Biopsych unit 3 PDF

Preview

Summary

Dr. Vincent Markowski...

Description

biopsych unit 3 markowski 

11/01/2016

Parkinson’s disease: progressive loss of dopamine-producing neurons  Behavioral symptoms: key symptoms are motor based, perhaps some attention deficits, maybe some depression; muscle rigidity, tremors, continual and involuntary shifts in position and posture, motor movements that are deployed are slow, gait (shuffle with forward stoop) (greater risk for falls), o Diseased brain regions: substantia nigra and amygdala (all involved in regulating voluntary motor behaviors)  Substantia nigra: headquarters or source of nigrostriatal pathway  Pathway provides input to the basal ganglia o Normal role of basal ganglia is to organize/refine movement  Movements are refined by inhibiting inappropriate options, synchronizing the output of the cortex 

Efferent connections: loop back to cortex and also out spinal cord.



Nigrostriatal destruction -> excessive inhibition of other motor regions o Possible causes: genetic predisposition, drug and/or environmental toxicant exposure (cumulative effect) o MPTP and the “Frozen Addicts”  People trying to synthesize heroin, created a drug (similar to Demerol) that caused Parkinson’s disease in young drug users.  MPTP contaminated drug, reactions caused decrease in dopamine neurons  MPTP -> MPP+ -> Parkinson’s 

Pharmacological treatments; o L-DOPA: crosses blood brain barrier, around dead dopamine systems, provides source of dopamine o MAO inhibitors: Monoamine oxidase inhibitors; prevents degradation monoamines, boosts dopamine  Monoamine oxidase B = worst one. o Individualized combination of the above o Neurosurgery



Deep brain stimulation of the subthalamic nucleus vs. lesions of the internal globus pallidus (younger people only; old people can’t handle it)



Stem cell therapy vs. fetal tissue transplants.

  

Eating behavior Overview of digestive system  Saliva -> carbohydrate metabolism  

Stomach -> Protein metabolism, meal storage Small intestine -> Completion of protein, carbohydrate, fat metabolism; cross from gastrointestinal to circulatory; absorption into bloodstream o Duodenum: first 6-8 inches of small intestine



Pancreas -> produces hormones that affect liver o Insulin (active with too much blood sugar): moves recently obtained glucose into cells so it can be utilized o Glucagon (active with too little blood sugar): releases stored glucose and free fatty acids o Absorptive phase: when food is ingested; “head phase” is when thinking about food releases insulin o Short term reservoir: stores glucose in liver; glucose is converted into glycogen via insulin. o Glucagon is high in “fasting” phase; pulls glycogen out of liver, converts it back to glucose, o Our long term reservoir consists of adipose tissue (fat).  Triglycerides: part of long-term reservoir; 

Glycerol:a substance (glycerine) derived from the breakdown of triglycerides, along with fatty acids; can be converted by the liver into glucose.



Speaking theoretically: why do we eat? o Set-point theories: have 3 main components: set point (ideal level of energy), figure out how close one is to ideal level, effector system to figure out how to fix problem.  Physiological deficit:

 

None of the theories explain obesity Have difficulty meal onset or offset. o Positive-incentive theories of food value  Anticipated pleasure (especially for foods high in carbohydrates and lipids  Cafeteria diet and sensory-specific satiety  Appetizer effect o Peripheral factors regulating food intake  Taste; bitter taste=avoid, sweet taste=consume, etc.  Mastication (chewing) 

Stomach distention: Abdominal distension occurs when substances, such as air (gas) or fluid, accumulate in the abdomen causing its outward expansion beyond the normal girth of the stomach and waist; “feeling bloated”



Contents of small intestine:  CCK released by high fat concentration (one example of a range of neuropeptides that have to do with satiety.



Liver hepatocytes monitor blood levels of glucose and lipids  If liver senses drop in glucose levels, feeling of hunger increases.



Brain structures regulating food intake and body weight set point o Lateral hypothalamus: stimulation and lesion studies  LH cell bodies produce and release melaninconcentrating hormone and orexin (post food fatigue from orexin)   

LH cell bodies -> nucleus of the solitary tract LH cell bodies -> dopamine neurons LH cell bodies -> forebrain motor system



LH cell bodies -> pancreatic insulin

o Ventromedial hypothalamus: stimulation and lesion studies:  Meal size, frequency, and content  Ascending norepinephrine pathway o Paraventricular nucleus: effects of stimulating PVN are similar to stimulating ventromedial: voracious eating o Eating disorders can cause change in brain function 

Neurotransmitters, hormones, and food intake o Leptin: provides feedback loop regarding body fat levels  Investigations with genetically altered mice: hyperphagic eaters, gained adipose.   

Humans may become insensitive to leptin. Leptin regulates other behaviors



KNOW ABOUT THE OB MOUSE, know that it’s different, but weight is not controlled by a single gene!



Both genes and environmental factors are involved in ALL of our body weight set points

In normal animals, body weight is not controlled by a single gene.



An important environmental factor for Americans = inexpensive, high calorie, readily available foods o Neuropeptide Y: inhibitory neurotransmitter released in the Pareventricular nucleus  Leptin inhibits neuropeptide Y    

Hormones and Behavior (read ALL of chapter 13) MAMAWAwA: men are men, women are women assumption Hormones: chemical communicators released into the bloodstream  They support chronic or long-term bodily processes

 

They are secreted by the hypothalamus and endocrine glands Mechanisms at the cellular level: o Bind to a membrane receptor OR o Bind to an intracellular receptor AND affect gene expression

 

Steroids (sex hormones) bind to intracellular receptors. The Hypothalamus and Feedback Loops  How are hormones in bloodstream controlled? Feedback loops  Involve hypothalamus, pituitary gland (interconnected system with hypothalamus), “target organs.” 321 in textbook.  General descriptions: hypothalamus/posterior pituitary -> vasopressin or oxytocin -> behavioral roles o Vasopressin: regulates perception of thirst; from pituitary to kidneys o Hypothalamus/ “releasing” hormones -> anterior pituitary/ “stimulating” hormones -> target gland/hormone -> feedback to hypothalamus



Example of a neuroendocrine feedback loop to regulate the function of adult female reproductive organs o In humans, this is a 28 day series of events o (begins with hypothalamus Gonadotropin Releasing hormone (GnRH) -> (from pituitary) follicle-stimulating hormone (FSH) and lutenizing hormone (LH) -> FSH interacts with cells of the follicle -> follicle produces, releases more estradiol -> LH peak, FSH, estradiol stimulates ovulation -> corpus luteum produces, releases progesterone (thickens uterine wall)-> fertilization? o The menstrual cycle is an example of an “activational” effect. o Manipulating the menstrual cycle with the birth control pill: lower levels of estrogen in pill prevent pituitary gland from releasing LH. With no LH present, egg does not mature and ovulation does not occur.

 

READ ABOUT EFFECTS OF STEROIDS

Hormones acting during critical periods: organizational effects (permanent)  Male and female embryos are similar until SRY gene is activated o SRY gene is on the Y chromosome

o SRY gene causes primitive gonad to produce testosterone (T)  SRY gene without SRY protein = intersex individuals o T leads to testes development – stimulates Wolffian ducts (turn into genitalia) o T (parent hormone) -> DHT (dihydro testosterone) -> male external genitalia o 5 alpha reductase: helps convert T to DHT o Organizes various regions of brain and spinal cord o In females, Mullerian ducts are not inhibited and primitive gonad automatically develops into ovaries (hormone -> Mullerian ducts degenerate) (“all females by default”) 

If steps 1-3 are disrupted, female structures/traits might develop (to some degree) in an XY individual



If step 4 is disrupted, male structures/traits might develop (to some degree) in a XX individual (i.e. diethylstilbestrol; thing in the 1940s through 60s that women could ingest to supposedly have healthier babies; caused rare form of cervical cancer in young women; behavioral effects, too, made girls more “tomboyish; high levels of bisexuality as well)



Sexually-differentiated brain structures  Males: circulating T crosses neuronal membrane -> conversion to estradiol -> receptor binding -> neuronal characteristics are altered o Occurs in hypothalamus and probably other regions as well o Testosterone is source for estrogen o Aromatization: the process by which the body converts anabolic steroids and/or testosterone into estrogen. o o o o Females: circulating estradiol does not masculinize hypothalamus during development  VMH and sexual behavior

 

Focus on: All sets of reproductive tissues, minus brain



Hormones vs neurotransmitters

  

Masculinization or not Lack of predictability Chapter 13 until 3.23

     

Presentation 1: Endocrine and energetic mediation of play behavior in free-living Belding’s ground squirrels  Purpose of study: to evaluate endocrine and energetic mediation of social play behavior through hormone and food manipulation, to determine whether testosterone injections increase sexual play behavior in females 

Experimental hypotheses: Newborn females treated with testosterone at birth should later exhibit play behaviors more closely resembling that of males than that of control females, Patterns of play among testosterone treated, provisioned females should resemble those of provisioned males, but differ from those of unprovisioned males, unprovisioned testosterone treated females, and control females



Both endocrine and energetic manipulation had no significant effect on the timing of play behavior.



T-treatment had no effect on play fighting, but increased rates of sexual play behavior in females to levels similar of juvenile males.



Food provisioning (energetic manipulation) increased rates of play among males and females in all conditions, suggesting that energy mediates play behavior.

 

Presentation 2: mapping phantom movement representations in the motor cortex of amputees  Wanted to test the belief that the motor region still maintains its same

function despite cortical reorganization following amputation  Artificially induce phantom hand movements?  

Phantom sensation related to stump muscles> 3 participants



TMS: transcranial magnetic stimulation maps muscle representation of two muscles  Results: phantom digit movements concentrated in motor cortex, not sensory cortex  Phantom limb sensations are a result of misinterpreting muscle movements, not the activation of hand movement in motor cortex   Presentation 3: words in melody; and H2^15O PET study of brain

activity during singing and speaking  Lateralization of cerebral function: identifies left/right brain hemispheres, each have own maximum capacity to perform specific skilled behaviors.  Fun fact: many stutterers can sing  

Gaussian filter: smoothes/blurs scanned images to rid of detail/noise…

 

Presentation 4: PTSD: inflammation in prefrontal cortex (PFC) and hippocampus (HC)

 

Imbalance of neurotransmitters. Blueberries: contain anthocyanins that are associated with antiinflammatory and antioxidant characteristics  SSRIs don’t always work.  Hypothesis: blueberry-enriched diet would reduce inflammation  Elevated plus maze: half enclosed, half open  ANOVA test utilized     

Blueberry group had less inflammation

 

Absorbative Fasting

3 phases of eating: Sophalic

11/01/2016 

11/01/2016 ...