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Cognitive Neuroscience 1.1-1.7 (History and Principles of Neuro to Chemical Senses)

by: Brianna René

Cognitive Neuroscience 1.1-1.7 (History and Principles of Neuro to Chemical Senses) PSYCH UA-25

Marketplace > New York University > Psychlogy > PSYCH UA-25 > Cognitive Neuroscience 1 1 1 7 History and Principles of Neuro to Chemical Senses
Brianna René
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This is the first couple units of cognitive neuroscience! These are topics for Exam 1 and also includes a brief analysis of one of the research papers required.
Cognitive Neuroscience
Clay Curtis
Class Notes
Cognitive Neuroscience, cog neuro, perception, sensation, Psychology, cognition, Neuro, neural science




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This 9 page Class Notes was uploaded by Brianna René on Thursday March 3, 2016. The Class Notes belongs to PSYCH UA-25 at New York University taught by Clay Curtis in Winter 2016. Since its upload, it has received 246 views. For similar materials see Cognitive Neuroscience in Psychlogy at New York University.


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Date Created: 03/03/16
1. Quiz 1 1.1. History and Principles of Neuroscience  Golgi- Allowed for visualization of individual neurons with a stain that turned them silver. Golgi Stain  Santiago Ramon y Cajal- Developed the idea of the “Neuron Doctrine.” Neurons in the the brain were not continuous but rather there were tiny gaps in between them (synapses). He deduced this by noticing that there was a significant time lag between stimulus and the manifestation of a reflex. Neurons couldn't be continuous if the signal travels that slowly  Glial Cells- support cells for the nervous system. Most important is myelin sheath that coats the axon. Schwann Cells are responsible for doing the myelinating. Other types of glial cells include Astrocytes and Oligodendrocytes.  Resting membrane potential is -70 millivolts. Electrical voltage triggers action potential in neurons . o First sodium channels open and Na rushes into the cell, making it more positive. The neuron reaches a peak in energy before potassium channels open and potassium rushes out of the cell making it increasingly more negative (positive charge leaving makes the remaining space negative). o The cell becomes so negative that it hyperpolarizes and falls below the equilibrium energy. At this point the cell is prevented from backfiring or firing again by inactivating its voltage gated channels. Both ion channels close in absence of electrical energy, and in order to return the neuron to its resting state, the sodium potassium pump uses energy (ATP) to pump sodium and potassium in and out of the membrane to restore the resting potential.  Saltatory conduction- more efficient way of travel for electrical signal down the axon. Jumps from myelinated node to node.  Voltage-gated ion channels- require electricity to modify the shape of the channel  Ligand-gated channels- require the binding of a ligand to modify the shape of a channel.  Inhibitory Post-Synaptic Potential (IPSP)- Signal that gets sent to neurons tomake them less likely to fire  Excitatory Postsynaptic Potential (EPSP)-Signal encourages neurons to fire more often.  Temporal Summation- the frequency at which a presynaptic neuron fires and causes the postsynaptic neuron to fire at the same time and these two potentials summate  Spatial Summation- Neurons near each other fire and summate.  Neurons integrate through neurotransmitters. This is how they communicate through chemical messengers. The electrical signal reaches the end of the axon and it causes vesicles of neurotransmitters to be released into the synapse via exocytosis. The NT’s then bind to the receptors on the postsynaptic dendrite and cause them to change shape and either influence or prohibit that neuron to fire. Neuromodulators: o Dopamine: Involved with motor function and a reward system in the brain. Deficiency linked to Parkinson’s Disease. Too much linked to Schizophrenia o Serotonin: Responsible for mood, sleep cycle, memory, body temperature. Deficiency: linked to depression, anxiety disorders, and OCD o Epinephrine/Norepinephrine: Excitatory neuromodulators. Fight or Flight o Acetylcholine: Induces contraction of skeletal muscles. Also inhibits contraction of cardiac muscle fibers. o GABA: Inhibitory effect on spinal cord and brain activity o Glutamate: Important for learning and memory. Creates a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously 1.2. Neuroanatomy  Phrenology is the study of the size and shape of the brain based on the idea that these physical attributes were related to mental function. (feeling up skulls)  Localization of Function vs. Aggregate Field Theory: AFT suggests that the brain functions as a whole LoF suggests that different areas of the brain have different functions.  Brodmann’s Areas: Cytoarchitectonic map of the brain based on cell type and neuron density that suggest differences in function  Anterior (rostral)and Posterior (caudal) refer to the front and back of the brain.  Superior (dorsal) and Inferior (ventral) describe the top and the bottom of the brain  Lateral refers to the outer surface and Medial refers to the center most part of the brain. 1.3. Gross Anatomy Parietal : Integrating sensory info and manipulating objects. Temporal: Located on the lateral sides of the brain and it’s responsible for olfaction and sound. Frontal: Responsible for conscious thought and social behavior. Occipital: Located in posterior portion of the brain, responsible for vision. Central Sulcus- prominent division between the frontal and parietal lobes as well as the separation between the somatosensory cortex and the motor cortex. Sylvian fissure- Division between frontal and temporal Lobes Limbic System- which is involved with emotion formation and processing, learning, and memory. Basal Ganglia  Amygdala-role in mood and anger  Cingulate Gyrus- highly influential in linking behavioral outcomes to motivation  Olfactory Bulbs- structures involved in sense of smell. Cerebellum: “little brain” smooth execution of movement Medulla: Involuntary/vital functions Primary visual cortex/striate cortex (V1): Located in occipital lobe of brain. Lines of Gennari are present in V1 as white strips that are actually myelinated axons. Extrastriate cortex would be the other visual areas, (V2,V3,V4, V5). Tonotopic Organization- certain cells respond to certain frequencies (basilar membrane in cochlea) Retinotopy in PVC: What we see in our retinas are mapped out in (V1). Motor & Somatosensory Cortex: Neighboring parts of the body take up space in neighboring parts of the brain. Space in the brain is dedicated to most sensitive areas. Homunculus (Hands, jaw, lips) Cortical layering is different in separate areas. For example, the motor cortex may have a larger output layer of neurons because it is responsible for execution, meanwhile the striate cortex has a large input layer because it is where visual information is received. Eye-->Optic Nerve→ Optic Chiasm→ LGN--->V1. 1.4. Cognitive Neuroscience Methods Behavioral Methods Cognitive Psychology: Aim to explain basic thought processes using an information processing approach. ex. Letter Matching Task (AA, Aa, SC). This showswe process physical differences first, then the phonetic identity, and then after that we must decipher between categories. Lesions Cerebrovascular Accidents (Strokes) Neuropsychological Studies: brain damage can be associated with cognitive impairments. ex. Spatial Neglect. Individuals with lesions on the left side of the brain ignore things that happen in the right visual field and vice versa. There isn't anything functionally wrong with their eyes, they just ignore one side of space due to the brain’s inability to coordinate with higher visual processing areas. Single Dissociation: Impairments on one type of task. ex. People with X type of injury are bad at task A Double Dissociation: Impairments on different types of task. ex. People with X condition are bad at task A but good with task B. People with Y condition are bad at task B but good at task A. Surgical Ablation Tissue removal or tissue destruction. Both of these methods are irreparable but precise. Tissue Destruction even more so since neurotoxins or excitotoxins can target a specific type of neuron in a certain area. Most reversible procedures in animal lesion studies do not have a very good specificity. Genetic Manipulations: Mostly irreversible. ex. Knockout Mice. Mice were missing a receptor important for learning and it became more fearless. As a result they did not learn from being endangered. Animal Lesion Studies  Avoids ethical complications of lesioning human brains. however animal brains aren't an exact representation of a human brain. Virtual Lesions Transcranial Magnetic Stimulation (TMS). Electric pulse generates a magnetic field that disrupts neural function. The disruptions are localized and temporary. ------------------------------------------------------------------- Semendeferi Article: Humans and Great Ape Cortices Hypothesis: Are human frontal cortices greater than monkey cortex? No. Human brains and great ape brains aren’t very different. Humans DO have larger frontal cortices but not proportionally larger. The paper acknowledges that the best way of assessing the subsectors of the frontal lobe would be through cytoarchitectonic studies but it is very expensive, and they had a limited supply of great ape material. So fMRI is second best and that’s what they used. Sample size was a problem. There was an underrepresentation of great ape species. The paper also suggests that a larger frontal cortex is not necessarily what could provide an explanation for our cognitive capabilities. Perhaps the neuronal connections have improved in the frontal lobe over time. Things to be skeptical about  sample size  how they defined the frontal cortex in each monkey  questions about sample size. were the monkeys wild or captive? gender differences? ----------------------------------------------------------------- 1.5. Types of Imaging Angiography: injecting dye into blood to diagnose potential disruptions in blood-flow. Computed Axial Tomography (CAT Scan): Based on the fact that different types of tissue absorb different levels of radiation. Magnetic Resonance Imaging (MRI): Spinning H atoms create a small magnetic field. The MRI’s magnetic field aligns H atoms with it. Radio frequencies get shot at the atoms and they get disrupted. RF pulse is turned off the scanner then detects the energy that is released when the atoms realign with the magnetic field. High resolution imaging technique.  fMRI uses BOLD signal(Blood Oxygen Level Dependent). It detects the time blood takes to rush to areas of the brain where neurons are active.  BOLD signal is dependent on % of deoxygenated hemoglobin due to the exposure of the iron in the heme unit. When activity is high, deoxyhemoglobin is low because the brain often overcompensates for high neural activity by dumping oxygen into the area. How do we get such strong magnets for an MRI? Electricity runs through the coil and dictates the magnitude of the electric field. HOwever, that generates a lot of heat so helium is used to keep the machine cool, and thus helps keep the magnetic field constant. The bulk magnetization is summarized by two components = longitudinal and transverse Longitudinal Magnetization: The RF pulse changes the orientation of the atoms (inverts them) and then the pulse turns off. The configuration returns to its original low energy state.  The speed of the “relaxation” is the T1 time constant.  T1 weighted MRI images help distinguish between white and grey matter Transverse Magnetization: The transverse component of different atoms are pointing in various directions. The RF pulse aligns them, and then they relax back to their original positions  The speed of the relaxation is the T2 time constant.  T2 weighted images are good for pathologies that involve fluid filled regions. MRI = Structural Imaging fMRI= Functional Imaging Diffusion Tensor Imaging (DTI): Viewing white matter tracts by measuring the density and motion of H2O in specific directions in the brain. H20 runs parallel with axon, and reveals directionality and connectivity of white matter. (rainbow image) Spatial Resolution=Good view of structure/localization Temporal Resolution= accuracy of time. Single Cell Recording: Measuring the individual activity of neurons via a microelectrode placed near the membrane. It records the changes in electrical potential.  excellent spatial & temporal resolution  extremely invasive and rarely used in humans Receptive fields of neurons = area in space they respond to specifically (Raster plots) Electroencephalography (EEG): Scalp electrodes measure summed activity of synchronously firing neurons.  Excellent Temporal resolution  Non-invasive  Poor spatial resolution Event Related Potentials: Changes in EEG signal time-locked to stimulus onset. The signals are averaged over trials. Magnetoencephalography (MEG): Detects magnetic fields generated by neurons. However this method requires the isolation of this field by blocking out the earth’s magnetic field. Superconducting Quantum Interference Device required to accomplish this. (SQUID).  good temporal resolution. but ok spatial res.  very expensive  can only measure neurons parallel to skull (sulci) Electrocorticogram (ECOG): Places electrodes DIRECTLY onto cerebral cortex.  good spatial and temporal resolution.  less signal distortion (Doesn't have to go thru scalp and skull)  Rare (limited clients) PET and fMRI detect changes in metabolism (blood flow). Neural events are not being directly measured. Positron Emission Tomography (PET): Measures changes in cerebral blood flow. Radioactive tracer is injected. It decays to positrons and those bump into electrons to produce photons. The photons are picked up by PET scanners.  very good spatial resolution very poor temporal (not measuring neural events directly) Computer Modeling/Simulation: Use computer algorithms to simulate cognitive processes. Generates testable theories of natural cognition.  models provide working theories  however it may force a simplification of the nervous system. We humans are more complex than a simulation! 1.6. Perception Sensation: The receiving of input to our senses Perception: How we process these inputs and make sense of them. Auditory System Hair Cells in inner ear vibrate when sound is introduced to them and this mechanical motion is transduced to a neural impulse that gets sent to the temporal lobe. Sound waves excite the cochlea (vibration of basilar membrane). The bending of the hair cells is what activates the action potentials Frequency tuning in cochlea (basilar membrane). High frequency sounds excite the base of the cochlea, and lower frequency sounds excite the apex. The basilar membrane is thicker at the base and thinner at the apex. Primary & Secondary auditory cortices also have frequency tuning (tonotopic maps). So certain cells are tuned to certain frequencies. Sound Localization: Being able to tell where a sound comes from in a region of space. Sounds differ as they arrive at the left and right ears in terms of timing and intensity. 1.7. The Chemical Senses: Olfaction, Gustation, Somatosensation Olfaction: Airborne chemical molecules enter the nose and circulate through the nasal cavity (or mouth). Smell is a very important part of taste. Its evolutionarily advantageous for organisms to smell! There is a difference in our brains between Sniffing and Smelling! Primary olfactory cortex is involved in sniffing and detecting changes in odor. Secondary OC involved in identifying them. Gustation: Taste buds (Papillae) on our tongue detect taste receptors. Salty, sour, sweet, bitter & umami! There aren't regions in the mouth for these senses, some taste buds are just more sensitive to some tastes than others.  Salt- Open sodium channels allow NaCl to come through. The concentration depends on the amount of Na+ in the environment (the mouth). Because these channels are always open, they act as sodium detectors.  Acid (Sour)- A K+ channel that is mediated by protons (H+). This makes sense because when proton density is high, an environment is typically acidic. So for this receptor a high proton density leads to more K+ channel activation leading to the perceptual experience of something ‘sour.’ Salt and Acid are Ionotropes  Sweet- The sweet receptor is a metabotrope. The ligand (sugar) binds to the receptor which activates a 2nd messenger (cAMP), and this opens channels and fuses vesicles to the postsynaptic cell.  Bitter- Metabotropic action leads to the mobilization of intracellular Ca+2 stores. Vesicles fuse and release neurotransmitters. This causes the cell to depolarize. THe NT release is directly controlled by the metabotropic receptor.  Umami is also a metabotrope  Ionotropic: open ion channels. Faster than metabotropic channels because they are fully integrated with the synapse.  Metabotropic: rely on 2 messengers in a signaling cascade. Slower because they depend on the activation of proteins but can amplify a signal by activating multiple proteins exponentially. o Excitatory: Tend to be Na+ channels the synapse activates. o Inhibitory: tend to be Cl- channels. Cl- drives the membrane potential down so if more Cl- channels are open than Na+, the signal will be inhibitory. Somatosensory: Detecting limbs, temperature, pressure and pain. Primary somatosensory cortex (S1) contains somatotopic representation of the body. Secondary somatosensory cortex (S2) contains more complex representations. Somatosensory plasticity/functional reorganization: if limbs are lost, the somatosensory maps adapt. Phantom Limb sensation occurs when the signal gets re-routed to the area of the brain that represents the limb.


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