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Neuroscience Exam 4

TMS, Neurogenisis, Parkinsons, Alzheimers, Addiction

Alvaro Pascual-Leone's main findings We can change our brain anatomy simply by using our imagination. He also pioneered the use of Transcranial Magnetic Stimulation to make neurons fire
TMS Transcranial Magnetic Stimulation
How does TMS work? A current is passed through a copper coil to generate a changing magnetic field that surges into the axons of neurons, from there to the outer layer of the cerebral cortex. The changing magnetic field induces an electric current around it
rTMS repetitive Transcranial Magnetic Stimulation: can activate neurons so much that they excite each other and keep firing even after the original burst of rTMS has stopped
Tortoise and Hare Effect Slower, more permanent 'monday' results from the formation of BRAND NEW structures. Faster, 'friday' changes are caused by the strengthening of EXISTING neuronal connections and unmask buried pathways
Study with braille when applying blocking TMS to the visual cortex of braille readers to create a virtual lesion, the subjects could not read braille or feel with the braille reading finger. The better someone could read braille, the more they use their visual cortex
'Easy' Problems of Consciousness -- addressed by cognitive neuroscience -How do we perceive and react to sensory stimuli? -How do we integrate information from many sources and use this information to control our behavior? -How do we describe our mental states?
'Hard' Problems of Consciousness -What is the basis for our individual thoughts and subjective experiences? -What is the cause of our internal feelings?
How do we explore nervous system processes that are uniquely human? -Elements of consciousness are not functionally definable -No theoretical replacement for Descarte's 'ghost in the machine' -The problem of correlation in neuroscience -Animal models are not possible
TMS -- recording data Electricity and magnetism are related, so you can use magnetism to both record activity of the nervous system, as well as to alter activity. --The stronger the magnetic field, the deeper the penetration
TMS -- Proof of Principle, verifying TMS can affect the nervous system 1.) TMS stimulation of motor cortex produces muscle twitches 2.) TMS stimulation of visual cortex (occipital lobe) produces phosphenes, that is, patterns of light (seeing stars)
Treating Disorders with TMS (single or dual pulse) -We can use the known effect of TMS to the motor cortex and its effect of motor movement. -Evaluate damage from Stroke, ALS, multiple sclerosis, and motor disorders
Treating Disorders with rTMS (repetitive stimulation) OCD, Tinnitus, Migraines, Major Depression, Stoke (especially aphasias), and Parkinson's Disease
Side Effects of TMS -TMS causes synchronous activity of some groups of neurons -Blink reflex and sometimes scalp twitching -A 50-250 ms silencing period follows stimulation -Those effects are similar to the start of an epileptic seizure -Loud 'click' during each pulse
July 2011, TMS, FDA approved for treating symptoms of major depressive disorder in patients that have not responded to anti-depressant medication
TMS modulating Braille reading speed -Low levels (1Hz) of occipital lobe stimulation cortical inhibition and worse performance -Higher levels (10Hz) of stimulation, long-term plasticity improves reading speed
Study of Moral Judgement, which group lead to ratings of events as morally OK that most people would see as questionable? Negative Intent leading to a neutral outcome (failed attempt to harm)
TMS and lying When applied to the RIGHT dorsolateral prefrontal cortex the people lied MORE. When applied to the LEFT dorsolateral prefrontal cortex people lied LESS.
Stem Cells continue to divide, making exact replicas of themselves, and can go on endlessly with no signs of aging. Described as 'eternally young' or the 'baby cells' of the brain
Two ways to increase the overrall number of neurons in the brain 1.) create new neurons 2.) extending the life of existing neurons
Mice Study -- Most effective contributor to the proliferation of NEW neurons Physical exercise -- running on a wheel, doubled new-neurons in the hippocampus after 1 month, anticipatory proliferation
Mice Study -- What extended the life of EXISTING neurons LEARNING -- learning to use other toys, balls, and tubes
Cognitive Reserve networks devoted to mental activity that we can call upon as our brains decline
Cognitive Reserve subjects 14-30 largely utilized TEMPORAL LOBES, more education, more utilization
Cognitive Reserve subjects 65+ largely utilized FRONTAL lobes, more education, more utilization
Rejuvenating effects of Physical Activity creates new neurons, the mind is based in the brain and the brain needs oxygen///strengthens heart and blood vessels that supply the brain///stimulates the production and release of the neuronal growth factor BDNF (crucial in plastic change)
What is the fastest form of brain atrophy, why? Being immobilized in the same environment. The monotony undermines our dopamine and attentional systems crucial to maintaining brain plasticity.
What strengthens neurons? Challenging mental activities increase the liklihood that our hippocampal neurons will survive.
Why is the Hippocampus Important? Critical brain region for spatial learning and memory
Eric Kandel -- The key to plasticity The key to plasticity is changes at the SYNAPSE
Advantages of using Aplysia for experiments -Total nervous system ~20,000 neurons -Many neurons are large and easy to record -Across animals, the same neuron is easily identified -Limited behaviors
What have we learned from Aplysia Habituation: becoming less responsive///Sensitization: becoming more responsive///Memory: short and long term changes in behavior
Presynaptic Plasticity More or less neurotransmitter RELEASE
Postsynaptic Plasticity More or less neurotransmitter RECEPTORS IN SYNAPSE
LTP Long Term Potentiation of Synaptic Strength
LTP: cellular basis of learning and memory Exhibits specificity and associative properties
SHORT TERM changes in NEURONAL PLASTICITY require the modulation of pre-existing proteins (changes in neurotransmitter release, localization of neurotransmitter receptors)
LONG TERM changes in NEURONAL PLASTICITY require fundamental changes in the synapse (more or less)
What is Parkinson's Disease named after? James Parkinson, an English doctor in 1817
Four components of the Basal Ganglia Striatum, Globus Pallidus, Substantia Nigra, and subthalamic nucleus
Striatum largest compent of the Basal Ganglia, comprised of CAUDATE and NUCLEUS ACCUMBENS
Globus Pallidus involved in the regulation of voluntary movement
Substantia Nigra important for reward, addiction and movement, contains dopamine producing cells
subthalamic nucleus function not well understood, may be in involved in action selection
What is Parkinson's Disease? Degenerative central nervous system disorder resulting from the death of dopamine-producing cells in the substantia nigra. (no release from inhibition)
Signs and Symptoms of Parkinson's Disease -- MOTOR Tremors (most common, effects most distal part of limb), Bradykinesia (difficulty planning, initiating, and executing movement. Also most disabling symptom of early stages), Rigidity, Postural Instability, Shuffing Gait
Signs and Symptoms of Parkinson's Disease -- Neuropsychiatric Disturbances in executive function (planning, cognitive flexibility, abstract thinking, rule acquisition, inhibiting inappropriate actions), slowed cognitive speed, memory deficits, and increased risk (2-6x greater) of Dementia
Who gets Parkinson's? 1/100 people over 60, mostly men
Risk Factors of Parkinson's Disease Age, head injury, and pesticide exposure
Protective Factors of Parkinson's Disease Caffeine, Nicotine
What causes Parkinson's? It is idiopathic - no single cause///no biomarkers///usually diagnosed by neurologist based on symptom examination and medicated alleviation of symptoms
Genetic Factors that affect Parkinson's RARE cases where a single mutation leads to PD -- Alpha synuclein -- a protein that is a major component of lewy bodies. Genetic mutation leads to an overproduction of Alpha synuclein
Environmental Factors that affect Parkinson's RARE cases where exposure to particular environmental toxins lead to PD. Isolated groups who took recreational opiate use contaminated with MPTP lead to the rapid onset (1 week) of PD.
Treatments for Parkinson's Disease Levodopa -- LDOPA, Deep Brain Stimulation (DBS), Ablative Brain Surgery, Focal Radiation (Gamma Knife)
Levodopa LDOPA///converted to dopamine in the brain///most widely used treatment for the past 30 years///many undesirable side effects (nausea, joint stiffness, excessive libido, diskineias [tics], psychosis [schizophrenic like behavior])
Deep Brain Stimulation DBS -- used for patients with advanced PD whom drugs are no longer working for///stimulating electrode placed into areas that are DOWNSTREAM substantia nigra (globus pallidus and thalamus or subthalamic nucleus)
Ablative Brain Surgery RARELY used today, surgical ablation of brain tissue in the globus pallidus, thalamus/// if motor symptoms are on one side, surgical destruction of the globus pallidus on the opposite side can improve symptoms, however bilateral destruction irreversible
Focal Radiation "Gamma Knife" -- powerful, highly focused gamma radiation into specific area
What is coming for Parkinson's Treatment? Neural Transplantation, Gene Therapy, Vaccine Against alpha-synuclein
Neural Transplantation cells are injected into the substantia nigra in hope that they will incorporate themselves into the brain and replace dopamine-producing cells (stem cells, fetal animal cells, retinal cells)
Gene Therapy uses a non infectious virus to shuttle a gene into a part of the brain -- AADC an enzyme that converts LDOPA into dopamine -- Neurturin a compound that protects cells in substantia nigra
Vaccine against alpha synuclein produces antibodies that bind alpha synuclein and clear it from the brain
Fundamental Components of the Aging Process Damage from oxidative stress///diminished ability to detoxify free radicals///decline in mitochondrial function///accumulation of injurious proteins///diminished cell signaling///diminished lipids (fat) --- all these lead to decreased integrity/cell death
Causes and description of Alzheimer's Disease Beta-Amyloid plaques - protein fragments that build up in the space between neurons///Tau-Tangles - tangles of a protein called Tau that builds up inside of cells
Diagnosis of Alzheimer's Disease Probably diagnosis ~90%---- spinal tap, PET or MRI scans, cognitive tests, patient history looking for differences in the HIPPOCAMPUS and TEMPORAL LOBE
Ways to maintain cognitive function while aging Physical exercise (increases size of the hippocampus and improves memory), mental exercise, and nutrition
What are 'Mental Exercises'? Activities that require you to use all your senses, break your routines, and engage in novel experiences///activities that involve planning (stimulate the frontal lobe), spatial skills (ballroom dancing/basketball), new language, painting
Components of Good nutrition for Improved Cognition Polyphenols from antioxidant rich fruits and vegetables (plants with rich colors), DHA rich foods, Olive Oil, Mediterranean Diet (high fruits and veg. and monounsaturated fats, low red meat), Polynunsaturated fats (walnuts, fish), moderate wine/alcohol
What is Addiction? A chronic relapsing brain disease, severely alters brain areas critical to decision making, learning and memory, and behavior control for long periods of time
DSM-IV Substance Abuse Criteria Definition A maladaptive pattern of substance use leading to significant impairment or distress as manifested by ONE(or more) criteria
DSM-IV Substance Abuse Criteria (4) 1.) Recurrent substance use resulting in failure to fulfill major role obligations 2.)Use in situations in which it is physically hazardous 3.) recurrent substance related legal problems 4.) continued use despite having persistent social problems from use
DSM-IV Substance Dependence Criteria Definition A maladaptive pattern of substance use leading to clinically significant impairment by THREE(or more) in a 12 month period
DSM-IV Substance Dependence Criteria 1.) Tolerance 2.)Withdrawal 3.)Substance taken in larger amounts over a longer period of time 4.) Persistent desire and unsuccessful efforts to control abuse 5.)time spent obtaining 6.)given up opportunities because of use 7.) using knowing their problem
Top Three Drug Dependences 1.) Marijuana - 4,165,000 2.) Pain Relivers - 1,768,000 3.) Cocaine - 821,000
Risk Factors for Addiction Genetics, Gender, Adolescence, Mental Disorders, Route/Pattern of Drug Administration, Early life stress/abuse, community/social acceptance, personality traits
#1 Risk factor for Addiction Making the voluntary choice to do drugs
Why do people take drugs? to feel good, to feel better, to do better, curiosity
Physiological Drug Tolerance The liver gets more efficient at breaking down the drug before it gets to the brain
Cellular Drug Tolerance Plasticity in nerve cells make them less responsive to the drug
Sensitization The same dose of the drug produces a much stronger action, (more so than tolerance is the basis for addiction)
The Drug Addiction Pathway Ventral Tegmental Area --- Nucleus Accumbens --- Prefrontal Cortex
Physiology of the Drug Addiction Pathway All drugs that people abuse have the same property of activating neurons of the ventral tegmentum to release dopamine in the nucleus accumbens///DENDRITIC SPINES FROM REPEATED ABUSE
Marijuana affects of blood flow to the brain Decreases blood flow to the Amygdala (attention to surroundings) and increases blood flow to the Hypothalamus (feeding and regulation)
Created by: 595032255
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