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emeraldwallaby818Lv1

28 Sep 2019

You have discovered a new area of the brain in the parietal lobe called the Shnoxocampus that seems to be responsible for âselfinessâ.

If I wanted to see if taking an excessive number of selfies affected the number of neurons in the area and the dendritic growth of neurons in the Shnoxocampus, what staining techniques should I use? If I then hypothesize that this brain area requires input from the visual cortex, how should I use a tracing technique to confirm the hypothesis?

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Bunny GreenfelderLv2

28 Sep 2019

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Related questions

Physiology Psychology

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2. Explain how an action potential occurs. Start with Glutamate release from the presynaptic neuron and end with neurotransmitter release from the postsynaptic neuron.

3. How does a neuron inhibit another neuron? Explain. {~1 paragraph}

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6. What is neural plasticity? Give an example and explain. [3-4 sentences]

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13. Discuss the Triune Brain model. Explain what happens to the functioning of the Triune Brain model when an individual is intoxicated by alcohol, and link that to drunk behavior.

14. Some patients develop disorders in which they believe that one of their limbs is not, in fact, their own limb. What could be happening in the nervous system that would lead to this peculiar phenomenon? Justify your answer and explain. (I am looking for you to come up with a reasonable hypothesis as to what could be causing it that you can sensibly justify and explain)

15a. What is schizophrenia? Describe 2 positive and 2 negative symptoms. Explain one way that the brains of schizophrenic patients are different from healthy controls, and link the brain abnormality to one of the symptoms of schizophrenia that you just described. 15b. What is the Dopamine (DA) Hypothesis for schizophrenia? Explain two pieces of evidence to support the DA Hypothesis. Explain one piece of evidence against the DA hypothesis. [~1 short paragraph] 15c. What is the Glutamate Hypothesis for schizophrenia? Explain two pieces of evidence to support the Glutamate hypothesis. Explain one piece of evidence against the Glutamate hypothesis. [~ 1 short paragraph] 15d. Schizophrenia is estimated to be about 80% heritable, but there are other factors that researchers have found to influence the development (or flare) of schizophrenia. Give an example of one of these other factors, and briefly explain the evidence for it. [2-3 sentences]

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17. Explain how the amygdala and brain stem are involved in the development of anxiety disorders such as PTSD, phobias or panic disorder.

18. Explain the basic function of the mesolimbic DA reward pathway. Discuss how drug use alters the pathway and contributes to the development of compulsive disorders like drug addictions/alcoholism.

19. If a stroke patient has damage to their right posterior parietal lobe, along the dorsal stream of visual processing, what syndrome would the patient have? Describe the major symptoms and explain what the personâs behavior would be like. What did we learn about the function of the parietal lobe from studying these patients? Explain.

20. If a stroke patient has damage to their temporal lobe, along the ventral stream of visual processing, what type of disorder would the patient have? Describe the major symptoms and explain what the personâs behavior would be like. What did we learn about the function of the temporal lobe from studying these patients? Explain.

21. What is blindsight? Explain how studying patients with blindsight informed our understanding of the visual system.

22. What are implicit and explicit memories? Do implicit and explicit memories represent independent neural systems for memory? Why or why not? Justify your answer with evidence.

23. What is retrograde amnesia? What did we learn about long-term memory from studying patients with retrograde amnesia (e.g., patient KC)? Explain.

24. What is our current understanding of how the Medial Temporal Lobe (MTL) stores and retrieves explicit memories? Discuss how the function of the MTL can explain cases of anterograde amnesia like HMâs.

25. Imagine that a doctor developed a drug called Memoryhole that is a Glutamate-NMDA receptor antagonist in the hippocampus. What effect would Memoryhole have on the process of Long-Term Potentiation (LTP), and, in turn, memory? Explain.

26. Do we have evidence for a biological basis for sexual preference? Discuss with respect to the Sexually Dimorphic Nucleus of the hypothalamus.

27. Helen Fisherâs research delineated 3 stages of love in the brain. Explain, with an emphasis on the brain-behavior relationships.

28. Parkinsonâs disease is a neurodegenerative disorder that results in severe motor impairments. What causes Parkinsonâs? Explain the major treatment for the disorder and the extent to which the treatment is successful. Are there any negative side-effects of that treatment? Explain.

29. What are mirror neurons? Explain two pieces of evidence for the hypothesis that mirror neurons are the neural substrate for empathy and theory of mind in humans. Do we have evidence linking mirror neurons to autism? Explain.

30. What was the most interesting thing you learned in class this semester? Why did you find it interesting? Explain.

31. What is a circadian rhythm? Explain how light acts as a zeitgeber to control our sleep/wake circadian rhythms. If someone had trouble falling asleep (insomnia), what advice would you give them? Justify your answer.

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Exercise #5: The Nervous system and Perception

Task #1: Color vision

Introduction

In the human retina, there are two kinds of light-sensitive cells: rods and cones. These cells are located on the outside of the retina, away from the vitreous humor and against the choroid layer, and are covered by a later of bipolar and ganglion cells as well as neurons. Light enters the posterior chamber through the lens and must pass through several cell layers before it is absorbed by the rods and cones.

Cones are involved in color vision at daylight intensities. Generator potentials in a cone excite one neuron, giving high-level resolution vision. Cones will not cause neural firing at low light intensities and are, therefore, nonfunctional at night.

Rods provoke black-and-white vision at low light intensities. A bipolar cell associates with several rods, so that generator potentials sum in their effect. This assures neuronal firing at low light intensities and provides a highly sensitive vision but with less resolution.

Receptor convergence. A ganglion cell, which receives input from a number of rods, spread out over the retina, cannot pinpoint the source of a light stimulus as well as a ganglion cell, which is stimulated by a single photoreceptor. In the case of a ganglion cell receiving the added input of several rods, light hitting any one of the rods can cause a neural spike in the ganglion cell, but the brain has no way to know which rod was excited. It is therefore harder to pinpoint the location of light stimuli on the retina when the stimulus is detected by rods (as compared to cones). The result is that our ability to see detail, or our resolving power, is considerably lower under dim light conditions than under bright light conditions.

Dark adaptation. If you go from a lighted area to a very dark room, you will not be able to see. After about ten minutes, however, you begin to be able to see again. This occurs because the rhodopsin pigment, which gets broken down when it absorbs light, is continually re-synthesized in the rods. When there is very little light, very little rhodopsin gets broken down and the amount of rhodopsin gradually builds up, making the rod much more sensitive to dim light.

When light strikes a receptor cell, it triggers a photo-chemical reaction that leads to neuronal firing. If a rod or cone receives high-intensity light, the visual pigments will be temporarily bleached and will not absorb any more light. Within a matter of a few seconds, enzyme systems in the cells will restore the visual pigment to its light-absorbing form. This can be easily demonstrated. If, after viewing a bright light, the eye is quickly shut or turned to a dark wall, the bright image will persist as a positive afterimage because the high generator potential causes the continued firing of neurons. If the eye is cast on a lighter background after a few seconds, a negative afterimage, or a dark image of the object will appear. This is because the still bleached cells are not receptive to the light coming from the light background.

According to the Young-Helmholtz theory of color vision, there are three types of cone cells, which respond respectively to red, green, and blue light.

All other colors are perceived as the brain interprets impulses coming from a mix of these receptors. If an object of one color is viewed for a long period of time at high light intensity, the cones for that color will become bleached. The afterimage of the object will be seen in the complementary color.

The Exercise 6 PowerPoint will demonstrate afterimages to you. Use the slide show option to project the square of red light on your entire screen in a dark room. After staring intensely at the square for 30 seconds or so, without shifting your gaze, click enter to change the slide to a soft white. Continue staring at the screen as the change is made. What do you see? What was the color of the afterimage?

Repeat this experiment using a blue square. Before doing the experiment, hypothesize what color the afterimage will be according to the Young-Helmholtz theory.

Hypothesis to be tested: (2 pts)

What did you see when the experiment was conducted? (2 pts)

Was you hypotheses accepted or rejected? (1 pt)

Explain the colors seen in these afterimages using the Young-Helmholtz theory. (5 pts)