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Lecture

NATS1860 Note 13

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Department
Natural Science
Course
NATS 1860
Professor
Keith Schneider
Semester
Winter

Description
NATS 1860 Note 13 Basics of vision: - Synapses conclusion - Eye - Photoreceptors (rods and cones) - Colour vision and colour blindness - Retina neurons - Lateral inhibition and edges - Projection to visual cortex - Neurons in visual cortex - Neurons and motion Review of Neural Communication - Spike (Action Potential) there is a threshold amount of depolarization that is necessary o Above polar levels causes Sodium to flow into the cell and depolarize it o Lower polar levels do nothing. o Potassium then flows out and the cell hyperpolarizes o Neurons signal using spike rate: up to 300spikes a second o This is how cells signal - If a spike travels down axon jumping from gap to gap in the myelin (it’s absence causes multiple sclerosis) at up to 100m/sec - It arrives at the synapses - Calcium enters and triggers neurotransmitter release - Neurotransmitter opens ion channels in dendrite - Ions flow into pout of postsynaptic cell changing its potential. Excitatory Synapses - Glutamate (GLU) is a neurotransmitter - Opens Sodium ion channels in post-synaptic neuron - Sodium ions enter and depolarize new ion - It’s called EPSP = Excitatory post synaptic potential THIS WILL BE ON THE EXAM o NO SPIKES ARE generated at the synapse, they’re generated at the cell body Inhibitory Synapses - GABA = Gamma acid. It’s the major inhibitory transmitter o It opens Potassium channels in the post-synaptic neuron o Potassium opens the ion charges and allowing them to exit and hyperpolarize the neuron o They’re called Inhibitory Post-Synaptic Potential = IPSP o If all cells fire at once, you may have an epilepsy - There must be a balance between EPSP and IPSP EPSP and IPSP Interaction - There is potentials spreading to soma and combining there. - The two synapses that have IPSP and EPSP produce slowly move down to the body and they combine. All the EPSPs (1000 synapses, 700 EPSP and 300 IPSP) - EPSP depolarization add - IPSPs hyperpolarization subtract from the EPSPs because they try to make the cell more negative. - If it’s not enough to depolarize, nothing happens, if it’ depolarizes to threshold, there is a spike o These must occur simultaneously for the interaction to take place o The spike itself is actually triggered if the Axon  The dendrites combine all the information from thousands nerve cells for stimulating and inhibiting. That combination determines whether the cell fires the spike. Drugs and the Brain - In every case where a drug has effects on our thought processes, it is active at synapses. - It releases at least 30 different neurotransmitters in the brain. o GLU and GABA are the two most popular and important ones o Each area in our brain uses Glutamate as primary source of excitation and GABA as the primary source of inhibition, and several others. - A drug that effects on only one neurotransmitters has a specific effect on one part of the brain and not on the other - All psychoactive drugs affect synapses o In moderate amount, these drugs do not kill you but may alter your life. - Cocaine: increase the effect of excitation in pleasure areas of the brain. - Opium and Morphine are mistaken by the brain for a natural neurotransmitter that blocks pain o It has very similar characteristics to this natural neurotransmitter  Runner’s high feel euphoric because its due to the release of a natural version of these chemicals in the brain  They’re called endorphins and encapholins - Valium (anti-anxiety and anti-panic) increases GABA hyperpolarization o It tends to lower the level of activity in the brain. The implication is that when you’re feeling anxious your brain is over active, over excited in areas that involve unhappiness and fear  By increasing inhibition you can damp that down. Dopamine and Parkinsonism - Dopamine is a neurotramsitter that is produced in the center of the skull where ther are specialized neurons that produce and transport it all over the brain - If an individual produces too little dopamine they develop Parkinson’s where they can’t move, shuffle, and have cognitive consequences - The treatment for this is drugs to help brain produce more dopamine (chemical precursors of dopamine that the brain uses to make more) o These can alleviate the symptoms of Parkinson’s - You can have electrodes implanted in the dopamine locations in the brain to produce more dopamine. o Stem cells can also be put into the areas that produce dopamine (it’s still experimental) - If someone takes too much of these drugs that produce more dopamine, it creates schizophrenia, especially in paranoid schizophrenia. o Since dopamine effects pleasure, too much pleasure would disrupt it - One of the goals of drugs research of the brain is to find treatments that can be limited to only one area o The current problem is the instability of specific areas that the drug affects it. Basic Neural Network in Brain - Excitation and Inhibition everywhere in brain o It’s how these cells are hooked up as well as how they get stimulated that determines what that part of the brain is doing o Excitatory and Inhibitory cells are all interconnected  One cells re-excites another cells  An E cell can excite an I cell, which in term is exciting it.  If the inhibition is strong, one will shut the other off. They compete  It fosters both competition and co-operation within the brain. Eye and Retina - An imagine is focused by the combination of a cornea, and the lens inside of our eye o It’s focused onto the retina at the back of the eye o For evolutionary reasons, our retina is created backwards in the sense that the photoreceptors are at the very back of the eye, and in front of them are two more layers of cells (ganglion)  The axons of the ganglion cells go off into the brain and form the optic nerve.  If the axons that are going into the optic nerve that are in the front of the eye, they have to cut back to the retina at some time, causing a blind spot (because this is where the optic nerve Photoreceptors: Rods and Codes - Photoreceptors: they are specialized neurons o How do neurons normally get stimulated?  By other neurons in synapses, or environmental energy  Light. Photoreceptors are specialized neurons is that proteins in their membranes (photopigments) evolved to capture photons of light of the wavelengths that we can see  When Light falls on these proteins in either rods or cones, it opens ion channels and excites the cells. o Afterwards, they transmit signals to the retina and along axons to the brain - Rods: specialized for night vision (low level) and there’s a majority of them. They’re very sensitive to light but do not code for colour. They send information even for 1 photon of light (smallest measure) o In a very dim illumination you can see shades of gray, but you cannot see colours. o If you want to determine whether only your rods are operating you have to be aware that if you can’t see colours in a dark hallway, your rods are only operating - Cones: you are using them right now because they’re specialized for daylight- bright intensity vision to light. o They code light colour using three different photopigments  Red (50% cones) in most of our retinas  Green (45% of cones)  Blue (5% of cones)  This is because in mammals, only monkeys, great apes, and humans have the red photo-pigments.  A hypothesis is that it evolved as a way of det
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