Depression has been linked to problems or imbalances in the brain, specifically with regard to the neurotransmitters serotonin, norepinephrine, and dopamine. The evidence is somewhat indirect on these points because it is very difficult to actually measure the level of neurotransmitter in a person’s brain. What we do know is that antidepressant medications (used to treat the symptoms of depression) are known to act upon these particular neurotransmitters and their receptors.
This powerpoint presentation was put together by Jordan Greenbaum, M.D., Children's Healthcare of Atlanta and presented on June 14th as part of our GA-CAN! Community Conversation on Timeout, Restraint and Spanking.
Book Review: Spark the Revolutionary New Science of Exercise and the BrainPatrick Moran
Fitness and Holistic Health expert, Patrick Moran presents an overview covering the book, Spark: The Revolutionary New Science of Exercise and The Brain
Depression has been linked to problems or imbalances in the brain, specifically with regard to the neurotransmitters serotonin, norepinephrine, and dopamine. The evidence is somewhat indirect on these points because it is very difficult to actually measure the level of neurotransmitter in a person’s brain. What we do know is that antidepressant medications (used to treat the symptoms of depression) are known to act upon these particular neurotransmitters and their receptors.
This powerpoint presentation was put together by Jordan Greenbaum, M.D., Children's Healthcare of Atlanta and presented on June 14th as part of our GA-CAN! Community Conversation on Timeout, Restraint and Spanking.
Book Review: Spark the Revolutionary New Science of Exercise and the BrainPatrick Moran
Fitness and Holistic Health expert, Patrick Moran presents an overview covering the book, Spark: The Revolutionary New Science of Exercise and The Brain
Anatomical localisation of function is a fundamental principle in the neurosciences. This presentation highlights the basics neuroanatomy and correlate major brain structure with their functions.
#36417 Topic Discussion 3Number of Pages 1 (Double Spaced).docxAASTHA76
#36417 Topic: Discussion 3
Number of Pages: 1 (Double Spaced)
Number of sources: 1
Writing Style: APA
Type of document: Essay
Academic Level:Master
Category: Psychology
Language Style: English (U.S.)
Order Instructions:
I will upload the instruction
Module Chapter 5 wk6 p630
chapter 5 Methods and Strategies of Research
Outline
· ■ Experimental Ablation
Evaluating the Behavioral Effects of Brain Damage
Producing Brain Lesions
Stereotaxic Surgery
Histological Methods
Tracing Neural Connections
Studying the Structure of the Living Human Brain
Section Summary
· ■ Recording and Stimulating Neural Activity
Recording Neural Activity
Recording the Brain’s Metabolic and Synaptic Activity
Stimulating Neural Activity
Section Summary
· ■ Neurochemical Methods
Finding Neurons That Produce Particular Neurochemicals
Localizing Particular Receptors
Measuring Chemicals Secreted in the Brain
Section Summary
· ■ Genetic Methods
Twin Studies
Adoption Studies
Genomic Studies
Targeted Mutations
Antisense Oligonucleotides
Section Summary
In July 1982, several young people began showing up at neurology clinics in northern California displaying dramatic, severe symptoms (Langston et al., 1983). The most severely affected patients were almost totally paralyzed. They were unable to speak intelligibly, they drooled constantly, and their eyes were open with a fixed stare. Others, less severely affected, walked with a slow, shuffling gait and moved slowly and with great difficulty. The symptoms looked like those of Parkinson’s disease, but that disorder has a very gradual onset. In addition, it rarely strikes people before late middle age, and the patients were all in their twenties or early thirties.
The common factor linking these patients was intravenous drug use; all of them had been taking a “new heroin,” a synthetic opiate related to meperidine (Demerol). Some detective work revealed that the illicit drug was contaminated with MPTP, a toxic chemical that damaged dopaminergic neurons and caused the neurological symptoms. Because the symptoms looked like those of Parkinson’s disease, the patients were given L-DOPA, the drug that is used to treat this disease, and they all showed significant improvement in their symptoms. Unfortunately, the improvement was temporary; the drug lost its effectiveness.
Fetal transplantation, an experimental neurosurgical method of treating parkinsonism, has shown some promise. The rationale for the procedure is this: The symptoms of parkinsonism, whether from Parkinson’s disease or the toxic effects of MPTP, are caused by the lack of dopamine in the caudate nucleus and putamen. There is at present no way to induce the brain to grow new dopaminergic neurons. However, if dopamine-secreting neurons can be introduced into the caudate nucleus and putamen and if they survive and secrete dopamine, then perhaps the parkinsonian symptoms will diminish. Because the implanted neurons must be healthy and vigorous and not trigger the.
#36421 Topic Discussion 7Number of Pages 1 (Double Spaced).docxAASTHA76
#36421 Topic: Discussion 7
Number of Pages: 1 (Double Spaced)
Number of sources: 1
Writing Style: APA
Type of document: Essay
Academic Level:Master
Category: Psychology
Language Style: English (U.S.)
Order Instructions: ATTACHED
I will upload the instruction
Module Chapter 5 wk6 p630
chapter 5 Methods and Strategies of Research
Outline
· ■ Experimental Ablation
Evaluating the Behavioral Effects of Brain Damage
Producing Brain Lesions
Stereotaxic Surgery
Histological Methods
Tracing Neural Connections
Studying the Structure of the Living Human Brain
Section Summary
· ■ Recording and Stimulating Neural Activity
Recording Neural Activity
Recording the Brain’s Metabolic and Synaptic Activity
Stimulating Neural Activity
Section Summary
· ■ Neurochemical Methods
Finding Neurons That Produce Particular Neurochemicals
Localizing Particular Receptors
Measuring Chemicals Secreted in the Brain
Section Summary
· ■ Genetic Methods
Twin Studies
Adoption Studies
Genomic Studies
Targeted Mutations
Antisense Oligonucleotides
Section Summary
In July 1982, several young people began showing up at neurology clinics in northern California displaying dramatic, severe symptoms (Langston et al., 1983). The most severely affected patients were almost totally paralyzed. They were unable to speak intelligibly, they drooled constantly, and their eyes were open with a fixed stare. Others, less severely affected, walked with a slow, shuffling gait and moved slowly and with great difficulty. The symptoms looked like those of Parkinson’s disease, but that disorder has a very gradual onset. In addition, it rarely strikes people before late middle age, and the patients were all in their twenties or early thirties.
The common factor linking these patients was intravenous drug use; all of them had been taking a “new heroin,” a synthetic opiate related to meperidine (Demerol). Some detective work revealed that the illicit drug was contaminated with MPTP, a toxic chemical that damaged dopaminergic neurons and caused the neurological symptoms. Because the symptoms looked like those of Parkinson’s disease, the patients were given L-DOPA, the drug that is used to treat this disease, and they all showed significant improvement in their symptoms. Unfortunately, the improvement was temporary; the drug lost its effectiveness.
Fetal transplantation, an experimental neurosurgical method of treating parkinsonism, has shown some promise. The rationale for the procedure is this: The symptoms of parkinsonism, whether from Parkinson’s disease or the toxic effects of MPTP, are caused by the lack of dopamine in the caudate nucleus and putamen. There is at present no way to induce the brain to grow new dopaminergic neurons. However, if dopamine-secreting neurons can be introduced into the caudate nucleus and putamen and if they survive and secrete dopamine, then perhaps the parkinsonian symptoms will diminish. Because the implanted neurons must be healthy and vigorous and not t.
#36420 Topic Discussion 6Number of Pages 1 (Double Spaced).docxAASTHA76
#36420 Topic: Discussion 6
Number of Pages: 1 (Double Spaced)
Number of sources: 1
Writing Style: APA
Type of document: Essay
Academic Level:Master
Category: Psychology
Language Style: English (U.S.)
Order Instructions:
I will upload the instruction
Module Chapter 5 wk6 p630
chapter 5 Methods and Strategies of Research
Outline
· ■ Experimental Ablation
Evaluating the Behavioral Effects of Brain Damage
Producing Brain Lesions
Stereotaxic Surgery
Histological Methods
Tracing Neural Connections
Studying the Structure of the Living Human Brain
Section Summary
· ■ Recording and Stimulating Neural Activity
Recording Neural Activity
Recording the Brain’s Metabolic and Synaptic Activity
Stimulating Neural Activity
Section Summary
· ■ Neurochemical Methods
Finding Neurons That Produce Particular Neurochemicals
Localizing Particular Receptors
Measuring Chemicals Secreted in the Brain
Section Summary
· ■ Genetic Methods
Twin Studies
Adoption Studies
Genomic Studies
Targeted Mutations
Antisense Oligonucleotides
Section Summary
In July 1982, several young people began showing up at neurology clinics in northern California displaying dramatic, severe symptoms (Langston et al., 1983). The most severely affected patients were almost totally paralyzed. They were unable to speak intelligibly, they drooled constantly, and their eyes were open with a fixed stare. Others, less severely affected, walked with a slow, shuffling gait and moved slowly and with great difficulty. The symptoms looked like those of Parkinson’s disease, but that disorder has a very gradual onset. In addition, it rarely strikes people before late middle age, and the patients were all in their twenties or early thirties.
The common factor linking these patients was intravenous drug use; all of them had been taking a “new heroin,” a synthetic opiate related to meperidine (Demerol). Some detective work revealed that the illicit drug was contaminated with MPTP, a toxic chemical that damaged dopaminergic neurons and caused the neurological symptoms. Because the symptoms looked like those of Parkinson’s disease, the patients were given L-DOPA, the drug that is used to treat this disease, and they all showed significant improvement in their symptoms. Unfortunately, the improvement was temporary; the drug lost its effectiveness.
Fetal transplantation, an experimental neurosurgical method of treating parkinsonism, has shown some promise. The rationale for the procedure is this: The symptoms of parkinsonism, whether from Parkinson’s disease or the toxic effects of MPTP, are caused by the lack of dopamine in the caudate nucleus and putamen. There is at present no way to induce the brain to grow new dopaminergic neurons. However, if dopamine-secreting neurons can be introduced into the caudate nucleus and putamen and if they survive and secrete dopamine, then perhaps the parkinsonian symptoms will diminish. Because the implanted neurons must be healthy and vigorous and not trigger the .
Running Head BACKGROUND AND SIGNIFICANCE1Running Head BACKGR.docxsusanschei
Running Head: BACKGROUND AND SIGNIFICANCE 1
Running Head: BACKGROUND AND SIGNIFICANCE 1
Background and Significance
Lana Eliot
Psychology 625
Professor Weniger
July 29, 2018
Specific Aims:
The effect of stress on human beings is terrible that leads them to different diseases. The stress comes from environment and change in human behavior. Stress profoundly impacts or minds that leads to damages of prefrontal cortex which plays a prominent role in cognition (Andrew Holmesa, 2010 ). The cognitive abilities of a human being the effect a lot in the presences of stress. That leads to mood swings, schizophrenia and anxiety disorder. Hence, numerous studies are carried out on the stress-induced cognitive abilities (Joëls, 2006).
Intense stress and even the minor stress is responsible for changes in cognition impairment. It is responsible for significant changes in the remodeling of neurons. It also brings changes in neuronal morphology and effects the working memory of human beings (Luine, 1994). This study demonstrates that how stress-induced cognitive impairment affects the different areas of the brain (Maroun, 2008). The impact of stress on the human brain is studied under molecular basis induced changes. There is numerous significance of this study that includes how the brain is affected by stress and what stress causes cognition problems. It will further demonstrate how molecular basis changes the prefrontal cortex. It also gives details about pathophysiology and its association with dysfunction in neuropsychiatric diseases. Further strategies will also have introduced for its treatment that helps in overcoming stress-induced cognitive impairments.
Background
Stress have destructive effects on human. These results are related to all internal and external development of human body and mind. Humans are exposed to multiple stressors in their daily routine that leads to severe problems. When the human body is exposed to stress at that time that time, they did notice that how this stress affects them. But later, when they are more frequently exposed to stress they feel changes in their behavior and brain as well. Mood swings and unpredicted behavior of humans are the results of this stress. As well as the brain is concerned, stress disturbs the chemical balance that restricts brains from performing their ordinary functions. Most importantly it affects the cognition problems in humans. They more frequently started to forget about different things that they did not realize initially. But with the passage of time when these things get severe, they know that how this stress negatively affect this stress. Furthermore, stress is the only factors that induce cognition and learning problems in humans.
Bondi et al. (2007) conducted a study on chronic unpredictable stress that induces cognitive deficit as well as anxiety problems. Keeping in view the aim of this study, he experiments on rats where he injected the chronic antidepr ...
Running Head STRESS-INDUCED COGNITIVE IMPAIRMENT1STRESS INDUC.docxtoltonkendal
Running Head: STRESS-INDUCED COGNITIVE IMPAIRMENT 1
STRESS INDUCED COGNITIVE IMOAIRMENT 6
Stress-induced cognitive impairment
Lana Eliot
Psychology 625
Professor Beharie
January 24, 2018
Stress-induced cognitive impairment
Bondi, Corina O., Gustavo Rodriguez, Georgianna G. Gould, Alan Frazer, and David A. Morilak, (2008). Chronic unpredictable stress induces a cognitive deficit and anxiety-like behavior in rats that is prevented by chronic antidepressant drug treatment. Neuropsychopharmacology, 33 (2), 320-331.
Bondi Cornia, Gustavo Rodriguez, Georgianna G. Gould and their fellows have published an article named Chronic unpredictable stress induces a cognitive deficit and anxiety-like behavior in rats that is prevented by chronic antidepressant drug treatment in the year 2008. Journal of Neuropsychopharmacology is the source where this article is submitted. In this article, the authors have mainly given several dimensions that are associated with stress which associates primarily with the cognitive deficit, in this concern an experiment was done on rats. This research would be helpful for us for our medical projects related to stress and its correlation with cognitive abilities of human beings.
Joëls, Marian, Zhenwei Pu, Olof Wiegert, Melly S. Oitzl, and Harm J. Krugers (2006). Learning under stress: how does it work? Trends in cognitive sciences, 10 (4), 152-158.Joëls, Marian, Zhenwei Pu, Olof Wiegert, Melly S. Oitzl, and Harm J. Krugers have published this research-based article in the year 2006 in the journal of trends in cognitive sciences. The central theme of this article moves around the concept of the consequence of stress on the learning ability of the individuals. In this article, it is also evaluated that the hormones of stress when released develops the transmitters in response to stress. This is an authentic article as is reviewed by expert authors so it could consider for a more profound study on the topic of Stress-induced cognitive dysfunction.
Luine, Victoria, Miriam Villegas, Carlos Martinez, and Bruce S. McEwen (1994). Repeated stress causes reversible impairments of spatial memory performance. Brain research, 639 (1), 167-170.
Line, Victoria, Miriam Villegas, Bruce S. McEwen and Carlos Martinez have published this article in the year 1994. The main ideology considered in this article is that the repeated stress has the impairments that are reversible and these could directly affect the spatial memory as the hormones inside the brain are released that negatively affects the cognitive ability of the individual. This article is authentic as the proper sources are given with the theory along with that it is reviewed by the scholars so it could be considered while working on the project related to stress-induced cognitive impairment.
Mizoguchi, K. Y. (2000). Chronic stress induces impairment of spatial working memory because of prefrontal dopaminergic dysfunction. Journal of Neuroscience, 20 (4), 1568-1574 ...
Top 24 team in the High School Utah Entrepreneur Challenge 2017. The program is managed by the Lassonde Entrepreneur Institute at the University of Utah. Learn more at lassonde.utah.edu/hsuec.
Running Head: DEPRESSION 1
DEPRESSION 3
Lana Eliot
Depression
Psychology 630
Professor Benton
August 25, 2018
Many people throughout the world experience some type of depression in their lives and it is one of the most common mental disorders. The current statistic show that depression is linked to genetic, environmental, biological and is also psychological. Depression can ben found with any age person. A small child or an adult may have to deal with the depression that is affecting them. Chemical imbalances in the brain is the leading cause for a person dealing with the depressive order. The neurotransmitter is the what we call the communicator between the brain and the limbic system. Researchers study the limbic system in the brain as this is where depression starts; especially for anxiety and stress. The 3 major neurotransmitters; serotonin, norepinephrine, and dopamine all have direct relations with a persons’ depression and anxiety.
Serotonin plays a crucial role in our brain. It is associated with many physical actions that we may portray. The actions associated with serotonin are mood altering, sleeping patterns, eating disorders, and aggression. If a persons’ serotonin levels decrease, they may experience these depressive symptoms. This can also make persons have a feeling of self-worth and suicidal feelings.
Another transmitter in the brain which is associated with the depressive disorder is dopamine. This is the part of the brain that deals with our motivation and how we gain the feeling of self-worth and self-pleasure. Early studies suggested that an existence of neurotransmitter norepinephrine deficiency in some certain areas of the brain resulted in depression. One main cause of depression is the reduction in the concentration of certain neurotransmitters in the brain, such as serotonin and dopamine. The decrease in the concentration of these neurotransmitters leads to disturbed neuronal signal processing which leads to alterations in the structure of the neuronal networks. These basic changes are accepted to be one of the fundamental purposes behind sorrow. The emergence of neuroimaging techniques, magnetic resonance imaging (MRI), positron emission tomography (PET) and functional fMRI, established the importance of the ‘neurocircuit of emotion’ which has been expanded to include other important brain areas and the prefrontal cortex (PFC). These brain sites and their connections, which have been widely studied, are responsible for maintaining emotional stability and their malfunction is considered central to the pathophysiology of depression (Palazidou, E., 2012).
Recent follow up studies also shows that there is a group of individuals with a depression disorder who exhibit low levels of the chemical norepinephrine. In autopsy studies, it has been shown that in comparison,.
4. Disfuntional Insular Cortex Hard time evaluating pain, and processing it. Plays a positive role in addiction.
5. Study 1: Sacktor, Weizmann Institute of Science (Rehovot, Israel) Aim: To determine result of blocking an enzyme that strengthens the neuron connections, creating long-term memory. Result: Memories erased by injecting the inhibitor into the insular cortex (taste-processing gustatory process).
6. Study 2: Dr. Urbanik Aim: To examine whether men and women respond differently to anger. Results: Men’s insular cortex is more activated than women’s, which creates a physical reaction of ‘fight or flight’ rather than an emotional.
7. Study 3: Nasir Naqvi, University of Iowa Aim: To see whether head injury that leads to dysfunction of the Insular Cortex will have an effect on drug addiction. Results: Cigarette smokers for example who suffer from damage of the Insular Cortex due to a stroke had their addiction to cigarettes almost eliminated. Up to 136 more likely to stop smoking then smokers who suffer damage to another part of the brain. Make this area of the brain a promising target for anti-addiction medications.
8. Works Cited Simon, Moss Dr. “Insular Cortex.” Psychlopedia. Web. 3 Nov 2009. <http://www.psych-it.com.au/Psychlopedia/article.asp?id=341> Swaminathan, Nikhil. “’Continuous Motor’ Underlies Long-Term Memory Storage.” Scientific American. 17 Aug 2007. Web. 2010. <http://www.scientificamerican.com/article.cfm?id=continuous-motor-underlies-memory> Podsiadlo, Lilianna. “Men and Women May Respond Differently to Danger.” ScienceDaily. 30 Nov 2009. Web. 2009. <http://www.sciencedaily.com/releases/2009/11/091129125131.htm> Craig, A. D. “Mapping Pain in the Brain.” The Welcome Trust. N.p., n.d. Web. 31 Mar. 2010. <http://www.wellcome.ac.uk/en/pain/microsite/science2.html> “Damage to the Insula Disrupts Addiction to Cigarette Smoking .” Science Mag. N.p., n.d. Web. 31 Mar. 2010. <http://www.sciencemag.org/cgi/content/abstract/315/5811/531> “Insular cortex.” Absolute Astronomy. N.p., n.d. Web. 31 Mar. 2010. <http://www.absoluteastronomy.com/topics/Insular_cortex> Nagai, K, K Kishi, and S Kato. “Insular cortex and neuropsychiatric disorders.” PubMed U.S. National Library of Medicine National Institutes of Health. N.p., n.d. Web. 31 Mar. 2010. <http://www.ncbi.nlm.nih.gov/pubmed/17416488>