Covers a range of topics including:
-Development of the nervous system
-Brain damage and neuroplasticity
-Learning, memory and amnesia
-Hunger, Eating and Health
-Drug use, drug addiction and the brain's reward circuits
-Hormones and sex
-Sleep, Dreaming and Circadian rhythms
-Biopsycho...
Experiments/Research/Article studies only
Tuesday, October 8, 2019 1:19 PM
Module 1 : Development of the nervous system
• Nun study
○ Hypothesis
▪ longitudinal model of aging and disease
○ Methodology
▪ Content archives provided info about potential early and middle-life risk factors for Alzheimer's and other disorders
▪ Annual examinations record changes in the cognitive and physical function of each participant during old age
▪ Structure and pathology of the brain can be related to early and middle-like risk factors and to late-life cognitive and physical function
○ Conclusion
▪ Dementia vs health aging depends on:
1. Degree of pathology present in the brain
2. Degree of resistance to the clinical expression of the neuropathology (ex, even if brain has some infarctions does it lead to
memory loss, etc. ?)
▪ (NYT) Positive emotional state in early life may contribute to longer life
• Evolving Diagnostic and Genetic Landscapes of Autism Spectrum Disorder
○ Hypothesis
▪ Discuss parallel evolution of diagnostic and genetic understanding of autism spectrum disorders
○ Methodology
▪ Identification of genomic loci and individual genes
- Karyotype
- Microarray technology (ex, comparative genomic hybridization)
- Next-generation sequencing , single nucleotide polymorphism (SNP) microarrays
○ Conclusion
▪ suggesting the number of rare mutations that can impart substantial risk for ASD is much larger than originally suspected
▪ average rate of mutations in individuals with ASD was not significantly different than control—or even unaffected siblings—unless the
analysis was restricted to genes that are known to be expressed during human brain development
▪ presence of multiple mutations and/or inherited protective or risk alleles—each at different loci within one individual—may interact
with each other to result in the emergent ASD phenotype
▪ Need to determine relationship between heterogenous and varied nature of ASD genomics to determine mechanism underlying ASD
• Autism may reflect excitation-inhibition imbalance in brain, study finds
○ Hypothesis:
▪ Key features of autism reflect an imbalance in signaling from excitatory and inhibitory neurons in a portion of the forebrain, and that
reversing the imbalance could alleviate some of its hallmark symptoms.
○ Methodology :
▪ Series of experiments on mouse models
- Reducing ratio of excitatory to inhibitory neurons
○ Conclusion :
▪ Autism-like behavioral deficits could be induced in ordinary mice by elevating the ratio of excitatory to inhibitory neuronal firing
patterns in the mice's medial prefrontal cortex. The new study shows that decreasing that ratio restores normal behavior pattern
• MRI reveals striking brain differences in people with genetic autism
○ Hypothesis:
○ Methodology:
▪ Cognitive and behavioral tests on participants
▪ MRI
▪ Involved any sort of participant (not only autistic)
○ Conclusion:
▪ identified structural abnormalities in the brains of people with one of the most common genetic causes of autism
• Phantom limb
○ Hypothesis
▪ Feelings in phantom limb caused by existing neural connections overtaking the "empty space"
○ Methodology
▪ Brain scan
○ Conclusion
▪ Hypothesis correct
▪ Ex, cheek expanding connection over phantom limb --> sensation on cheek = sensation on phantom limb
• Brain gain
Hypothesis
PSYC370 Page 1
, ○ Hypothesis
▪ Does neurogenesis occur in adult humans?
○ Methodology
▪ BrdU (artificial nucleoside that can replace thymidine), neuron-specific protein markers and confocal imaging, which enabled
researchers to identify newly generated cells
○ Conclusion
▪ Confirmation that neurogenesis occurs in adults
▪ neurogenesis may continue for most of one’s life
• Sperry's frog eye rotation study
○ Chemoaffinity hypothesis: growing axons are attracted to the correct targets by different chemicals released by the target sites
○ Topographic gradient hypothesis: axonal growth is guided by the relative position of the cell bodies on intersecting gradients, rather than by
point-to-point coding of neural connections
○ Methodology: cut the optic nerves of frogs, rotated their eyeballs 180 degrees, and waited for the axons to regenerate
○ Axon growth during development or regeneration is precise, with each axon growing to its intended target
○ Synaptic connections established before, then shift as they mature to be precisely mapped
○ Revised hypothesis: growth cones seem to be influenced by a series of a chemical and physical signals along the route
▪ Signals that guide growing axons come from adjacent growing axons
▪ Cut axons grew out to fill the available space rather than growing out to their original points of connection
Module 2- Brain damage and neuroplasticity
• Canadian-made blood test for concussions could radically simplify diagnosis
○ Blood test uses a small sample of blood drawn from someone within 72 hours of a sudden blow to the head to measure 174 brain chemicals
that change in response to a brain injury.
○ Difficulty being accurate about concussion diagnosis
▪ Parker smith - didn’t know he had concussion since signs weren't apparent, couldn’t play hockey anymore
• Big idea: Brain trauma
○ Head collisions linked with behavioral and cognitive changes
○ Methodology
▪ Analyzing impact data from video recordings and helmets equipped with accelerometers
○ Key mark of chronic traumatic encephalopathy (CTE), a disorder found in athletes who have sustained repetitive head blows, reveals itself in
the details of stained slices of brain
▪ Presence of tau protein, loss of brain matter
▪ Need better tests, can only diagnose after patient dies
• Rowan's law
○ Rugby player, teen who died due to 2 concussions within a week
▪ Wasn’t aware she had concussion
○ "Rowan’s Law,” an act governing the management of youth concussions in all sports.
• Stroke of insight
○ Neuroanatomist Jill Bolte Taylor realized she was having a massive stroke one morning. As it happened -- as she felt her brain functions slip
away one by one, speech, movement, understanding -- she studied and remembered every moment.
• Study finds damage in 90% of former football players' brains
○ chronic traumatic encephalopathy, or CTE, a debilitating brain disease that can cause a range of health problems including memory loss,
depression, confusion and dementia, symptoms that can arise years after the collisions occur
▪ Caused by repeated blows to the head
• Neuronal reorganization
○ Kaas and colleagues (1990)
- Assessed effect of making a small lesion in one retina and removing the other
- Several months after, primary visual cortex neurons that originally had receptive fields in the lesioned area of the retina were found to
have receptive fields in the area of the retina next to the lesion
- This change began within minutes of the lesion
○ Pons and colleagues (1991)
- Mapped the primary somatosensory cortex of monkeys whose contralateral arm sensory neurons had been cut 10 years before
- Found that the cortical face representation had systematically expanded into the original arm area
- Scale of reorganization was greater than assumed possible
▪ The primary somatosensory cortex face area had expanded its border by >1cm over the 10 year interval between surgery and
testing
○ Sanes, Suner, and Donoghue (1990)
- Transected the motor neurons that controlled the muscles of rats' vibrissae (whiskers)
- Few weeks later, stimulation of the area of motor cortex that previously elicited vibrissae movement now activated other muscles of t
face
PSYC370 Page 2
, face
○ In humans:
- Blind volunteers had skills superior to those of sighted control volunteers on a variety of auditory and somatosensory tasks
• Cognitive reserve
○ Kapur (1997)
- Conducted biographical study of doctors and neuroscientists with brain damage, and observed a great degree of cognitive recovery
- Observed improvement didn’t occur due to actual recovery of brain function, but because their cognitive reserve allowed them to
accomplish tasks in alternative ways
- Used to explain why highly educated people are less susceptible to the effects of brain deterioration associated with aging
• Neurotransplantation as a Treatment for CNS Damage- early research (see notes for more details)
○ Reparation of damaged CNS tissue by implanting embryonic tissue near the damaged area
➢ Fetal tissue into substantia nigra for treatment of Parkinson's
▪ Lack dopamine-releasing cells of the nigrostriatal pathway
▪ Cured by transplanting the appropriate fetal tissue into the substantia nigra
▪ some patients started to display variety of uncontrollable writing and chewing movements ~ 1 year after surgery
➢ Adrenal medulla cells for treatment of Parkinson's
▪ Adrenal medulla cells release small amounts of dopamine, so, adrenal medulla autotransplantation could alleviate symptoms of
the disease?
▪ Not successful
➢ Implanting nonneural cells
▪ Xu and colleagues (1999)
- Induced cerebral ischemia in rats
- Hippocampus of rats treated with virus that releases apoptosis inhibitor, reducing loss of hippocampal neurons
➢ Implanting Schwann cell sheaths
▪ Promote regeneration and guide axon growth
▪ Cheng, Cao, and Olson (1996)
- Transected spinal cords of rats, rendering them paraplegic (paralyzed in the posterior portion of their bodies)
- Researchers then transplanted sections of myelinated peripheral nerve across the transection
- Spinal cord neurons regenerated through the implanted Schwann cell myelin sheaths, and regeneration allowed the rats to
regain use of their hindquarters
○ Modern research
➢ Induced stem cells have been the focus of research, but genetic manipulation required to create them (ex, insertion of 4 genes) makes
difficult to predict how they might behave in a human patient
▪ Stem-cell cultures deteriorate as chromosomal abnormalities gradually accumulate during repeated cell division
➢ Effects of implanting stem cells genetically programmed to release neurotrophins or to develop into glial cells are currently under
investigation
• Treating strokes
○ Nudo and colleagues (1996)
▪ Produced small ischemic lesions in the hand area of the motor cortex of monkeys
▪ Program of hand training and practice was initiated, where the monkeys plucked 100s of tiny food pellets from food wells of different
sizes
▪ Significantly reduced the expansion of cortical damage into the surrounding penumbra
○ Weiller and Rijntjes (1999); neuronal competition for synaptic sites
- Constraint-induced therapy: tied down the functioning arm for 2 weeks while the affected arm received intensive training
- Performance of the affected arm improved markedly over the 2 weeks, and there was an increase in the area of motor cortex
controlling that arm
Module 3: Learning, memory and amnesia
• Experts excited by brain 'wonder-drug'//Scientists discover two repurposed drugs that arrest neurodegeneration in mice
○ Prevent both a form of dementia and prion disease by stopping brain cells dying
○ Tested more than 1,000 ready-made drugs on nematode worms, human cells in a dish and mice
○ Trazodone and DBM (dibenzoylmethane)
○ Highly protective and prevented memory deficits, paralysis and dysfunction of brain cells
• My 'smart drugs' nightmare
○ Benjamin zand took modafinil (smart drug)
○ Decreased attention span over time (before, attention span was at the top 15-20% of people my age. After, it was in the top 5-10%.)
○ Dehydration, insomnia, distracted (increased focus, but on the wrong things)
• Oh Where, Oh Where Have Those Early Memories Gone? A Developmental Perspective on Childhood Amnesia
○ from the ages of 3 to 7 years, adults have fewer memories than would be expected, based on forgetting alone
○ within the period eventually obscured by childhood amnesia, children had remarkably rich autobiographies
adults lack memories from early in life because no memories were formed or memories were formed, but later became inaccessible as a
PSYC370 Page 3
, ○ adults lack memories from early in life because no memories were formed or memories were formed, but later became inaccessible as a
result of cognitive changes
• Adult recollections of childhood memories: What details can be recalled?
○ Questionnaire
○ Few differences were found between positive and negative memories, which on average had 4/5 details and dated to the age of 6/6.5 years
○ Memory for details about activity, location, and who was present was good; memory for all other details was poorer or at floor
• Cognitive enhancement by drugs in health and disease
○ experimental and clinical studies have demonstrated relatively modest overall effects, most probably because of substantial variability in
response both across and within individuals
○ evidence that there might be more significant effects in subgroups, such as those whose baseline performance is poorest or individuals with
particular genotype.
○ possible that these effects could be due simply to a generalized improvement in arousal
• Case of H.M.
○ Got bilateral medial temporal lobectomy- removal of the medial portions of both temporal lobes including most of the hippocampus,
amygdala, and adjacent cortex due to his seizures
○ Surgery caused retrograde and anterograde amnesia
○ His case lead to 3 major scientific contributions;
1. Challenged the current view at the time that memory functions are diffusely and equivalently distributed throughout the brain (by
showing medial temporal lobes play an important role in memory)
2. Supported the theory that there are different modes of storage for ST, LT and remote memory (since he couldn’t form certain types o
long term memories, but his performance on tests of short-term memory or his remote memory was still good)
3. First to reveal that a patient with amnesia might claim no recollection of a previous experience while demonstrating memory for it by
improved performance (Led to categorization of LTM ; explicit and implicit)
• Retrograde amnesia and memory reconsolidation
○ Hebb's theory - memories of experiences are stored in the short term by neural activity reverberating (circulating) in closed circuits. These
reverberating patterns of neural activity are vulnerable to disruption (ex, a blow to the head) but eventually they induce structural changes
the involved synapses which provide stable long-term storage
○ Method: differences between the before- and after- ECS scores serves as an estimate of memory loss for the events of each year
○ Current view of memory consolidation is that it continues for a very long time, if not indefinitely
• Hippocampus and consolidation
○ Nadel and Moscovich
▪ Retained memories become progressively more resistant to disruption by hippocampal damage because each time a similar experienc
occurs or the original memory is recalled, a new engram (change in the brain that stores a memory) is established and linked to the
original engram, making the memory easier to recall and the original engram more difficult to disrupt
• Reconsolidation
○ Theory that each time a memory is retrieved from long-term storage, it is temporarily held in an unstable state in STM, where it is susceptib
to posttraumatic amnesia (remains until consolidated again)
○ Nader, Schafe, and Ledoux (2000)
▪ Infused the protein-synthesis inhibitor anisomycin into the amygdala of rats shortly after they had been required to recall a fear-
conditioning trial
▪ Infusion produced retrograde amnesia for the fear conditioning, even though the original conditioning trial had occurred many days
before
• Delayed non-matching to sample test (monkeys)
○ Gaffan (1974) & Mishkin and Delacour (1975)
▪ Showed that monkeys with bilateral medial temporal lobectomies have major problems forming long-term memories for objects
encountered in the delayed nonmatching-to-sample test
- Monkey is presented with a distinctive object (sample object) where food is found under
- After a delay, the monkey is presented with 2 test objects: the sample object and an unfamiliar object
- The monkey must remember the sample object so that it can select the unfamiliar object to obtain food hidden beneath it
▪ Well trained monkeys, 90% correct , while monkeys with bilateral medial temporal lobe lesions had major object-recognition deficits
▪ Modeled deficits of H.M.
○ Rats;
▪ Bilateral lesions of the rats' hippocampus, amygdala and medial temporal cortex combined produce major deficits at all of the interva
except the shortest intervals
• Object-recognition deficits resulting from bilateral medial temporal lobectomy
○ Case of R.M
▪ Left amnesic following an ischemic accident that occurred during heart surgery. Brain revealed cell loss was restricted largely to the
pyramidal cell layer of his CA1 hippocampal subfield
PSYC370 Page 4
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