Description
Focus on slide 14
35 multiple choice percentage entered in tracs, not points out of 35
3322 Midterm 1 Review sheet: Spring 2017
Methods (animal and human studies: Lecture 1, Chapter 2) In vivo cell and brain being studied in live animals. In vitro cells studied outside of living organism (usually rodents/ monkeys)
∙ Ablation/lesion studies
∙ Electropysiological studies 2 types 1. Electrocephalography/evoked potentials (scalp recordings) [done in epilepsy patients] measures electricity produced by the brain 2. Intracranial (cortical recordings from elcetrodes implanted to monitor seizures) If you want to learn more check out What is the process of reproducing new dna and dna molecules?
∙ PET and fMRI provide information about which areas are active based on metabolic activity. High metabolic demand=active area. Tell you where BUT cant tell you exactly when the activity is occurring. Good structural resolution.
∙ fMRI uses magnetic fields to see where there’s high oxygen in blood. Don't forget about the age old question of What are the formed elements of blood?
∙ PET uses radioactive substances like glucose, oxygen, radioactively tagged drugs (more invasively risky) We also discuss several other topics like What is the definition of compensation theory in art?
∙ EEG eceltrodes on the scalp to detect brain activity. Poor structural resolution. Cant tell you where but tells you when. MUCH CHEAPER AND NO RISK FOR PARTICIPANT.
∙ Transcranial Magnetic Stimulation (TMS) big magnet to interrupt brain activity
Organelles (parts of the cell, esp. from Lecture 1 – 2, and from review) slide 14
∙ DNA in the nucleus.
∙ [cytoplasm] Mitochondria gives energy
∙ ribosomes and mitochondria important for proteins like amino acid, turn it into neuro transmitters like serotonin
Similarities and differences between PET and fMRI (Lecture 1, Chapter 2)
∙ thefMRI is less invasive than PET (which uses radioactive injections)
∙ both have good structural resolution
∙ both tell where activity occurs altho fmri is better
∙ temporal resolution is poor
Bloodbrain barrier (Lectures 2 and 3, Chapter 2)
∙ these cells make up capillary walls Don't forget about the age old question of What is the vedic society?
∙ enodphileal cells (site of exchange)
∙ keeps large molecules out
∙ glial cells
∙ keep crap from being in blood
Glial cells, esp. Similarities and differences between Schwann cells and oligodendrocytes (Lectures 2 and 3, Chapter 2)
∙ GLIAL CELLS are support cells
∙ Both produce myelin)
∙ Difference CNS(oligodendrocytes) or PNS(schwanna)
∙ Neurons are nerve cells
Neuron cant do the job properly without glia cells
There are more glia cells than neurons
Understand the resting potential and the action potential and the chemical/ionic events that occur to create it. (Lectures 3 and 4, Chapter 3) – esp. what is going on with ion channels and why an action potential only travels in one direction down an axon (Lectures 3 and 4, Chapter 4) slide 9
Exocytosis and the events that cause it to occur (Lectures 4 and 5, Chapters 3 and 4) ∙
Postsynaptic effects (inhibition, excitation – IPSPs and EPSPs and why they occur), (Lectures 4 and 5, Chapter 4). Slide 11, 21, 22
∙ When one neuron sends message to another it can either have excitatory effect or inhibitory effect ∙ Graded depolarization (excitatory effects) Don't forget about the age old question of What is putnam’s primary focus that he dissects throughout the book?
∙ Hyperpolarization (becoming more negative, less likely to fire, inhibitory effect); negative ions come in
Summation – what is it and what are the two types? (Lectures 4 and 5, Chapter 3) slide 23, 24 ∙ Neuron either fires or it doesn’t
∙ Summation getting added together
∙ 2 ways 1. Close enough in time 2. Close enough in space
Saltatory conduction and the role of myelin (Lectures 3 and 4, Chapter 3) slide 14
∙ MAKES ACTION POTENTIAL QUICKER
∙ Ion exchange at little gaps
∙ Generates itself from node to node
The two types of receptors and how they differ (Lectures 4 and 5, Chapter 4) slide 10, 29, 33 ∙ The difference is how the channel opens to let ions in
∙ Ionotropic
∙ Metabotropic (lasts longer)
What makes something excitatory or inhibitory is how it opens? If you want to learn more check out What are okazaki fragments?
*Mechanisms (or different ways) by which drugs can affect activity at the synapse (Lecture 5 – esp. slide #26) + agonists/antagonists (also lecture 6 slide 3) slide 23
∙ production, release, storage of neurotransmitters; binding of transmitters to receptors; interfering with reuptake, inactivation, second messengers
∙ excitotoxicity neurons that fired too much
example question: what is a way that a drug can affect communication?
Drugs: agonists and antagonists (slide 24) – Lecture 5 slide 24, Chapter 4 pp. 8889 (also know the terms affinity, specificity, and efficacy – Lecture 5 slide 21) slide 24
∙ How speficic a drug will work on certain nuerotransmiters
∙ How strongly a drug affects a neurontransmitter
Describe the effects of nicotine on acetylcholine receptors (Lecture 5 slide 29 and Lecture 6 slide 4, Chapter 4 p. 97) slide
∙ Nicotine is the same shape and size so it sticks and mimics acetlcholine
Describe the effect of alcohol at GABA receptors and the effects of nicotine on acetylcholine receptors (Lecture 5, Chapter 4 for GABA and its role in the brain) (slide 9)
∙ ALCOHOL: binds directly to receptors; alters membranes as well as ion channels, enzymes, and receptors
∙ gaba major inhibitory neurotransmitter; opens ion channel; when it attachs to receptor site it implifies, strengthens affects. Gaba is relaxing.
∙ Nicotine mimics particular kind of acetylcholine receptor.
∙ Gaba has inhibitory effect
The three views of the brain (axial, sagittal, coronal) and how they are obtained (i.e., top to bottom, side to side, back to front) (Lecture 6, Chapter 2) slide 19; coronal , axialfrom top to bottom, sagittal from ear to ear
Adjectives to describe the brain (Lecture 6, Chapter 2) slide 19
∙ Dorsal is on top and the ventral is underneath
∙ Lateral is the outside, medial is on the inside
∙ No inspiralteral
∙ No provinal vs
∙ Study Planes of View slide
∙ From front to back coronal section
∙ Horizontal from top to bottom
∙ Sagittal from ear to ear
The two major divisions of the autonomic nervous system and the major differences between them (Lecture 6, Chapter 2) slide 16
CNS (Central nervous system spinal cord, brain) and PNS (peripheral nervous system nerves outside of the CNS [somatic nervous system: senses, muscles, glands. Autonomic nervous system:sympatheic and parasympathetic]
What are two main divisions of
Lecture 7 slide 11 and 12
Hindbrain and midbrain structures and their basic functions (Chapter 2, Lecture 6) slide 13: hindbrain The posterior of the brain, MEDULLA: reflexes, source of many cranial nerves, reticular formation (arousal, attention), cerebellum (movement, balance, coordination, memory, humor, cognition) HIGHLY SENSITIVE TO ALCOHOL
Somatic system
Autonomic system
Sympathetic nervous system to expand energy
Anatomy (or the ability to name structures in) the limbic system and the basal ganglia (Lecture 7, Chapter 2)
The role of the thalamus (Lecture 7 slide 22, Chapter 2 pp. 3940) slide 22
∙ Where information travels on its way to being conscious
∙ Every sense except smell
The four lobes of the brain and their putative functions (Chapter 2, Lecture 7) slide 26,27,28,29 The meninges (Lecture 7, Chapter 2)
Diagrams to study: You will be required to identify some of these structures from a diagram provided on the exam
*please note that these diagrams are not exactly like the ones you will get on the exam. Therefore, it’s important that you know what/where all the bits really are and don’t just memorize the order of the names