BIOL 300 Chapter Notes - Chapter 5: Golgi Apparatus, The Terminal, Cytosol

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ochreporcupine180

3 Feb 2017

School

Department

Biology

Course

BIOL 300

Professor

Moody Bill

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Document Summary

The transfer of information from one neuron to another occurs at specialized sites of contact called synapses. The process of information transfer at a synapse is called synaptic transmission. Electrical current flowing from one neuron to the next: electrical synapses. Chemical neurotransmitters transfer information from one neuron to another at the synapse: chemical synapses. A synapse is the specialized junction where one part of a neuron contacts and communicates with another neuron or cell type (such as a muscle or glandular cell). Information tends to flow in one direction, from a neuron to its target cell. The first neuron is said to be presynaptic and the target cell is said to be postsynaptic. Electrical synapses are relatively simple in structure and function, and they allow direct transfer of ionic current from one cell to the next. Electrical synapses occur at specialized sites called gap junctions.

Related Questions

The junction specialized for the transmission between a neuron and another cell is called a (1) _____ ______. Usually, the signal being sent to the receiving cell is carried by chemical messengers called (2) _____. (3) _____ is an example of this type of chemical messenger, which diffuses across the synaptic cleft, combines with protein receptor molecules on the muscle cell membrane, and soon thereafter is rapidly broken down by enzymes. At an (4) ____ synapse, the membrane potential is driven toward the threshold value and increases the likelihood that depolarization and an action potential will occur. At an (5) ____ synapse, the membrane potential is driven away form the threshold value, and the receiving neuron becomes hyperpolarized and is less likely to achieve an action potential. A specific transmitter substance can have either excitatory or inhibitory effects depending on which type of protein channel it opens up in the (6) ____ membrane. (7) ____ are neuromodulators that inhibit perceptions of pain and may have roles in memory and learning, emotional states, temperature regulation, and sexual behavior. (8) ____ ________ at the cellular level is the moment-by-moment tallying of all excitatory and inhibitory signals acting on a neuron. Incoming information is (9) ____ by the cell bodies, and the charge differences across the membranes are either enhanced or inhibited. Some narrow-diameter neurons are wrapped in lipid-rich (10) _______ produced by specialized neuroglial called Schwann cells; each of these is separated from the next by a(n) (11) ________ ________ - a small gap where the axon is exposed to extracellular fluid. A (12) ____ is an involuntary sequence of events elicited by a stimulus. During a (13) _______ ________, a muscle contracts involuntary whenever conditions cause a stretch in length; many of these help you maintain an upright posture despite small shifts in balance. Imbalances can occur at chemical synapses; a neurotoxin produced by Clostridium tetani blocks the release of GABA and glycine, thus freeing the motor neurons from (14) _____ control, which may cause tetanus â a prolonged, spastic paralysis that can lead to death. A. Excitatory H. Stretch reflex B. Inhibitory I. Summed C. Myelin J. Neurotransmitters D. Chemical synapse K. Postsynaptic E. Synaptic integration L. Endorphins F. Exposed node M. Acetylcholine (ACh)

lilacchinchilla331

Physiology Psychology

1. The mind-body problem is a fundamental philosophical issue at the base of all cognitive/behavioral neuroscience research. Why? Discuss the mind-body problem and give an example of how it relates to an issue in cognitive/behavioral neuroscience. Explain.

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}

4. Design a drug that would increase Dopamine (DA) and/or Norepinephrine (NE) levels and explain its mechanism of action (explain how it works to increase DA and/or NE). What kind of disorder could this drug be used to treat? What would be some side-effects you might expect from taking such a drug? Would there be any risks expected from long-term treatment? Explain.

5. Alzheimerâs dementia is a neurodegenerative disorder that results in severe cognitive impairment. Researchers hypothesize that Alzheimerâs is due to low Acetylcholine activity in the cerebral cortex. How could a researcher test this hypothesis? Justify your answer.

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

7. Dr. Butthurt, a prominent pain researcher, has recently discovered that a Chinese form of meditation called Tai Chi can be a very effective pain-relief method. In Dr. Butthurtâs studies, he found that people in pain experience profound pain relief after participating in just 30 minutes of Tai Chi meditation. Now, Dr. Butthurt wants to determine the neural mechanism by which Tai Chi works to relieve pain. The first hypothesis he wants to test is that Tai Chi works because it stimulates endorphin activity in the brain. How can Dr. Butt-hurt test this hypothesis? Explain. [~1 paragraph]

8. A dominant view in neuroscience is that the human brain is âmodularâ. For example, many have claimed that the Fusiform Face Area (FFA) is a specialized, domain-specific module for recognizing faces. Discuss the issue, giving evidence for and against the claim that the FFA is domain-specific for face-processing. (1-2 paragraphs)

9. The Wernicke-Geschwind model of language was the dogma in neuroscience and psychology for many years. According to the W-G model, Brocaâs Area and Wernickeâs area are the two main language modules in the brain. What does the model argue is the function of Brocaâs area? Explain one piece of evidence to support it. What does the model argue is the function of Wernickeâs area? Explain one piece of evidence to support it. Why has the current theory of language moved away from the W-G Model? Explain.

10. If a person has the genes associated with a particular psychopathological disorder (e.g., depression, schizophrenia, bipolar, etc), will that person definitely develop the disorder? Why or why not? Explain. Use an example to help you explain. (few sentences to a short paragraph)

11. Why is it the case that there are some very high-pitched ringtones that are typically only audible to people under 18 years old? Why canât (most) adults hear these high-pitched tones? Explain. (few sentences)

12. How does Miraculin act on the nervous system to change our perception of taste? Explain.

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]

16. Major depression (unipolar) is a psychiatric disorder affecting over 15% of the U.S. population. Explain two of the dominant hypotheses about the biological factors in depression, discussing the evidence for and against those hypotheses. What is the most effective treatment for long-term relief from depression? Why? Explain. (~2 paragraphs)

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.

32. Seasonal Affective Disorder is a type of depression that occurs when depression symptoms consistently flare in the winter season and abate in the summer season. One successful treatment for this type of depression is âlight therapyâ in which the patient sits in front of a sunlight-emitting device for a certain number of hours a week. How could this type of depression and its treatment be explained by what we know about the neural basis of arousal and circadian rhythms?

Tetraethylammonium (TEA) is a drug that blocks voltage-gated potassium channels. What effect would this have on an action potential?

(a)Prevent the rising phase

(b)Prevent the cell from reaching the threshold to trigger an action potential

(c)Prevent or prolong the falling phase

(d)None of the above

The hyperpolarization phase of the action potential is due to:

(a)The opening of voltage-gated Cl- channels

(b)Prolonged opening of voltage gated K+ channels

(c)The closure of resting Na+ channels

(d)Rapid inactivation of voltage-gated K+ channels

The period when it is difficult to initiate another action potential for several milliseconds due to voltage-gated sodium channel inactivation is referred to as the:

(a)Relative refractory period

(b)Absolute refractory period

(c)Resting period

(d)Hyperpolarization period

In the human central nervous system, Gap junctions are found:

(a)Only between neurons

(b)Only between astrocytes

(c)In both neurons and astrocytes

(d)In all cells

Small molecule transmitters such as acetylcholine are synthesized in:

(a)The nerve terminal

B) The cell body and transported to the nerve terminal

C) Synaptic vesicles

D) Endoplasmic reticulum

Prior to Otto Loewiâs classical experiment, which of the following was not known:

(a)stimulation of the vagus nerve slows the heart

(b)extracts of frog heart, made following vagal nerve stimulation, slow the heart

(c)some acetylcholine effects are similar to those produced by muscarine

(d)vagal nerve stimulation releases a substance which slows the heart

Which of the following is most important in determining if neurotransmission is excitatory or inhibitory?

(a)The structure of the synapse

(b)The neurotransmitter released by the presynaptic neuron

(c)The neurotransmitter receptor

(d)The strength of the stimulus

Benzodiazepines such as Valium allosterically regulate GABA receptors by:

(a)Binding at receptor sites other than the transmitter binding site

(b)Binding at the transmitter (GABA) binding site on the receptor

(c)Blocking the action of the endogenous transmitter

(d)Mimicking the action of the endogenous transmitter

GABA-A receptors are ligand-gated Cl- channels. The equilibrium potential of Cl- is -65 mV. At the neuronal resting membrane potential of -65 mV, GABA binding to the GABA-A receptor would result in the opening the Cl- channel, resulting in:

(a)no net flow of Cl- ions

(b)Cl- inflow and hyperpolarization

(c)Cl- outflow and depolarization

(d)Cl- outflow and hyperpolarization

At the mammalian neuromuscular junction, the released neurotransmitter acts on:

(a)muscarinic receptors

(b)nicotinic receptors

(c)adrenergic receptors

(d)Beta receptors

Neurotransmitters are packaged into synaptic vesicles by:

(a)endocytosis following transmitter release

(b)presynaptic membrane transporters

(c)vesicular transporters

(d)all of the above

. Which of the following are NOT types of ion channels?

Voltage-gated

(a)Ligand-gated

(b)G protein coupled receptor (GPCR)-gated

(c)Leak channels

(d)NONE of the above

NMDA receptors are unique in that their ion channel is:

(a)Ligand-gated

(b)Voltage-gated

(c)Ligand- and voltage-gated ion channels

(d)GPCR-gated

. Which of the following is INCORRECT regarding Catecholamine neurotransmitters

(a)Includes Dopamine, Norepinerphrine, and Epinephrine

(b)Contain a Catechol Ring

(c)Synthesized from Tryptophan

(d)Are produced by neurons whose cell bodies are located in the upper brainstem

The largest and most diverse group of receptors in eukaryotes is:

(a)Ligand gated receptors

(b)Glutamate receptors

(c)G-Protein coupled receptors

(d)Allosteric receptors

The most abundant G-protein coupled receptor in the brain is:

(a)Glutamate receptors

(b)Acetylcholine receptors

(c)Cannabinoid receptors

(d)Dopamine receptors

Which of the following drugs DOES NOT block voltage-gated Na+ channels

(a)Lidocaine

(b)Riluzole

(c)Reserpine

(d)Tetrodotoxin

Sarin, a nerve gas, exerts its toxicity by:

(a)blocking nicotinic receptors

(b)inhibiting choline acetyltransferase

(c)inhibiting acetylcholinesterase

(d)inhibiting voltage-gated Na+ channels

Botulinum Toxin (BoTox) interferes with transmitter release by:

(a)cleaving protein(s) involved in transmitter release

(b)blocking voltage-gated Ca2+ channels

(c)blocking voltage-gated Na+ channels

(d)blocking voltage-gated K+ channels

Atropine is:

(a)An agonist of the acetylcholine ionotropic receptor

(b)An antagonist of the acetylcholine ionotropic receptor

(c)An agonist of the acetylcholine metabotropic receptor

(d)An antagonist of the acetylcholine metabotropic receptor

BIOL 300 Chapter Notes - Chapter 5: Golgi Apparatus, The Terminal, Cytosol

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