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133 Cards in this Set
- Front
- Back
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Homeostasis |
the process by which the body's substances and characteristics (such as temperature and glucose level) are maintained at their optimal level. |
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Negative feedback |
a process whereby the effect produced by an action serves to diminish or terminate that action, a characteristic of regulatory systems |
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Satiety mechanism |
a brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water. uses negative feedback system |
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Lipocyte |
place in cells where excess fat is stored, which expand in size until the fat is used for fuel. Lipocytes in obese individuals grow in size (hypertrophic growth) and in number (hyperplastic growth).When obese individuals lose weight their lipocytes reduce in size but not number. |
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Body Mass Index |
Weight (kg) / Height (m) squared Inaccurate measure for individuals with high muscle mass |
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Obesity |
Globally more women are obese than men. It has doubled since 1980 Factors influencing this disease: Genes (monogenic syndrome/susceptibility genes) and Environment (metabolic rate/exercise/food intake/culture) Causes: pregnancy, lack of sleep, medical condition, medications, lack of exercise Health risks: cancer, stroke, renal failure, hypertension, heart failure, sleep apnea |
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Control of food intake |
Homeostatic: defends well against energy deficit but not excess. Assymetrical system which allows for weight gain easier than it tolerates weight loss. Hedonic: mediated by reward pathways activated by palatable good, stimulates overconsumption based on sensory pleasure and reward rather than biological need |
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Hunger and Satiety cues |
1- Environmental factors 2- Gastrointestinal system 3- Metabolic factors 4- Central Nervous System |
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Environmental Influences on H&S |
- food availability - social variables - cultural/ethnic factors - sight and smell of food - taste |
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Cephalic Phase |
- Physiological responses initiated by the sight and smell of food (anticipatory salivation) - Prepares the digestive system for the onset of the meal - Receptors in the nose and mouth send olfactory and gustatory signals to the nucleus of the solitary tract in the medulla via the cranial nerves (olfactory, trigeminal, facial, glossopharmygeal, vagus) |
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Peripheral Physiological Signals |
1- Episodic signals: short term inputs generated by recent consumption (CCK, ghrelin) 2- Tonic factors: signals generated by the body's constant metabolic need for energy (leptin) |
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Cannon and Washburn's Hunger Experiment |
Swallowed balloon and told to push button when feeling hungry Hypothesis: hunger is caused by stomach contractions |
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Gut Hormones that Decrease Food Intake |
1- Cholecystokinin (CCK; duodenum) 2- Peptide tyrosine-tyrosine (PYY; colon/ileum) 3- Pancreatic polypeptide (PP, pancreas) 4- Glucagon-like peptide (GLP-1; colon) 5- Oxyntomodulin (OXM; colon) |
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Cholecytoskinin (CCK) |
- peptide hormone released from the duodenum in response to food intake - receptors found in gut and CNS - Causes the pylorus to constrict and decreases gastric contraction, inhibiting stomach emptying -information about CCK sent to brain via the vagus nerve by increasing the rate of firing of the vagal neurons - Treatment for obesity: repeated administration decreases meal size, but increases the meal frequency. Chronic administration decreases sensitivity of the receptors to the effects of CCK |
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Peptide Tyrosine-Tyrosine (PYY) |
- released from the intestines after a meal in amount proportional to the calories that were just ingested - Tmnt: continuous administration of PPY reduces body weight and adiposity - Evidence: KO mice for PYY ate more and gained more weight than wild-type mice. Treating PYY KO mice with PYY reversed increased food intake and BW |
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Ghrelin |
- hormone that increases food intake - secreted by stomach and small intestine - fasting associated with increases in ghrelin, while feeding is associated with decreases in ghrelin - Ghrelin receptors found in hypothalamus - Obese individuals do not experience a decrease in ghrelin after meals - Tmnt: injections of ghrelin increase food intake and BW. Gastric bypass decreases basal levels of ghrelin. |
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Prader-Willi Syndrome |
-Genetic defect on chromosome 15 leads to hypothalamic problems Symptoms: - decreased muscle tone, insatiable appetite (polyphagia), short stature, hypogonadism, mild mental retardation, increased basal levels of ghrelin. |
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Ghrelin mechanisms |
- Ghrelin from the stomach: inhibits the activity of the vagus nerve, reducing the discharge of NT in the brain - This in turn may cause the local release of ghrelin in the hypothalamus. Ghrelin stimulates appetite by increasing the activity of orexigenic neurons in the arcuate neucleus. |
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Leptin |
- Adiposity negative feedback signal - a hormone secreted by adipose tissues that decreases food intake and increases metabolic rate, by inhibiting NPY-secreting neurons in the arcuate nucleus - within the hypothalamus, leptin inhibits appetite stimulating neurons (NPY) and stimulates appetite inhibiting neurons (alpha-msh) -diminishes perception of food reward and enhances the response to satiety signals - Mutations in the gene encoding leptin (LEP) lead to an absence of leptin and extreme obesity - Both ghrelin and leptin target the arcuate nucleus, but ghrelin stimulates NPY and agouti and leptin surpress it. |
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ob/ob mouse |
- A strain of mice whose obesity is caused by a a mutation that decreases the ability to produce leptin -Symptoms: increased food intake, increased BW, decreased metabolic rate, decreased energy output |
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db/db mouse |
Mice with uncontrolled rise in blood sugar, severe depletion of insulin-producing beta cells and death by 10 months old. Impaired leptin receptors |
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Experiments with ob and db mice |
ob/ob x WT: obese mice loses weight and increases MR when paired with WT mice that produce leptin. db/db x WT: wild type mouse loses weight when pair with diabetic mouse indicating that the diabetic mouse produces excess leptin but does not respond to it. ob/ob x db/db: obese mice lose weight because their receptors use leptin produced by diabetic mice that db cannot use |
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Weigh loss & gain |
Weight loss --> leptin levels fall --> food intake up, temperature down, energy expenditure down, reproductive function down Weight gain --> leptin levels rise --> food intake down, energy expenditure up, sympathetic activity up |
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Orexigenic (increase food intake) peptides |
1- Neuropeptide Y 2- Melanin concentrating hormone 3- Orexin (hypocretin) 4- Agouti-related protein 5- Endocannabinoids |
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Anorectic (decrease food intake) peptides |
1- Cocaine and amphetamine-regulated transcript 2- alpha-MSH |
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Melanin Concentrating Hormone |
- Expressed in lateral hypothalamus - Administration of MCH increases food intake in satiated animals - Over-expression of MCH increases fat intake and BW.Food deprivation increases mRNA for MCH in lat. hypothalamus |
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Orexin (hypocretin) |
- expressed in lateral hypothalamus - administration of orexin increases food intake - restricting food intake increases mRNA for orexin - may play a role in relationship between eating and sleeping |
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Neuropeptide Y (NPY) |
- Neurons in the arcuate nucleus of the hypothalamus. Appetite regulation in the hypothalamus is controlled thru the NPY signalling pathway. - Ghrelin receptors are on the NPY neurons, NPY released in response to ghrelin stimulates apetite and increases BW -Food deprivation increases NPY - Eating decreases NPY -Glucoprivation activates NPY |
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alpha-MSH |
- stimulation of alpha-MSH decreases food intake - derived from pro-opiomelanocortin (POMC) - POMC is synthesized in arcuate nucleus - Neurons project to: brainstem, CCK, dopamine neurons in nucleus accumbens |
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Cocaine and Amphetamine reg. transcript (CART) |
- Cocaine and amphetamine increase levels of CART and decrease food intake - neurons located in the arcuate nucleus - administration of CART decreases food intake - injections of anti-CART antibodies increases food intake |
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Thrifty Gene Hypothesis |
- For most of human history, individuals have live with an inconsistent food supply (feast or famine). - Individuals who could store food within their bodies better during feasts could survive better during famines |
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Type II Diabetes |
-The stomach converts food to glucose and the rising glucose levels signals the pancreas to produce insulin. The body does not respond to insulin and glucose is prevented from entering the cells. The sugar builds up in blood vessels and creates a spike in a body's blood sugar level. - Symptoms: dehydration, hunger, numbness of hands and feet, fatigue, nausea |
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Yo-Yo Dieting |
1- Diet starts and there is an initial weight loss 2- Your metabolic rate lowers due to the lack of calories and your body burns less calories 3- Brain releases chemicals that tell the body to store fat, and your body enters famine mode 4- You reach your weight loss plateau and you become frustrated 5- Resume old eating habits but your MR is still slow so you gain more weight than you started with |
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Treatments for Obesity |
- reducing caloric intake - increasing physical activity - pharmacological - surgery |
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Phentermine |
- appetite suppressant pill intended for obese patients that are medical risk due to weight - is designed for short-term use with combination of exercise and healthy diet - phentermine works in the hypothalamus and stimulates adrenal glands to release norepinephrine, reducing hunger. |
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Orlistat |
- inhibits pancreatic lipase, an enzyme that breaks down triglycerides in the intestine. Triglycerides are prevented from being hydrolyzed into absorbable free fatty acids and are excreted undigested. - prevent absorption of 30% dietary fat - side effects: malabsorption of fat soluble vitamins |
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Lorcaserin |
- used for obese ppl with at least one weight-related health condition - Activates receptors in the hypothalamus that activate POMC production and therefore weight loss thru satiety |
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Contrave |
- super new weight loss drug for obese and overweight individuals - works probably by lessening appetite and curbing cravings |
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Maestro |
- subcutaneously implanted rechargeable neuroregulator and 2 electrodes that are implanted via surgery in the stomach - vagal blocking therapy (VBLOC): blocks transmission of messages involving food intake and processing between the brain and the stomach. Limiting expansion of stomach, reducing stomach contraction, decrease secretion of digestive enzymes. |
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Surgical Treatments |
- gastric bypass - stomach stapling |
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Adiposity Negative Feedback Signal |
- Circulating signals inform the brain of changes in body fat mass - In response to input from signals, brain mounts adaptive adjustments of energy balance to stabilize fat stores. - Criteria: peptide circulates in blood at levels proportional to body fat content and enter CNS in proportion to their plasma levels. Administration of peptide into CNS decreases food intake and vice versa |
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Learning and Types |
- Def: long-term changes in brain functioning and behavior as a consequence of experience - Types: 1. Perceptual- improvements in the ability to detect, discriminate and classify sensory stimuli of a particular category (wine) 2. Stimulus response- classical conditioning and instrumental conditioning 3. Motor: procedural |
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Memory and Types |
- Def: how the changes are stored and reactivated or retrieved - Types: 1. Procedural: non-declarative, skill memory (playing the piano) 2. Declarative: semantic memory (facts) and episodic memory (past event, autobiographic) |
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Procedural Memory |
- skills and procedures, "knowing how" - information is modality specific - preserved in amnesia - phylogenetically/developmentally early - inaccessible to conscious recollection - rely on cerebellum and striatum |
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Declarative Memory |
- facts, episodes and data "knowing that" - phylogenetically/developmentally late - impaired in amnesia - accessible to conscious recollection |
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Episodic memory |
Type of declarative memory that: - stores events - organized temporally -reported as remembrance - based on personal experience - affect is important - very susceptible to amnesia |
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Semantic memory |
Type of declarative memory that: - ideas and concepts - organized conceptually - reported as knowledge - affect is unimportant - kinda unsusceptible to amnesia |
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Formation of Explicit Memory |
1- Encoding: info for memory is assembled from different sensory systems 2- Consolidation: encoded memory info is converted into a form that can be permanently stored 3- Storage: deposition of memories into resting places (association cortex) 4- Retrieval |
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Stages/Model of Memory |
Incoming information --> sensory memory --> (thru selective attention) short term memory/working memory -->(coded for storage in LTM) Long term memory |
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Long-term potentiation (LTP) |
- underpinnings of memory -long-term increase in the magnitude of excitatory postsynaptic potential (EPSP) in postsynaptic neurons - persistent increase in synaptic strength as measured by EPSP in postsynaptic neuron - Morphological changes: increase in spine head volume, widening & shortening of spine neck, spine perforation, increase in number of spines - Mechanisms: increases the number of receptors for NT (AMPA), increases number of connections among neurons, increases production of NT |
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Associative LTP |
if a weak stimulus and a strong stimulus are applied at the same time, the synapses activated by the weak stimulus will be strengthened. |
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Summation LTP |
if axons are stimulated rapidly, the EPSPs produced by the terminal buttons will summate, and the postsynaptic membrane will depolarize enough for LTP to occur. If axons are sitmulated slowly, the EPSPs will not summate, and LTP will not occur. |
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NMDA receptor |
a specialized ionotropic glutamate receptor - When the postsynaptic membrane is at the resting potential, Mg blocks the ion channel, preventing calcium from entering. - When the membrane is depolarized sufficiently, the Mg ion is evicted. Thus the attachment of glutamate to the binding causes the ion channel to open, allowing Ca ions to enter the dendritic spine. |
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AMPA receptor |
-an ionotropic glutamate receptor that controls a sodium channel, when open it produces EPSPs. - When the conditions for LTP are met, calcium ions enter the dendritic spine through NMDA receptors. The calcium ions activate enzymes in the spine. The enzymes cause AMPA receptors to move into the spine. This increase in the AMPA receptors strengthens the synapse. |
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CREB |
- a protein that needs to be activated to strengthen the synapse permanently. - Inside the cell nucleus, CREB activates select genes causing them to be transcribed into mRNA versions that leave the nucleus. Cellular machinery translates mRNA into synapse-strengthening proteins that diffuse. |
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Steps for LTP |
1. NMDA receptor stimulated by glutamate in depolarized dendritic spine 2. Calcium enters cell 3. Activate calcium calmodin kinase II 4. Movement of AMPA receptors from base of dendritic spines to tips 5. Alteraion in synaptic structure 6. Growth of new dendritic spines 7. NO released by spines 8. Travels to presynaptic neuron and increases glutamate release |
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Factors modifying hippocampal functioning |
- exercise (high fats decrease memory and omega-3-fatty acids benefit cognitive function) - environmental enrichment -caloric restriction - nutrition -age |
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Brain-derived Neurotrophic Factor (BDNF) |
- neurotrophin - enhance survival and differentiation of neurons - protect against neurological disorders - neurotrophins can produce both rapid and enduring changes in synaptic efficacy - transgenic mice with decreased BDNF expression lose their ability to induce LTP and are impaired in learning a spatial memory task - replenishing depleted hippocampal BDNF with exogenous BDNF ameliorates deficits in learning and LTP. |
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BDNF and Exercise |
- voluntary exercise increases BNDF mRNA and protein in the hippocampus - Beneficial effects of exercise on cognition inhibited when BDNF activity is blocked in the hippocampus - Daily activity appears to elevate BDNF proteins more rapidly, although same levels are attained with alternating days. Remain elevated for several days after that too. - Exercise induces growth factor cascades and reduces peripheral risk factors for cognitive decline. |
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Aging and the Brain |
- decrease brain weight - decreased blood flow to brain - increased oxidative damage and free radicals - decreased growth factors - problems with neurotransmission - decrease dopamine/serotonin receptors and synthesis - age-related decline in glutamate especially in cerebral cortex and hippocampus - impairments in LTP due to decreased NMDA receptors, drug that enhance NMDA improve LTP in aged animals - diets: strawberries, blueberries, spinach |
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Morris Water Maze |
- typical age-related loss of spatial memory seen in old rats - environmental cues present in the room provide info that permits the animals to orient themselves in space. Start positions are variable or fixed depending on the task. The rat is supposed to hide the hidden platform inside the pool. |
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Hebbian Theory |
If a synapse repeatedly becomes active at about the same time that the postsynaptic neuron fires, changes will take places in the structure or chemistry of the synapse that will strengthen it |
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Blackout |
- can result from the intake of any substance in which long term memory creation is impaired, therefore causing a complete inability to recall the past. - "en bloc" blackout: inability to later recall any memories from the intoxication period, even when prompted, can carry out conversations - "fragmentary" blackout: having the ability to recall certain events from intoxicated period, and yet being unaware that other memories are missing until reminded of the existence of those gaps in the memory |
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Alcohol and Memory |
- Alcohol primarily interfere with the transfer of information from short-term to long-term storage -alcohol impairs episodic encoding - large amount of alcohol block LTP in rat brains - alcohol stimulates GABA receptors and inhibits NMDA receptors by inhibiting ion current by glutamate |
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Blueberries |
Decreased LTP in brains of older rats supplementation with blueberries reversed age-related deficit in LTP |
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Hyperthymesia |
a condition where you possess an extremely detailed autobiographical memory |
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Retrograde amnesia |
inability to recall past events |
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Anterograde amnesia |
inability to recall future events |
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HM |
- ability to retain information for a short-time was preserved - linguistic comprehension remained, but difficulty interpreting ambiguous sentences - vividly remembered childhood but was unable to encode long-term episodic memory - did not recognize himself in mirror - mirror drawing task: HM improved with repeated training, procedural memory is intact, but he cannot recall ever performing task before - Conclusions: hippocampus is not the location of LT memories, nor necessary for their retrieval/ hippocampus is involved in consolidating immediate memories into LT memories |
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KC |
- lost both hippocampi in motorcycle accident - could remember semantic info - could not remember episodic info - Brain scans revealed that hippocampus helps access personal memories, but brain seems to use parahippocampus for semantic memories |
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Korsakoff's syndrome |
- memory impairment caused by thiamine deficiency as a result of chronic alcoholism - Vitamine B1 (thiamine) helps the body convert food into energy, and aids the function of the heart and cardiovascular system and nervous system. Korsakoff's syndrome is a memory deficiency cause by lack of thiamine. - Damage occurs in mammillary bodies and basal frontal lobes which produces anterograde amnesia. - Alcoholics: enlarged corpus callosum and ventricles - Confabulation |
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Wernicke-Korsakoff's Syndrome |
- Wernicke's encephalopathy develops first - Evidence of malnutrition, involuntary jerky movements, poor balance, disorientation - difficulty in acquiring new info, learning new skills, change in personality, confabulation -Permanent brain damage may result if not treated. - Tmnt: thiamine |
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Dementia |
- the progressive decline in cognitive function due to damage or disease in the brain beyond what might be expected from normal aging -Symptoms: loss of memory, judgment and reasoning, change in mood and behavior, |
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Vascular dementia |
- decrease in cognitive abilities as a function on decrease blood flow to the brain (stroke) - changes in cognition occur rapidly - may coexist with AD - impaired on executive function (frontal lobe tasks) - Symptoms: nighttime wandering, depression, incontinence, one-sided body weakness, confusion, disorientation, trouble speaking, decreased ability to pay attention - Risk factors: age, prior heart attacks, HBP, obesity, diabetes, smoking, sedentary lifestyle |
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Lewy Bodies Dementia |
- Lewy bodies are accumulated bits of alpha-synuclein inside the nuclei nerve cells causing them to work less effectively and eventually die - lewy body accumulation is also linked to PD - Symptoms: fluctuating cognition, recurrent complex visual hallucinations, REM sleep disorder, spontaneous features of PD, sensitivity to neuroleptic drugs |
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Frontal Temporal Dementia |
- Genes are related - several disorders that affect the frontal and temporal lobes of the brain and cause brain to lose brain cell function. - progressive behavior/personality decline (apathy, compulsive eating, social disinhibition) - progressive language decline (aphasia, dysarthria) - progressive motor decline (tremor, gait, muscle rigidity) |
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Alzheimer's Disease |
Symptoms: - memory loss, difficulty performing familiar tasks, problems with language, disorientation in time and place, poor judgment, misplacing things, changes in mood, loss of initiative Hallmarks: - Beta-amyloid plaques (dense deposits of protein that accumulate outside and around nerve cells) - Neurofibrillary tangles (twisted fibers that build up inside the nerve cell) - Cerebral cortex (affected areas) shrink Risks: -Age, genetics, diabete, down's syndrome, HBP, sedentary life style |
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Beta-amyloid plaques/Amyloid hypothesis |
- Amyloid precursor protein (APP) is the precursor to amyloid plaque - APP sticks through the neuron membrane - Enzymes cut APP into fragments of proteins - Beta-amyloid fragments come together in clumps to form plaques - Affect hippocampus and other areas of cerebral cortex |
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Tau |
neurons have an internal support structure made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes, causing microtubules to collapse, and tau proteins clump together to form neurofibrillary tangles |
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Early onset AD |
rare, usually affecting people 30-60 and running in families. researchers have identified mutations in three genes that causes early-onset AD |
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Late onset AD |
more common, usually affect people over 65, researchers have identified a gene that produces a protein called apolipoprotein which is believed to be involved in the formation of beta-amyloid plaques |
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Major Cholinergic Changes in AD |
- Depletion of acetylcholine, especially in moderate to severe disease strategies - Decline in ChAT activity - Loss of cholinergic neurons (both nicotonic and muscarinic receptors) |
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Treatment of AD |
1. Donepezil (side effect: nausea, vomiting) 2. Galantamine (same) 3. Memantine (headache,constipation) 4. Tacrine (liver damage, nausea) |
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Omega-3-Fatty-Acids and AD |
- Decrease in Omega-3s in brains of individuals with AD -fish intake and cognitive behavior correlated |
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Hemorrhagic stroke |
- weakened/disease blood vessels rupture - blood leaks into brain tissue |
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Ischemic stroke |
- blood clots stop the flow of blood to an area of the brain - 87% of strokes - Without oxygen and glucose, neurons begin to depolarize. The neurons reach threshold and produce a barrage of AP. APs release glutamate and the NT is not reabsorbed. Excess Ca and Zn enter cell with APs and they trigger cell death. |
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Treatment for Strokes |
1-Thromobolytics: dissolve blood clots 2- Drugs that inhibit sodium channel may reduce APs generated 3- Drugs that block glutamate receptors may combat excessive stimulation 4-Drugs that block calcium channels may avert the intracellular buildup of Ca 5- Dripping tPA directly on clot thru a catheter on femoral artery |
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Stroke symptoms |
- sudden numbness or weakness of the face, arm, leg - sudden confusion, trouble speaking or understanding - sudden trouble seeing in one or both eyes - sudden trouble walking, dizziness, loss of balance - sudden, severe headache |
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Non fluent aphasia / Broca's aphasia |
-there are difficulties in articulating but relatively good auditory verbal communication - expressive aphasia, non fluent speech, omits function words, good comprehension, mispronunciation - Patient was only able to speak with the syllable 'tan', brain showed damaged to left ventral frontal lobe (speech production) - area 44 (phonological processing) and area 45 (selecting and manipulating semantic elements) |
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Fluent aphasia/ Wernicke's aphasia |
-fluent speech but difficulties either in auditory verbal comprehension or in the repetition of words, phrases can speak normally but what the person is saying makes no sense |
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Pure aphasia |
there are selective impairments in reading, writing, or recognition of words (agraphia, alexia) |
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PKU |
-disease that arises from the absence of a single enzyme (phenylalanine hydroxylase). -This enzyme converts phenyalanine to tyrosine. Failure to carry out conversion leads to build up of phenylalanine which is toxic to the CNS. Not everyone has same level of deficiency (autosomal recessive inheritance). ---Diet that is high in phenyalanine is the treatment. -Effects: mental retardation, infantile irritability, seizures, peculiar stance and sitting posture, pale pigmentation, dry skin |
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Capgras Syndrome |
condition where individuals suffer from defective detection due to malfunctioning of are in the brain responsible for face processing. Belief that loved ones have been replaced by impostors. |
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Methylmercury poisoning |
- Coal burning and mining of iron can contaminate water resources with MM which is later absorbed in bodies of fish Symptoms: gait disturbance, loss of balance, disturbance of sensation, muscle weakness, hearing disturbance, sight disturbance to peripheral areas, dementia - Exposure to this chemical in the womb, resulting from the mother's consumption of fish, can adversely affect baby's growing brain and NS |
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Prosapagnosia |
cognitive disorder of face perception where ability to recognize familiar faces is impaired can be caused by posterior cerebral artery infarcts almost always in the right hemisphere |
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Symptoms of schizophrenia |
1- Positive symptoms: thought disorders, dellusions, hallucinations, irrational thinking, bizarre behaviors 2- Negative symptoms: flattened affect, lack of initiative, poverty of speech, social withdrawal 3- Cognitive symptoms: difficulty with attention, poor abstract thinking, impaired working memory, eye tracking dsyfunction, hypofrontality |
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Physical abnormalities associated with Schizo. |
- head circumference is outside normal range - wide set eyes - low seated ears - furrowed tongue - curved 5th finger - third toe longer than second toe |
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Structural Schizo. Brain Changes |
- brain decreases size - enlargement of cerebral ventricles - limbic system abnormalities (smaller hippocampus and amygdala) - reduction in frontal lobe volume and activation |
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Risk Factors for Schizophrenia |
- Maternal infections during 2nd and 3rd trimester - nutriotional deficiencies - maternal stress during pregnancy - birth complications - increased parental age - birth in winter and early spring (sunlight exposure, vit D deficiency) |
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Treatment for Schizophrenia |
Antipsychotic (neuroleptic) meds: decrease activity of dopamine pathways in brain - Chloropromazine - Halperiodol Side effects: - Parkinsonian syndrome (resting tremor, rigidity, dampened facial expression) / sense of anxiety and restlessness (akathesia)/sudden and severe spasms (dystonia)/ drowsiness/dry mouth/ weight gain/ rapid heartbeat/low BP |
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Dopamine Hypothesis |
- antipsychotic drugs like chloropromazine blocks dopamine receptors and reduce schizo symptoms (long term usage develop PD symptoms) - L-DOPA increases dopamine levels and can produce many schizo symptoms - amphetamine psychosis resemble schizophrenia and makes it worse - Problems: many patients do not respond to neuroleptics, intolerable side effects, studies show mixed results |
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Tardive dyskinesia |
- involuntary movements (rolling movements of tongue, smacking lips, twisting and sudden jerking movements) - occurs in patients taking antipsychotics - more prevalent in older individuals - caused by upregulation of receptors in dopamine pathway |
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Clozapine |
atypical antipsychotic acts on a variety of NTs including dopamine, serotonin, norepinephrine, acetylcholine decreases severity of positive and negative symptoms few motor sides effect Side effects: decrease in WBCs (agranulocytosis), weight gain, diabetes, seizure risk, costly |
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Angel Dust (PCP) and Schizophrenia |
- PCP induces symptoms that resemble positive symptoms and negative manifestation of schizophrenia - In normal individuals causes: difficulty to think abstractly, learning new info, hallucinations, delusions -Replicate the molecular disturbance in the brains of schizos, block NMDA receptor which participates in regulating dopamine release |
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Glutamate Hypothesis |
- non competitive NMDA receptor antagonists (like PCP and ketamine) induce both positive and negative symptoms of schizo - unmedicated schizo patients are more sensitive to the effects of NMDA receptor antagonists - adjunctive treatment with NMDA agonists may provide a modest improvement in symptoms |
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Hypofrontality and Schizophrenia |
- Negative symptoms of schizo may be associated with decreased activity in the dorsolateral prefrontal cortex - Schizos do poorly on neuropsychological tests that are sensitive to prefrontal damage |
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Affective Disorders |
1. Major Depression (reactive, endogenous, seasonal affective) 2. Bipolar Disorder |
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Depression |
-Symptoms: persistent sad, anxious or empty mood/feelings of hopelessness/feelings of guilt/ loss of interest in activities/decreased energy or fatigue/ difficulty concentrating/changes in food intake/ suicidal thoughts - Affected brain areas: frontal & temporal lobes, parts of limbic system (cingulate gyrus) -Tmnt: meds and exercise |
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Medications for Depression |
1. Monoamine oxidase inhibitors 2. Tricyclic antidepressants 3. Selective serotonin reuptake inhibitors 4. Serotonin Norepinephrine reuptake inhibitors |
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MAO inhibitors |
- inhibit the enzyme monoamine oxidase which breaks down serotonin, norepinephrine and dopamine - MAO inhibitors inhibit breakdown tyramine which can lead to increased blood pressure and heart failure |
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Tricyclic Antidepressants |
- inhibit reuptake of serotonin and norepinephrine -3 to 6 weeks for full effect -side effects: constipation, blurred vision, sedation, nausea, photosensitivity, weight gain, dry mouth |
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Selective Serotonin Reuptake Inhibitors |
- Fluozetine (Prozac) / Paroxetine (Paxil)/ Setraline (Zoloft)/ Fluvoxamine (Luvox) - blocks normal reuptake of NT serotonin, excess serotonin in synapse enhances its mood-lifting effect |
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Serotonin-norepinephrine reuptake inhibitors |
- slightly greater efficacy and fewer side effects than SSRIs - Effexor and Cymbalta - Mechanisms of action and side effects are similar to SSRIs but with higher rates of suicide |
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Electroconvulsive Therapy |
-involves applying a brief electrical pulse to the scalp while the patient is under anesthesia. this pulse excites the brain cells causing them to fire in unison and produces a seizure -works more quickly than antidepressant meds -useful for individuals who are suicidal or for whom other treatments have not workerd - side effects: headaches, nausea, muscle aches, memory loss (ST memory loss during time of tmnt and permanent memory loss) |
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Deep Brain Stimulation |
uses surgically placed electrodes (subcallosal cingulate) to send an electric current thru neural circuits. These circuits do no function properly in people suffering from major depression. The therapy has yet to be approved for routine medical use. It can somtimes correct signalling impairments and thereby dissipate feelings of hopelessness and lack of pleasure. |
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Monoamine Theory of Depression |
- Depression is associated with a decrease in the activity of the monoamine NTs, serotonin and norepinephrine - Drugs which decrease serotonin and norepinephrine may lead to depression - Drugs used in the tmnt of depression increase serotonin and norepi |
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BDNF and stress |
- Stress decreases the expression genes that make neurotrophic factors that are critical to the survival and function of neurons - Decreased BDNF levels lead to neuronal atrophy and self-pruning - reduction in dendritiv arborization |
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Forced Swimming Test |
- animal model of depression - measures a rodent's response to threat of drowning and used to assess antidepressant efficacy |
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Neurogenesis and Depression |
- Neurogenesis is necessary for antidepressant effects - BDNF has antidepressant like effects in animal models of depression - Behavioral effects of antidepressants are eliminated in BDNF-deficient mice - Levels of BDNF increased in brains of depressed individuals who were treated with antidepressants |
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Neurotrophin Hypothesis of Depression |
- Decreases in hippocampal BDNF are correlated with stress-induced depressive behaviors -Antidepressant tmnt enhances the expression of BDNF |
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Bipolar Disorder |
- Bipolar I Disorder : recurrent episodes of mania and depression - Bipolar II Disorder: Milder episodes of hypomania that alternate with depression - Rapidly cycling BD: 4 or more episodes occur within a year Typically develops in late adolescence or early adulthood and has a strong genetic predisposition |
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Bipolar Disorder Symptoms |
- Inflated self-esteem, feelings of grandiosity - decreased need for sleep - more talkative than usual - flight of ideas - distractibility - psychomotor agitation - excessive involvement in activities that have a high potential for painful outcomes |
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Lithium |
- first mood stabilizing medication for mania - low therapeutic index (there is little difference between an effective dose and an overdose) - Side effects: reduced appetite, nausea, hair loss, acne, tremors, weight gain, fatigue, seizures, memory problems, confusion, coma - Compliance with treatment is low because of positive aspects of manic periods |
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Anticonvulsants for BP |
- may help stabilize mood - may be used in conjunction with lithium or antidepressants - manic episodes are associated with an increase in norepinephrine and depression with a decrease in norepinephrine |
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Addiction |
-primary chronic disease of brain reward, motivation and memory -characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of siginificant problems with one's behavior and interpersonal relationships and a dsyfunctional emotional response. -involves cycles of relapse and remission |
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Substance Use Disorder |
Symptoms: impaired control, social impairment, risky use, pharmacological criteria Signs: tolerance, obsession, increase intake, loss of control, abuse despite harm, withdrawal symptoms |
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Drug Tolerance |
-a need for markedly increased amounts of the substance to achieve intoxication or desired effect -a markedly diminished effect with continued use of the same amount of the substance -cross tolerance: development of tolerance to one drug decreases the effectiveness of a second drug |
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Psychoactive Drugs |
1. Sedatives and antianxiety drugs (valium, alcohol) 2. Antipsychotic agents (chlorpromazine) 3. Antidepressants (MAO, tricyclics) 4. Mood stabilizers (Li) 5. Narcotics (heroin, morphine) 6. Stimulants (cocaine, amphetamine, caffein) 7. Psychedelics and hallucinogens |
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Controlled Substances |
Schedule 1: high potential for abuse, no medical use (marijuana, heroin, ectasy) Schedule 2: high potential for abuse, medical use (cocaine, ritalin) Schedule 3-5 |
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Drug Administration (fastest acting order) |
1. Intravenous 2. Intranasal 3. Oral 4. Smoked |
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Rewarding Effect of Addictive Agents |
- the more immediate the reward, the more addictive the agent (heroin vs morphine, crack cocaine vs oral cocaine) - drugs of abuse activate the medical prefrontal cortex and nucleus accumbens |
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Chronic tolerance |
1. Drug dispositional tolerance: chronic alcohol use increases alcohol dehydorgenase leading to more rapid metabolism of alcohol 2. Pharmacodynamic tolerance: neurons adapt to the continue presence of alcohol by making compensatory changes such as decrease receptors 3. Behavioral tolerance: individuals adjust their behaviors when they have learned the effects of alcohol |
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Withdrawal symptoms |
Vary with each drug - Psychological: anxiety, restlessness, irritability, insomnia, headaches - Physical: sweating, heart palpitations, muscle tension, tightness in the chest, tremors, nausea, vomiting |
