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192 Cards in this Set
- Front
- Back
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synapse
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gap bw neurons
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reflex arc
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circuit from a sensory neuron to a muscle receptor
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sherrington
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the speed of conduction through a reflex arc is slower then that of an axon , delay occurs when one neuron communicates wit hthe other..sp,e process slows conduction through the reflex
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temporal summation
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repeated stimuli occuring within abrief period of time are cummultive and produces a reflex (as opposed to a single stimuli)
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postsynaptic neuron
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cell that recieves the message
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presynaptic neuron
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neuron that delivers the synaptic transmission
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EPSP- excitatory postsynaptic potential
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magnitude decreases across membrane, depolarization, not enough sodium gates are opened to reach the threshold (3 consecutive EPSPs combined were able to reach the threshold and produce an ap)`
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spatial summation
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several synaptic inputs originating from separate locations combine their effect on a neuron (2 pinches in different spots elicit a reflex) also depolarizes the cells
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IPSP-inhibitory postsynaptic potential
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hyperpolarization of membrane, synaptic input slectively opens the gate for potassium ions to leave the cell, chloride enter and the cell is mor enegative
interneuron that excitred a motor neuron also inhibited a motor neuron connected to the extensor muslce |
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probability of an ap depends on
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ratio of epsps to ipsps at any given moment
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spontaneous firing rate
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a periodic production of ap even without synaptic input, epsps increase the frequency of aps above the spontanteous rate where ipsps decrease it below the rate.....make firing rate higher or lower the sp firing rate...
most neurons are actually firing all the time |
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Elliot/Loewi experiment proved that
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synaptic transmission depends on chemical (neurotransmitters) rather then electrical stimulation
vagus nerve-transferenc eof fluid from 1st to 2nd heart the 2nd heart also decreased in heartbeat- chemical=acetylcholine |
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the sequence of chemical events at a synapse 1
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neuron synthesizes chemicals to be used as neurotransmitters
the larger chemicals (peptides) are sysnthesized in the cell body the smaller chemicals are synthesized in the axon terminals |
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2
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transport of large neuro (peptides) in vesicales down to the axon terminal
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3
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ap causes calcium (stored in extracellular space) to enter releasing neurotransmitters
nt are release from the terminals into the synaptic cleft ( the space bw the pre and post synaptic neurons) |
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4
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nt binds to receptors of postsynaptic neuron and alters its activity
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5
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nt separate from receptors-molecules detatch- may be converted into inactive chemicals
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6
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nt may be taken back up into presynaptic neuron-REUPTAKE- to be used again, some chemically inactivated. vesicles are also transported back to cell body to be packed again with nt
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7
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negative feedback messages to slow further release of nt by presynaptic cell- dont send anymore nt!
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neurotransmitters
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at a synapse one neuron releases chemicals that affect a second neuron-affect either another muslce, gland etc.
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dopamine
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pleasure, too little-Parkinsons, too much-schitz
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amino acids
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acids containing an amine group
glutamate, gaba, glycine, asparate |
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glutamate
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most prolific excitatory transmittor
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gaba
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most prolific inhibitory transmittor
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monoamines
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non acidic nt containing a namine group, formed by a metabolic change in certain aa.
indolemines (serotonin) catecholamines- 1st dopamine, 2nd- norepinephrine, epinephrine |
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peptides
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chains of aa. even longer chains are polypeptides(proteins)
endorphins, substance P |
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substance P
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transmits intense P, counteracts endorphins
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endorphins
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morphin, heroine like, built in narcotic-feel good, reduce pain
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purine
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ATP, adenosine, metabolism
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gases
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NO-nitric oxide,---related to blood flow, how blood knows an area of the barin has becom emore active, dilates blood vessels so that increased blood flow is sent to ares of the barin, also involved with erections
CO, HO? very toxic, not sure whether these really exist |
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most nt are
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derivitaives of amino acids wit hthe exception of NO
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the neuron synthesizes chemicals it needs from the
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diet
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tryptophan
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the amount of this substanc ein the diet controls the amount of serotonin in the brain
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carbohydrates
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release fo insulin
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acetylcholine
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ina category by itself, amine group replaced by N(CH3)3 group
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transport from cell body to terminal may take as long as
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hours or even days long, after releasing their supply neurons replenish their supply slowly, neurons do not reabsorb and recycle peptides, neuron exhausts its supply of this nt faster then other nt
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vesicles
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where high concentrations of nt are stored in presynaptic terminal, but NO is not stored in vesicles, neurons release NO as soon as it is stored
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Exocytosis
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after calcium enters the presynaptic terminal-release of nt in bursts from the presynaptic terminal into the synaptic cleft
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acetylcholine
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sysnthesized from choline, abundunt in cauliflower and milk
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catecholamines
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(dopamine, norepinephrine, epinephrine) start with the aa phenylaline &tyrosine (from diet) which combine to make DOPA--> then the 3 other things
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substantia nigra
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depletion of dopamine leads to parkinsons disease, L DOPa which is fat soluble crosses the blood barin barrier and is synthesized to make dopamine
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Dales Principle
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assumption that each neuron only releases 1 nt, but neurons usually release 2 or 3 in the same cobination
alhoiugh a neuron only releases a limited number of nt, it may receive and respond to many nt at different synapses. |
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when nt bind to the active site of its receptor the receptor either
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opens a channel (iontropic) or produces slower and longer effects (metabotropic)
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Iontropic
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rapid, short lived, most direct
when the nt bids to the receptore on the membrane it alsmot immeditaly opens gates for some kind of ion (NA, K)-effects localized to one point on the membrane most depend on just glutamate (EPSPS) and GABA (IPSPS) for quick events such as visual stimulation, muscle movements |
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metabotropic effects
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initiation of a sequenceof metabloic reactions that are alower and more long lasting
use a variety of nt longer term activity like memory- as well as hunger, thirst, fear, anger nt binds to the rest of the protain, allowing the protin inside the neuron to react with other molecules |
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G Protein
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coupled to guanosine triphosphate (GTP) an energy storing molecule...and is activated by the neuron---when the transmitter molecule attaches to the receptor the receptor bends releasing the G Protein, the activated G Protein in turn increases the activity of a second messenger molecule such as cyclic AMP
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Second messenger
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communicates to different areas in the cell, influences activity in a lager area of the cell over longer periods of time it can-
1)alter a metabolic pathway 2)turn a gene on in the nucleus 3)open or close an ion chanel 4)alter structure of cell |
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attachment of acetylcholine on to cell
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twists open th eborders of sodium channels. iotropic effects- there are 9 typesof acetycholine receptors that are activated by acety
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neuromodulators
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mainly peptide nt
do not directly excite or inhibit, but increase or decrease the release of other nt, or alter the response of postsynaptic cells to various inputs (intermedate bw nt and hormones) |
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hormone
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a chemical that is secreted in most cases by a gland and is conveyed by the blood to other organs whose activity it influences, long lasting change sin many different part sof the body
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protein hormones
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bound receptors activate somethig inside (enzymes that alter cell activity) like metabotropic process
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pituitary gland-posterior pituitary
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neural tissue, extension of hypothalmus, neurons in th ehypothalmus sysnthesize oxytocin and vasopressin which migrate down the axons to the posterior pituitary and are later released into the blood
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hypothalmic piuitary portal system
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recieve hormones from hypothalmus-no synthesis
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anterior
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composed of glandular tissue, synthesizes 6 hormones-releasing or inhibiting hormones produced by hypothalmus which travel to anterior and control the relase of the 6 hormones- GH, ACTH, TSH, FSH, LH, prolactin
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hypothamlus maintains constant circulating levels of hormones through
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negative feedback system
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acetycholinesterase
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breaks down acetycholine into two fragments choline and acetate, inactivation by chemical process
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myasthenia gravis
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in the absence of acetyl. aceytcholine nt remains and continues stimulkating receptor, drugs thatblock actylkjhlkh are helpful for ppl with diseases that impair acetyylcholine transmission
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reuptake
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presynaptic neuron takes up most of neurotransmitters molecules and reuses them, occurs through special membrane proteins called transporters
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COMT MAO
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enzymes that convert catecholamine transmitters into inactive chemicals
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autoreceptors
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receptors that detect the amount of transmitter released and inhibit further synthesis and release after it reaches a certain level
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retrograde transmitters
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postsynaptic neurons that release special chemicals that travel back to the presynaptic terminal where they inhibit further release of transmitter (NO)
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Heteroreceptors
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receive info from the axon of another cell-excitation or inhibition from another cells input
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human cns beings to form when the embryo is
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2 weeks old, neural tube surrounding a fluid-filled cavity
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proliferation
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production of new cells some cells remain where they are as stem cells and continue to divide while others become neurons or glia and migrate to other locations
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chemicals that help giude neuron migration
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immunoglobins and chemokines
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differentiate
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of neuron, forming of axons and dendritesin some cases the axon grows first, in other cases the axon grows towards its toarget
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ferret experiment
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ferrets turned the way they had been taught to turn when they saw something, rewired temporal cortex received input from optic nerve-producing visual response
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myelination
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process by which glia produce insulating fatty sheaths, grow first in the spinal cord, and then in hin, mid and forebrain
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synaptogenesis
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formation of synapses which constinues throughout life
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exception that the brian can gain new neurons
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olfactory receptor, neurons in the nose remain immature throughout life, they deveolop to replace lost ones
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other exception-stem cells
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undifferentiated cells in the interior of the brain that generaate daughter cells that migrate to ethe olfactory bulb and transform into neurons or glia
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other exception-
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cells in adult hippocampus-prob important contributors to learning
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Paul Weiss
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nerves attach to muscles at random and send a variety of messages, muscles receive many signals but respond only to one---> WRONg
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sperry
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when he cut the nerve connections in newts the axons regenarted to the area of the tectum where it had oiginally been, presumably following a chemical trail-->narly all axons grow to almost exactly their correct target
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a growing axon follows a path of
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cell surface molecules--attracted and repelled by chemicals, follow trails based on attractive chemicals follow until they become insensitive to thaht chemical and thenf ollow another on ehow handy dandy is that!
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neural darwinism
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we start with more neurons and synapses then we keep, selection process keeps some synapses and rejects others, postsynaptic cells strengthen some synapses and eliminates others
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Rita Levi-Montalcini
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muscles determine how many axons SURVIe
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Nerve Growth Factor
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after a neuron forms a synapse on a muscle the muscle delivers a protein called the NGF that promotes the growth and survival of the axon, axons that do not recieve NGF die
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apoptosis
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if the axon does not make contact with the appropiate postsynaptic cell it kills itself
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neurotrophin
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(NGF) a chemical thaht promotes survival and activity of neurons
the most abundunt one in the brain is BDNF |
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to survive neurons must receive neurotrophins from its target cell and from
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incoming axons brining stimulation
nt release neurotrophins when they are released |
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# of motor neurons is highest
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at 11 weeks in the human fetus-decreases from there
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loss of brain cells in a particular area of the brain can indicate
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development and maturation
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after maturity neurons no longer need
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neurotrophins for survival
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fetal alcohol syndrom
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children born of mothers who drank heavily during oregnancy, dendrties are short branches, defects in facial patterns
relates to apoptosis- alcohol supresses release of glutamate, many neurons receie less excitation and neurotrophins and die |
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Dale Purves/RD Hadley
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axons and dendtries modify their structures throughout life, when dendrites grow new spins some last for days and others for life- gain or loss of spines means gain or loss of synapses
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an enriched environment
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enhances sprouting of axons and dendrites
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thickness of cerebral cortex
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is thicker in ppl who remain physically active in older age, but usually decreases with age
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losing one sense
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increases attention to other senses
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in blind people
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touch info had invaded the cortical area which is normally dedicated to vision alone. occiptal section of blind ppl serves verbal and touch functions
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practicing a skill reorganizes the brain to
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maximize performance of that skills- doing a skill over an dover again can make you more adapt to that skill but neccessarily anything else. , sustained attention to anything releazses dopamine and dopamine acts on the cortex to expand the reposne of stimuli, gray metter will be thicker in skilled proffesional musicians
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focal hand dystonia (musicians cramp)
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stimulation on one finger excites mostly or entirely the same cortical ares as another finger, trouble distinguising one finger from the other, this happens in a portion of the somatosensory cortex
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closed head injury
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blow to the head not resulting in puncturing of the brain, rotational forces damage brain tissue against the insid eof the skull
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stroke or cerebrovascular accident
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temporary loss of blood flow to the brain
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ischemia
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bood clot, neurons are deprived of blood and do not receive oxygnen or glucose
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hemorrhage
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ruptured artery, flooded with blood and with excess O, CA
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edema
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casued by ischemia or hemorrhage, accumulation of fluid, increases pressure on brain
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isch and hemm also
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impair ths sodium potasium pump and neurons die
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tissue plasminogen activator
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breaks up blood clots, for treatment of strokes
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penumbra
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area surrounding the immediate damage cells can be saved in this area after strokes occur they survive at least temporarily
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beneifts of a cooled brain
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less activity, lower energy needs, less risk for overstimulation
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cannabinoids
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decrease release of glutumate, prevent excess glutumate from overstimulating the neurons, drugs related to marijuana, reduce cell loss after stroke
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diachisis
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decreased activity of surviving neurons after damage to other neurons, damage to any area of the brain deprives other areas of their normal stimulation
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stimulint drugs
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drugs should promote recovery by decreasing effects of diachisis, should be given during the next weeks and days
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cell bodies cannot be replaced
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but axons can grow back and sometimes they attach to the wrong muscle
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collateral sprouts
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a surviving axon grows a new branch to replace the synapses left vacant by a damaged axon, , cells secrete neurotrophins to induce other axons to form new branches, damage also sometimes induces sprouting by unrelated axons
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gangliosides
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combined carbohydrates and fat molecules promote the restoration of damaged brains, may increase sprouting
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progesterone
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increases release of neurotrphin progesterone, which promtes axon sprouting and formation of new synapses
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denervation supersensitivity
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muscle cell bilds additional receptors when the axonis cut or inactive for days- and it becomes sensitive to acetylcholine over a wider area of its surface
heightened sensitivity to a nt deneravition refers specifically to when the axon has been destroyed may help ppl maintain normal behavior |
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disuse supersensitivity
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due to inactivity of the incoming axon
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phantom limb
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a continuing sensation in an amputated body part, occasional tingeling to intense pain
develop when relevant portion of the somatosensory cortex reorganizes and becomes responsive to alternative inputs--> connections in the brain remain plastic throughout klife |
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deafferented
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limb has lost its sensory or affernt input, but still has connections to motor neurons, brain damaged is based on learning-still capable of using these limbs
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thomas lavere
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lesion to the visual cortex impairs retrieval of a memory but does not destroy it completly
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wide variation of drug effects are accounted for by
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ppl who differ widly in proportions of various receptor types
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antagonist
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a drug that blocks the effects of a neurotransmitter, blocks manufacturing or enhances reuptake
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agonist
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mimics or increases the effects of a nt
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what drugs can do
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increase or decrease synthesis, cause it to leak from vesicles, decrease uptake, block breakdown into inactive chemicals, stimulate or block postsynaptic receptors
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affinity
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if the drug binds to a receptor, vary in strong to weak affinities
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efficacy
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tendedncy for drug to activate its receptor, if it fails to stimulate then it has a low efficacy
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nucleus accumbens
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a small subcortical area rich in dopamine receptors, drugs influence the relase of dopamine here, sustanied bursts of dop inhibit cells that release GABA
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stimulant drugs
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highly addictive, increase excitement, alertness, motor activity, whle elevating mood, decrease fatigue
amphetamine, cocaine, methylphenidate (ritalin), MDMA-ecstacy |
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amphetamine
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stimulates doopamine synapses by increasing the release of dopamine from the presynaptic terminal
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dopamine transporter
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presynaptic terminal normally reabsorbs released dopamine through this protein, amphetamine reverses this process
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cocaine
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blocks the reuptake of dopamine, norepherine, serotoni, prolonging their effects, short lived due t odevelopment of tolerance-classical conditioning, stimulant drugs are known for their short term effects
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methylphenidate
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prescribed for ADD, longer lasting less intense then cocaine, clock reupake of dopamine, children who take this drug are lesslikley to abuse drugs later in life
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MDMA-ectsacy
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release of dopamine, serotonin-hallucinations
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Nicotine
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stimulates all 4 nicotine receptors, present in tobacco, stimulates the nicotine receptor foudnin cns and skeletal muscle, increase of dopamine release
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opiate drugs
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opium poppy, relax ppl, decrease attention to real world problems, decrease sensitvity to pain
morphin, heroin, methadone brain produces peptides (endorphins) inhibit GABA-release of GABA, block locus coueruleus, that responds to arousing stmulis and memory storage os you have less stress response and l ess memory storage |
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marijuana
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THC and cannabinoids
there are no cannabinoid receptors in medulla (wher eneurons are that control heart beat and breathing rate)-cannot od on marijuana , intensifaication of sensory experiences and illusion tim eis passing very slowly, cannibinoids dissolve in the bodys fats, canniboid receptors are the most abundunt in the mammalian brain anandamine/2-AG bind to cannaboid receptors, the cannaboid receptors are located on the presynaptic neuroninhibit glkutamate and gaba |
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hallucinoenic drugs
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distort preception, stimulate serotonin
post synaptic neurons increase number of receptors making lsd more effective |
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electronic synapses/gap junctions
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direct electrical connections bw neurons
ap-->ap-->ap-true synapse but very close, synapses in eye- rapid sesnory systems |
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peripheral nervous system
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somatic-voluntary, sensory info to cns
autonomic-ivoluntary muscles |
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dorsal
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back, top of the brain
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ventral
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towards stomach, away from back
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anterior
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front
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posterior
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reear
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superior
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above
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inferior
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below
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lateral
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towards teh side
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medial
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toward the middle
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proximal
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close t opoint of attacment
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dital
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farther away
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ipsilateral
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on the same side o fthe body
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contralateral
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on opposite side of the body
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coronal plane
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brain structures as seen from the front
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sagital plane
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as seen from the side
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horizontal
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as seen from above
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lamina
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a row or layer of cell bodies separated from other cell bodies by a layer of axons and dendrites, 6 layers in cortex
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column
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columns functionally distinct-each column extends through several laminae, a set of cells perpendicular to the surface of the cortex, neurons have simiilar properties in each column
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tract
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a set of axons within the cns, also known as a projection, fibers projecting from neuron a to b
in spinal cord--> tracts on rght-descending tracts on left-ascending, tracts carry different info to brain |
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nerve
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a set of axons in th eperihperary, cns to muscle, sensory organ to muslce
12 cranial nerves 31 spinal nerves |
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nucleus
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a cluster of neuron cell bodies within CNS
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ganglion
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cluster of neuron cell bodies outside the SNs (dorsal root ganglia)
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gyrus
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proturbance on surface of brain
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sulcus
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fold or groove that separates one gyrus from another
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fissure
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a long deep sulcus
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bell-magendie law
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the entering dorsal roots carry sesnroy information and exiting ventral roots carry motor information
spinal cord sends inf oto the brain and recieves motor commands from th ebrain |
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dorsal root ganglia
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cell bodies of sensory neurons are located in clusters of neurons outside the spinal cord, sensory in....motor neuron-sensory out
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grey matter
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H centered in th emiddle of the spinal cord- cell bodies and dendrites
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white matter
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axons-myeination around axnns makes it white
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sympathetic
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prepares the organs for vigourous activity...increase breaathing, heart rate, decrease in digestive
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parasympathetic
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nonemergency responses by organs
both are constantly active to various degrees aka craniosacral system |
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sympathetic outflow
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most of the ganglia are near the spinal cord
postganglionic axons-norepinepherine released, farther away from taregt axons |
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presympathetic outflow
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all output comes from brain to vagus or pelvic nerve, postganglionic axons a are closer to taarger organs-secrete acetylcholine by pre-post ganglionic neurons
-rest/rejuvination |
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because the two systems secrete different transmitters
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certain drugs may excite or inhibit one system or the oher
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hindbrain
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rhombencephalon (medulla, pons, cerebellum)=brainstem
metencephalon (pons, cerebellum) myelencephalon (medulla) |
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medulla
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above spinal cord, heart rate, breathing rate, vomiting, salivation, coughing, sneezing
controls these reflexes through the |
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cranial nerves
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control sensations from th ehead, muscle movements in head, sympathetic output to organs
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pons
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location where axons from each half of the brain cross to the opposite side of the spinal cod, so that the left hemisphere controls th eright sid eof the body and the rght hemisphere controls th eleft side of the body
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reticular formation
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descending portion=controls motor areas of spinal cord
ascending-arousal, attention |
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raphe system
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sends axons to much of th e forebrain modifying brains rediness to respond to stimuli
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cerebellum
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balance, coordination, shiftng attention back and forth bw auditiry and visual stimuli
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midbrain
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mesencephalaon-tectum, tegmentum, superior collicuus, inferior colliculus, substantia nigra
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tectum
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roof of midbrain
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superior/inferior colliculus
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swellings on side of th etectum, important routes for sensory info
superior-vision inferior-audition |
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tegmentum
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under tectum, intermediate level of hindbrain
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substantia nigra
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dopamine containing pathway that deteriorates in parkinsons disease
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forebrain
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prpsencephalon
diencephalaon-thalmus, hypothalmsu telencephalon-cerebral cortex, hippocampus, basal ganglia consists of two cerebral hemispheres |
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basal ganglia
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movement
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limbic system
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olfactoy bulb, hypothalmus (pituitary gland), hippocampus (emotions), amygdala, cingulate gyrus
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thalmus
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relay center, processes all info except olfactory info
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hypothalmus
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feeding, flighting, fighting, sexual behavior, ventral to thalmus
conveys message sto the pituitary gland-release of hormones superchismatic nuclei-sleep/dreams, variety f nuclei within hypothalmus |
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pituitary gland
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hypothalmus release hormones
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basal ganglia
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caudate nucleus, putamen, globus pallidua exchange of info within cerebral cortex-movement emotional expression
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hippocampus
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memories
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central canal
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fluid filled channel in the center of th espinal cord
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ventrucles
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four fluid filled cavities within th ebrain`
1, 2-lateral ventricles in brain 3 separates the thalamus in half 4 continues down to central canal |
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cerebrospinal fluid
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a clear fluid similar to blood plasma foudn in central canal and ventricles, comes into contact with tissue to provide nutrietns, cushions brain against mechanical shock when th ebrain moves
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amygdala
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fear
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central solcus
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separates precentral gyrus and postcentral gyrus
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precentral gyrus
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motor
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postcetralgyrus
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sensory
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