Behavioral Neuroscience FINAL

Describe the evidence for unconscious decision making

Blindsight and unilateral neglect show that people can process and act on visual information accurately without conscious awareness of seeing it, proving that some decisions are made unconsciously.​

Blindsight

a condition where a cortically blind person can correctly respond to visual stimuli in their blind field without conscious awareness of seeing them.

Unilateral neglect

a post-brain-injury disorder where a person fails to attend to or respond to stimuli on the side of space opposite the lesion, despite intact primary sensation and motor function.

Define Charles Bonnet Syndrome and the symptoms that accompany its diagnosis.

a condition in which people who have lost vision experience complex visual hallucinations, often with increased activity in secondary visual cortex, while knowing the images are not real.​

What is cognition?

information processing that includes higher-level mental operations such as thinking, reasoning, and other processes that contribute to conscious experience.​

What is the galvanic response?

a change in the skin’s electrical conductance caused by sweat gland activity during emotional arousal.

what do backwards masking, prosopagnosia, and Capgras syndrome tell us about brain activity and awareness?

Visual backward masking, prosopagnosia, and Capgras syndrome show that the brain can process visual and facial information (including emotion) unconsciously, and that conscious recognition depends on specific cortical pathways that can be selectively damaged.​

Capgras syndrome

a delusional misidentification disorder in which a person believes that someone emotionally close to them has been replaced by an identical-looking imposter.

Prosopagnosia

a neurological disorder where a person cannot recognize familiar faces despite normal vision and intelligence.

Backward masking

when a brief target stimulus is rendered hard to perceive or recognize because a second “masking” stimulus appears immediately afterward and overwrites its sensory trace.

Detail the brain areas associated with facial recognition, both consciously and unconsciously.

the fusiform face area

amygdala and associated limbic circuits.​

What is form agnosia?

an impairment in consciously recognizing shapes and objects despite intact low-level vision, often with preserved ability to use visual information to guide actions.​

What do choice-reaction tasks tell us about unconscious processing?

show that people can learn and speed up correct responses based on patterns they are not consciously aware of, indicating unconscious learning and decision processes.​

Be familiar with the arguments for and against conscious awareness in decision making (i.e., Benjamin Libet’s experiment on the readiness potential and the criticisms of his conclusions).

Libet’s experiments found that brain activity (readiness potential) predicting a movement appears before conscious intention, suggesting unconscious initiation, but critics argue that the task is artificial, the timing of “intention” is unreliable, and that consciousness may still veto or shape actions.​

Hysteria

involves unconscious production of symptoms

malingering

involves deliberate, conscious exaggeration or faking of symptoms for external gain.

What are false memories?

Vivid recollections of events or details that did not occur or occurred differently, arising because memory recall is a creative, reconstructive process.​

What is hemineglect?

a condition, usually after parietal damage, in which a person fails to attend to or respond to stimuli on one side of space, despite intact primary sensory function.

Positive symptoms of Schizophrenia

add abnormal experiences like hallucinations and delusions

Negative symptoms of schizophrenia

reflect a loss of normal functions like flattened emotion and social withdrawal

cognitive symptoms of schizophrenia

involve problems with attention, working memory, and executive function

Identify the genetic and environmental risk factors of schizophrenia

Schizophrenia risk comes from many genes (such as DISC1 and 22q11.2 variants) plus environmental factors like low socioeconomic status, winter or early-spring birth, urban birth, perinatal or obstetrical complications, maternal viral infection or malnutrition, and increased paternal age.​

Do children of monozygotic twins discordant for schizophrenia have the same or different chances of developing schizophrenia?

Children of monozygotic twins where only one twin has schizophrenia have similar elevated risks whether their parent is the affected or the unaffected twin, showing strong genetic loading.​

What is schizotypal personality disorder?

a milder, nonpsychotic condition with odd beliefs, unusual perceptual experiences, and social/interpersonal deficits that may share genetic risk and subtle brain changes with schizophrenia.​

Know the neuronal and neuroanatomical findings associated with schizophrenia.

Schizophrenia is associated with decreased gray matter in prefrontal, temporal, and parietal cortices, enlarged ventricles, reduced thalamic volume (especially mediodorsal nucleus), abnormal prefrontal function and connectivity, and synaptic rather than massive neuronal loss.​

Discuss how abnormal brain development in adolescence could contribute to the onset of schizophrenia (neurodevelopmental vs neurodegenerative hypotheses).

The neurodevelopmental view holds that early brain insults plus excessive adolescent synaptic pruning in associative cortices (especially prefrontal) unmask schizophrenia,

whereas the neurodegenerative view emphasizes ongoing post-onset gray-matter loss and ventricular enlargement; evidence suggests early developmental abnormalities with some later progressive changes.​

What is the dopamine hypothesis of schizophrenia? What brain areas are specifically involved with this theory? In what brain region might dopamine transmission be high, and where might dopamine transmission be low?

proposes overactive mesolimbic dopamine signaling (contributing to positive symptoms) and

relatively reduced mesocortical dopamine to prefrontal cortex (contributing to negative and cognitive symptoms),

involving midbrain dopamine neurons projecting to limbic areas and frontal cortex.​

Detail the differences between the effects of antipsychotic drugs on the positive, negative, and cognitive symptoms of schizophrenia

D2 receptor antagonists mainly reduce positive symptoms but often have limited benefit for negative and cognitive symptoms,

while partial dopamine agonists aim to dampen excessive dopamine in overactive pathways yet preserve some dopaminergic tone in underactive prefrontal circuits to better spare negative and cognitive functions.​

Be familiar with the glutamate theory of schizophrenia and what effect an NMDA antagonist (e.g., phencyclidine or ketamine) might have on schizophrenia symptoms.

suggests that hypofunction of NMDA-type glutamate receptors contributes to schizophrenia, supported by the fact that NMDA antagonists like phencyclidine or ketamine can induce or worsen both positive and negative/cognitive symptoms in healthy people and patients.​

Overall, what is the most effective drug to treat schizophrenia?

Clozapine

What is the comorbidity of anxiety and major depressive disorders?

Around 60%

Describe the differences between unipolar depression and bipolar disorder.

Unipolar depression involves only depressive episodes,

whereas bipolar disorder includes both depressive episodes and episodes of mania or hypomania.​

How do women and men differ in major depression?

Major depression is more common in women than in men, with roughly about twice the prevalence in women.​

Know the role of the anterior cingulate cortex in depression.

The anterior cingulate cortex shows abnormal function in depression, with its rostral (emotional) and caudal (cognitive) divisions both implicated in disturbed emotional processing and cognitive control.​

What are the diagnostic criteria for depression and mania?

Depression is diagnosed based on a persistent low mood and loss of interest plus other symptoms like sleep, appetite, and concentration changes, whereas mania is diagnosed by a sustained period of abnormally elevated or irritable mood with increased energy, decreased need for sleep, and risky or grandiose behavior.​

Be familiar with the role of the amygdala and hippocampus in depression (i.e., size and activity).

In depression, the amygdala tends to be hyperactive and sometimes enlarged, while the hippocampus is often reduced in volume and functionally impaired.​

What other brain regions are involved in depression?

Depression also involves abnormal activity in the dorsolateral prefrontal cortex, anterior cingulate cortex, and other regions in emotional-salience and cognitive-control networks.​

How are stress and depression interrelated?

Chronic stress can increase cortisol, which may damage the hippocampus through glutamate-mediated excitotoxicity and reduced neurogenesis, thereby increasing vulnerability to depression.​

What is the monoamine hypothesis of depression?

proposes that depression is linked to deficient signaling of monoamine neurotransmitters such as serotonin, norepinephrine, and dopamine in key brain circuits.​

Describe the function of antidepressant treatments (i.e., MOAIs, TCAs, CBT, ECT, DBS, TMS, SSRIs).

MAOIs, TCAs, and SSRIs boost monoamine signaling by blocking degradation or reuptake; CBT changes maladaptive thoughts and behaviors; ECT, TMS, and DBS modulate activity in mood-related circuits like the prefrontal cortex and cingulate to relieve severe or treatment-resistant depression.​

Know the function of both ketamine (what receptors it affects and what neurotransmitter system is involved with) and lithium.

a fast-acting antidepressant that blocks NMDA-type glutamate receptors, altering glutamatergic transmission, whereas lithium is a mood stabilizer for bipolar disorder that, among other actions, influences inositol metabolism and intracellular signaling.​

What are the major anxiety disorders?

Major anxiety disorders include generalized anxiety disorder, panic disorder, social anxiety disorder, specific phobias, posttraumatic stress disorder, and obsessive-compulsive disorder.​

What is known about brain regions associated with the anxiety disorders?

often involve hyperactivity of the amygdala and related fear circuits, altered hippocampal function, and abnormal regulation by prefrontal regions that normally modulate fear and worry.​

Explain what symptoms are common in OCD patients and what environmental risk factors are associated with its development.

characterized by intrusive obsessions and repetitive compulsions, with risk increased by factors such as infections or immune-related insults (e.g., PANDAS/PANS) in susceptible individuals.​

Describe panic attacks and the role of GABA in these episodes.

Panic attacks are sudden episodes of intense fear with symptoms like palpitations, shortness of breath, and dizziness, and reduced GABAergic inhibition in anxiety circuits may lower the threshold for these episodes.​

What medications are used to treat anxiety disorders?

Anxiety disorders are commonly treated with SSRIs and SNRIs, sometimes benzodiazepines for short-term relief, and other agents such as certain anticonvulsants or buspirone depending on the specific disorder.

What are the genetic and environmental factors associated with autism?

Autism involves many genetic variants (including neuroligin and other synaptic genes, copy-number variants, and de novo mutations) plus environmental risks such as certain prenatal viral infections and immune factors.​

Know the brain areas possibly associated with autism spectrum disorders.

Autism has been linked to early overgrowth and later differences in cortex, abnormal amygdala development and timing, atypical white matter, reduced Purkinje cells in the cerebellum, and abnormalities in regions like superior temporal sulcus involved in social perception.​

Explain the Sally-Anne test and what problems people with autism-spectrum disorders have with mentalizing.

In the Sally-Anne false-belief test, many autistic children fail to predict that Sally will look where she last saw an object, showing a delay or impairment in mentalizing (attributing beliefs to others).​

What is mind blindness?

difficulty understanding and representing other people’s thoughts, beliefs, and intentions, a common theory-of-mind problem in autism.​

What are “islets of ability” in autism-spectrum disorder?

circumscribed areas of exceptional skill, such as music, art, calculation, or memory (including perfect pitch in some), seen in some autistic individuals despite broader cognitive or social difficulties.​

What are the features of autism-spectrum disorder?

Core features include impaired social interaction, impaired verbal and nonverbal communication, restricted and repetitive behaviors and interests, insistence on routines, atypical sensory responses, and frequent comorbid intellectual disability or seizures.​

What are female to male ratios for autism-spectrum disorder?

Autism is around three times more common in males than in females.​

Understand Fragile-X syndrome and the percentage of individuals with fragile-X syndrome that also meet the criteria for autism. What is the genetic basis of Fragile-X syndrome?

Fragile-X syndrome is caused by a CGG repeat expansion and methylation in the FMR1 gene on the X chromosome, eliminating FMRP; about 30% of boys with Fragile-X meet diagnostic criteria for autism spectrum disorder.​

What is Rett syndrome? Know the details of its development and progression. What is the genetic abnormality associated with Rett syndrome?

Rett syndrome is an X-linked disorder mainly in girls, with normal early development followed by loss of language and hand skills, motor and cognitive regression, and lifelong disability, caused by mutations in the MeCP2 gene that regulates gene expression.​

Differentiate between Down Syndrome, Turner Syndrome, Prader-Willi Syndrome, and Angelman Syndrome. How do these conditions relate to autism-spectrum disorders? What are the genetic abnormalities associated with these conditions?

Down syndrome (trisomy 21) causes intellectual disability and sometimes autism; Turner syndrome (single X chromosome) can include social difficulties; Prader-Willi (paternal 15q11–q13 loss) involves hyperphagia and obsessive traits; Angelman (maternal 15q11–q13 loss) involves severe intellectual disability and a happy affect, and both Prader-Willi and Angelman illustrate links between chromosomal abnormalities and ASD-like features.​

What is genetic imprinting?

parent-specific gene expression where only the maternal or paternal allele is active, as in the 15q11–q13 region in Prader-Willi and Angelman syndromes.​

What is haploinsufficiency?

Haploinsufficiency is when a single functional copy of a gene is not enough for normal function, so loss of one allele (for example in certain deletion syndromes) produces disease.

Define learning and understand how learning and memory work in conjunction.

Learning is a change in behavior due to experience, and memory is the encoding, storage, and retrieval process that allows learned information to be retained and used later.​

Know what role the medial temporal lobe including the hippocampus has in declarative and procedural memory.

The medial temporal lobe, especially the hippocampus, is critical for forming and consolidating new declarative (explicit) memories but is not required for procedural (skill and habit) memory.​

Be familiar with patient H.M. and what his injury and memory function help us understand about working memory, short and long-term memory, and implicit memory. How did H.M. perform on tests of explicit memory? How did he perform on tests of implicit memory? What does this tell us about the neuroanatomy involved with explicit and implicit memory?

H.M., who had bilateral medial temporal lobe and hippocampal removal, had normal working memory and old long-term memories but could not form new explicit memories, yet showed normal implicit learning (e.g., priming and skill learning), demonstrating that medial temporal structures are essential for explicit memory but not for implicit memory systems like basal ganglia and cerebellum.​

Differentiate between implicit and explicit memory.

Explicit (declarative) memory involves conscious recall of facts and events, whereas implicit (nondeclarative) memory supports skills, habits, priming, and conditioning without conscious awareness.​

Know the two subtypes of explicit memory (semantic and episodic).

Semantic memory stores facts and concepts (word meanings, general knowledge), while episodic memory stores autobiographical events with their spatial and temporal context.​

How is explicit memory consolidated?

Explicit memory consolidation involves time-dependent stabilization of traces through gene activation and protein synthesis that change synapses, with medial temporal lobe structures temporarily linking distributed cortical representations.​

What brain regions are involved with encoding?

Deep encoding of explicit memories engages the medial temporal lobe (including hippocampus) together with association and left prefrontal cortices.​

Know the definition and examples of priming, habituation, sensitization, habit learning, associative learning, non-associative learning, episodic memory, and semantic memory.

Priming is improved processing of a stimulus after prior exposure; habituation is decreased response to a repeated harmless stimulus; sensitization is increased response after a strong or noxious stimulus; habit learning is gradual acquisition of automatic behaviors; associative learning links stimuli or actions with outcomes (classical and operant conditioning); non-associative learning includes habituation and sensitization; episodic and semantic memory are the event-based and fact-based forms of explicit memory.​

Explain what happens when a memory is formed (i.e., capacity of storage, physical process associated with consolidation, retrieval, etc.).

When a memory is formed, information is encoded with essentially unlimited long-term storage capacity, consolidation strengthens synaptic connections via gene- and protein-dependent plasticity, and retrieval later reactivates the distributed network, often reconstructively.​

Where are long-term explicit and implicit memories stored in the brain?

Long-term explicit memories are stored in distributed association cortices, while long-term implicit memories are stored in circuits supporting specific skills and conditioning, such as basal ganglia, cerebellum, and relevant sensory and motor cortices.​

What is operant conditioning? What is classical conditioning?

Operant conditioning links a behavior with a reinforcing or punishing outcome (action–outcome learning), whereas classical conditioning links two stimuli so that a previously neutral cue predicts an unconditioned stimulus.​

What are some common memory errors?

Common memory errors include absent-mindedness (poor encoding), blocking (tip-of-the-tongue), misattribution (wrong time, place, or person), suggestibility, bias, and persistence of unwanted memories.

The role of the amygdala in fear conditioning.

The amygdala, especially its lateral nucleus, is required to form and store associations between neutral cues and aversive events, so damage to it blocks Pavlovian fear conditioning.​

The role of the amygdala in determining the emotional valence of stimuli.

The amygdala evaluates the emotional significance (valence) of sensory inputs and then drives appropriate autonomic, endocrine, and behavioral responses via its projections to hypothalamus, brainstem, and cortex.​

Neurotransmitters associated with seizures and neurotoxicity.

Excessive glutamate and resulting overactivation of its receptors, especially NMDA receptors, drive excitotoxicity and seizure-related brain damage, while reduced GABAergic inhibition can also promote seizure activity.​

Composition of neurofibrillary tangles.

Neurofibrillary tangles in Alzheimer’s disease are intracellular aggregates of abnormally hyperphosphorylated tau, a microtubule-associated protein.​

Genes associated with Alzheimer’s disease.

Key Alzheimer’s-related genes include APP (amyloid precursor protein), presenilin-1, presenilin-2, and APOE (with the APOE4 allele increasing risk).​

Risk factors for Alzheimer’s disease.

Major risk factors include advanced age, APOE4 genotype, family history and other genetic variants, plus vascular and lifestyle factors.​

Ghrelin, CART, MSH, leptin, orexin.

Ghrelin is a stomach hormone that stimulates hunger; leptin is an adipose hormone that signals fat stores and suppresses appetite; CART and MSH are hypothalamic peptides that reduce feeding; orexin (hypocretin) from the lateral hypothalamus promotes wakefulness and stabilizes the sleep–wake cycle.​

The different types of aphasia including Broca’s and Wernicke’s aphasias.

Broca’s aphasia involves nonfluent, effortful speech with relatively better comprehension, whereas Wernicke’s aphasia involves fluent but often meaningless speech with poor comprehension; other types include conduction aphasia, global aphasia, and transcortical aphasias.​

The stages of sleep and how they occur across the sleep cycle.

Sleep cycles through NREM stages N1, N2, N3 (slow-wave sleep) and REM in roughly 90-minute ultradian cycles, with more N3 early in the night and more REM toward morning.​

Sleep disorders.

Common sleep disorders include insomnia, obstructive and central sleep apnea, narcolepsy, restless legs syndrome, parasomnias (sleepwalking, night terrors), REM behavior disorder, circadian rhythm disorders, and the rare fatal familial insomnia.​

Vomeronasal organ.

The vomeronasal organ is a chemosensory structure that detects pheromones and sends information to the medial amygdala and hypothalamus, influencing social and reproductive behaviors.​

What is a partial agonist? How would it act under conditions of low neurotransmitter concentrations and high neurotransmitter concentrations?

A partial agonist activates a receptor but produces a submaximal response; at low transmitter levels it can increase receptor activation, while at high transmitter levels it can compete with the full agonist and effectively reduce overall receptor activation.