SPIKE TIMING has been shown to be important in SYNAPTIC STRENGTH.

PAST EXAM — Nucleus accumbens: rostral vs. caudal, and the stress finding

Activation of ROSTRAL areas of the medial shell of the nucleus accumbens enhances APPETITIVE behaviors; activation of CAUDAL areas enhances AGGRESSIVE/AVERSIVE behaviors. Lambert's text: in rats housed in a stressful environment (extra bright and loud), the AVERSIVE ZONE EXPANDED to fill more than 80% of the medial shell.

PAST EXAM — Opioid and dopamine roles in reward

Neural secretion of DOPAMINE PREDICTS a reward, while activating OPIOID receptors SIGNIFIES reward (the 'wanting' vs 'liking' split). Activation of MU opioid receptors produces euphoria; activating KAPPA receptors is NEGATIVELY reinforcing and mediates the anti-rewarding effects of opioids. Enkephalins, beta-endorphins, and dynorphins all activate OPIOID receptors.

PAST EXAM — Jim Olds' accidental discovery

Olds and his graduate student were implanting electrodes to study something else — the reticular formation and arousal/avoidance learning — and a misplaced electrode landed near the MEDIAL FOREBRAIN BUNDLE as it runs through the LATERAL HYPOTHALAMUS. The rat kept returning to the spot where it had been stimulated, and would press a lever to self-stimulate. What they discovered by accident was that this stimulation apparently produces feelings of PLEASURE — the brain's reward system. This exact question has appeared on two past Exam 4s AND on your last oral, where it cost you 5 points.

PAST EXAM — Prediction error

The discrepancy between the EXPECTED outcome of an action and the outcome that ACTUALLY occurs. This is what Lambert's probe trial tests in the dry land maze — the animal predicted food would be there and it was not.

PAST EXAM — Why is a dolphin's hippocampus proportionately small?

Because their HABITAT IS MORE HOMOGENOUS than that of land mammals — less spatial detail to map. Not oxygen conservation, not limited cognition.

PAST EXAM — Urinary oxytocin in dog owners

HIGHER in dog owners who were allowed to look at (gaze at) their dogs for 30 minutes compared with owners who were not. Ties to Lambert's point that affiliative social contact raises oxytocin.

WHO DID WHAT — Berthold

1849. Castrated roosters, then reimplanted their own or transplanted another male's testicle, with NO nerve or blood connections. Plumage and behavior returned. Showed the factor must be BLOOD-BORNE. First behavioral endocrinology experiment.

WHO DID WHAT — Pavlov

Russian physiologist studying DIGESTION and salivation; implanted a cannula into dogs' salivary glands to measure output. Noticed dogs salivated before food arrived. Discovered/formalized CLASSICAL (respondent) conditioning — stimulus paired with stimulus.

WHO DID WHAT — Thorndike

Puzzle box with a cat and a chain that opened the door. Cats initially did nothing until a motivating factor (food outside) was added; once one escaped by accident, escape times shortened day by day. Produced the LAW OF EFFECT — consequences shape the probability of a behavior.

WHO DID WHAT — Skinner

OPERANT conditioning. Animals emit random behaviors called OPERANTS; those followed by reward increase in probability. Interested in contingency and schedules, not brain mechanisms. Pigeon work: key pecking, discriminating color/brightness/light, detecting carbon monoxide, recognizing people. Argued behavior is shaped by external factors rather than autonomous thought.

WHO DID WHAT — Richard Thompson

Rabbit NICTITATING MEMBRANE (third eyelid) eyeblink conditioning: air puff as UCS, tone as CS. Localized the learning to the LATERAL INTERPOSITUS NUCLEUS of the cerebellum using permanent lesions and reversible cryoprobe cooling; showed the RED NUCLEUS is needed to PERFORM but not to LEARN the response.

WHO DID WHAT — Karl Lashley

Cut series of cortical lesions in rats and ran them in mazes searching for the engram in the CEREBRAL CORTEX. Concluded MASS ACTION (deficit scales with amount of tissue removed) and EQUIPOTENTIALITY (all cortex contributes equally to complex learning). Thought Pavlov's localization idea was wrong.

WHO DID WHAT — Eric Kandel

Used APLYSIA, the sea slug, to find the cellular basis of learning in the gill/siphon withdrawal reflex. Habituation = decreased quantal release from reduced presynaptic calcium channel opening. Sensitization = a facilitating interneuron releasing serotonin onto the presynaptic terminal, blocking potassium channels.

WHO DID WHAT — Donald Hebb (and Carla Shatz)

Hebb's rule: if a presynaptic cell consistently helps drive a postsynaptic cell, that connection is strengthened. Shatz's phrasing: cells that fire together wire together. LTP is the experimental demonstration, with specificity, cooperativity, and associativity.

WHO DID WHAT — Joseph LeDoux

Operationalized FEAR with tone-plus-shock conditioning. Traced the auditory route ear → cochlear nucleus → inferior colliculus → medial geniculate nucleus → cortex AND amygdala, and showed the direct thalamo-amygdala route is sufficient for the fear response. Localized emotional learning to the AMYGDALA.

WHO DID WHAT — James Olds

With his graduate student, accidentally discovered brain self-stimulation reward while aiming for another target; stimulation of the medial forebrain bundle through the lateral hypothalamus produced apparent PLEASURE and rats would lever-press for it.

WHO DID WHAT — Simon LeVay

Postmortem comparison of INAH 1-4 in the anterior hypothalamus between homosexual and heterosexual men; found INAH 3 larger in heterosexual men. Confound: the homosexual men in the sample died of AIDS.

WHO DID WHAT — Egas Moniz and Walter Freeman

Psychosurgery and LOBOTOMY, performed with a leucotome. Moniz was a Portuguese asylum head who removed prefrontal tissue after seeing the effect in a monkey, and was later shot by a patient. Freeman popularized the procedure and performed it in public lectures. Irreversible, and done on tissue with nothing structurally wrong with it.

WHO DID WHAT — James McGaugh

Two things. (1) Stress and memory: epinephrine antagonists impair water maze memory, beta-adrenergic agonists enhance consolidation — moderate arousal helps memory. (2) With Larry Cahill, identified and verified HIGHLY SUPERIOR AUTOBIOGRAPHICAL MEMORY, starting with Jill Price.

WHO DID WHAT — David Diamond

Stress and memory impairment. Developed the cat-exposure predator stress model in rats: stressed rats showed less low-threshold LTP and more spatial memory errors, plus reduced neural cell adhesion molecules. Also the neuroscientist who explained the hot-car forgetting cases in terms of stress rather than parenting.

WHO DID WHAT — Wilder Penfield

Stimulated parts of the cerebral cortex and removed small pieces attempting to cure EPILEPSY. His insula seizure work supports the anterior/posterior division: a posterior focus gives an aura of bodily sensation, an anterior focus gives an aura of emotion.

WHO DID WHAT — Paul MacLean

Named the LIMBIC SYSTEM and proposed the TRIUNE BRAIN (reptilian, paleomammalian, neomammalian). Argued vocalization, nursing, and play distinguish mammals and all three tie back to parenting.

WHO DID WHAT — Kelly Lambert and Craig Kinsley

Flipped the maternal-care question to ask how the maternal experience changes the MOTHER'S brain. Behavioral tasks (radial arm maze, elevated plus maze, dry land maze, cricket hunting), hippocampal dendritic spines, the resource restriction/low SES model, the Iron Curtain task, the paternal deer mouse comparison, and the degu study.