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Download doc Nerve and synapses
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Nerve/Synapse [“not a single atom that is in your body today was there when that event took place” – Steve Grand (computer scientist)] -spinal cord=highway of processing information (relaying up to brain and down to periphery of body) and mediates automated activities (ex. walking) -afferent fibers or sensory neurons bring information from periphery to spinal cord (ex. skin sensations) -efferent fibers or motor neurons allow movement -nervous system comprises about 100 billion neurons. -neurons use electricity to propagate information from a place to another -there is probably from a hundred trillion to a quadrillion of synapses in human nerv.syst. ∙soma: cell body, containing nucleus, where metabolic and synthetic activities take place, maintaining neuron in living state ∙dendrites: “antennas” of neuron, for information to flow in -axon: unique, for information to flow out (initial segment inserts in cell soma, presynaptic terminal=swelling at axon’s end) Resting membrane potential: the inside of a neuron has a slightly negative voltage(=electrical pressure) compared to the outside (-60mV to -70mV, tiny fraction of unpaired negatives charges, less than 1%). Neurons use it as a starting point for propagating electrical signals. [almost all cells have a resting membrane potential] -at rest, neurons still have great permeability to potassium ions (because of leak potassium channels), but Ca&others can’t flow in nor out. -negative voltage of neurons is then due to high concentration of potassium ion -When the chemical and electrical gradients are equal, the system is at equilibrium(quickly attained). The membrane potential at equilibrium is described by the Nernst equation. -Nernst equation tells us exactly what the voltage is going to be W/ the Nernst equation, we find E(Na)=+50mV and E(Cl)=-70mV The resting membrane potential is a bit more positive than EK, because there is a small inward leak of Na+, which pushes the membrane slightly toward ENa. -The membrane potential is determined by concentration gradients and relative permeabilities of membrane to different physiological ions. -The dominant permeability makes greatest contribution to the membrane potential. (At rest, the dominant permeability is to potassium, so the membrane potential is close to EK.) -Action potential is a jump in membrane potential, from negative to positive compared to the outside (all or none event). -Three types of channels: •leak potassium channels •voltage-gated sodium channels •voltage-gated potassium channels (accelerate falling phase, open w/ depolarization of axon, open slowly) -These flows don’t change very much ions concentration (too small numbers), sodium-potassium pump are continuously in action (maintaining gradients in background). -Since the action potential always start at initial segment, it always goes from initial segment down to presynaptic terminal (inactivation of sodium channels). [if you stimulate presynaptic terminal, action potential will go up to soma, middle of axon: both directions] -Action potential have same size and duration: differences are encoded in terms of frequency and pattern. Sodium channels are the molecular targets for numerous naturally occurring neurotoxins: •Puffer fish make tetrodotoxin, an extremely potent inhibitor of sodium channels. •Phyllobates frogs secrete batrachotoxin, a powerful sodium channel activator. •Sodium channels are also modulated by pyrethroid insecticides, as well as scorpion and anemonae toxins. Sodium channels are blocked by therapeutically important drugs, including local anesthetics and some antiepileptic agents: •Local anesthetics •Antiepileptics Lidocaine Phenytoin (Dilantin) Benzocaine Carbamazepine (Tegretol) Tetracaine Lamotrigi Cocaine Rapid propagation of action potentials is important for survival, especially in situations that require rapid, reflexive responses. In squids, evolution solved the problem of how to send fast-moving signals from one end of the body to the other by making giant axons, 1000 times fatter than our axons. This strategy works because the propagation rate of the action potential is proportional to axon diameter. Vertebrate neurons solve the problem of how to make a small axon with a high conduction velocity by wrapping the axon in an insulator called myelin. Myelin is formed by Schwann cells (in the PNS) or oligodendrocytes (in the CNS). -metaphor speed skater vs runner (push and glide vs step by step) or people handing sandbags (close to each other or tossing from a distance) -Multiple sclerosis is cause by loss of myelin. -white matter: regions of nervous system containing large bundle of myelinated axons -grey part is composed of cell bodies, dendrites and synapses -Axon is unique but has many embranchments. -Botox & tetanus toxins chews up some of proteins invovled in this process (so vesicle don’t fuse w/ membrane anymore), black widow venom makes vesicles fuse spontaneously w/ membrane. -excitatory synapses are only found on spines, inhibitory synapses are found on dendrites shafts or soma -The main excitatory neurotransmitter in the brain is glutamate (amino acid), the most prevalent neurotransmitter in nervous system. -The EPSP is a small, transient depolarization of the postsynaptic spine (1 to 2 mV and about 20 msec). -From 50 to 100 EPSPs must sum at the initial segment to initiate an action potential. These near-simultaneous EPSPs can come from multiple synapses acting in synchrony and/or from individual synapses, activated at high frequencies. NMDA receptors will only conduct calcium if: -activated by glutamate -postsynaptic spine already depolarized They are then coincidence receptors -Long-term potentiation (LTP) is a model of synaptic plasticity. -High frequency activity depolarizes postsynaptic spine, removing Mg2+ block of NMDA receptors and enabling them to conduct Ca2+. -EPSPs are larger, hours after induction of LTP. (more AMPA receptors inserted into postsynaptic spine) -Excitotoxicity is likely to contribute to neuronal degeneration after stroke and in neurodegenerative diseases. . -Epilepsy is caused by an imbalance of excitation over inhibition. -GABAA receptors are potentiated by a variety of drugs, including benzodiazepines (e.g. xanax), barbiturates (e.g. pentobarbital) and ethanol. -Glutamate synapses have both ionotropic receptors (AMPA and NMDA receptors) and metabotropic glutamate receptors (mGluR’s) -Glutamate makes mGluR change shape. That leads to a biochemical event inside of the cell which generates the formation of small soluble molecules (2nd messenger). -2nd messengers activate a range of cellular proteins, including ion channels, protein kinases and transcription factors. -Glutamate&GABA activate both ionotropic& metabotropic receptors. -Many types of neurotransmitters interact mainly or entirely with metabotropic receptors. These substances, such as dopamine, serotonin and norepinephrine, as well as neuropeptides like substance Y and endorphins, are often referred to as neuromodulators. They are not directly involved in the fast flow of neural information, but modulate global neural states, influencing alertness, attention and mood. -Neuromodulator systems are important targets for a wide range drugs. For example, antidepressants, such as Prozac, affect serotonergic transmission, whereas amphetamines, cocaine and other stimulants typically affect dopamine and norepinephrine transmission. -Axoaxonic synapses modulate neurotransmitter release from the presynaptic terminal. -Most of inhibitory neurons have short axons and most of excitatory have long axons.