What are some ways that impulses at the synapse can be altered?
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Impulses at the synapse can be altered by:\n\n1.) Up-or-down regulation of receptors\n\n2.) Levels of enzymes that break down excess neurotransmitters (such as MAO, monoamine-oxidase).\n\n3.) Release of Nitric Oxide by post-synaptic neuron\n\n4.) Inhibitory synapse at axon
734307
Restore celll membrane potential, restore normal membrane transport and ionic balance.
888477
Yes.  The more you use a neuron network the stronger it becomes.  The increase is minuscule, but certainly large enough to measure.  Good luck in your quest for more knowledge. Ciao!\n-C
846839
My hunch is that with a bit more time separation between the stimuli, that the nerve cells would have time to recover between firing signals, and that they could build a greater action potential.  \n\nI'm a bit perplexed as to why you'd be tackling this problem at 7:30 AM on Thanksgiving Day......or are you in Europe?
416619
C) By interfering with the electron transport chain, energy production (in the form of ATP) would be significantly reduced.  Neurons use a great amount of energy to maintain the ionic gradient that allows synaptic transmission.  In he absence of ATP, the ionic pumps, primarily sodium/potassium, would not function, the ionic gradient would break down, and it would halt neuronal transmission.
471751
a synapse is also called a junction. it's a space between neurons where neurotransmitters are released. to transmit information from one neuron to another, the neurotransmitters travel through the cell body of the neuron and are released though the axon. after chillin in the synaptic gaps they are received from the dendrite of another neuron. i'm assuming you know what an action potential is? anyway as it travels through the nueron it can't really leave so it lets the neurotransmitters escape and go to another neuron. if the action potential is great enough you react to the stimulus. if it doesn't reach the threshold then you don't.
314995
Within the cells, small-molecule neurotransmitter molecules are usually packaged in vesicles. When an action potential travels to the synapse, the rapid depolarization causes calcium ion channels to open. Calcium then stimulates the transport of vesicles to the synaptic membrane; the vesicle and cell membrane fuse, leading to the release of the packaged neurotransmitter, a mechanism called exocytosis.\n\nThe neurotransmitters then diffuse across the synaptic cleft to bind to receptors. The receptors are broadly classified into ionotropic and metabotropic receptors. Ionotropic receptors are ligand-gated ion channels that open or close through neurotransmitter binding. Metabotropic receptors, which can have a diverse range of effects on a cell, transduct the signal by secondary messenger systems, or G-proteins.
97213
Both inhibition and stimulation begin with the same action, release of some signal from a presynaptic neuron onto a postsynaptic neuron.  In most cases, this is a chemical signal where the presynaptic neuron releases small amounts of neurotransmitter into the synaptic cleft between the pre and postysnaptic neurons.  The neurotransmitter then binds to a receptor on the postsynaptic membrane which then leads to some change in the postsynaptic neuron.  This change could be immediate (opening and/or closing of channels in the membrane) or delayed (activation of some chemical cascade within the neuron).\n\nGenerally, inhibition of a postsynaptic neuron occurs when these changes result in a decrease in the likelihood that the postsynaptic cell will fire an action potential.  This could be by increasing the polarization of the cell membrane or by interfering with processes/channels that would otherwise cause the cell to depolarize.\n\nExcitatation of a postsynaptic neuron is when the effect of the cell causes the cell to increase it's likelihood of firing either by opening channels that cause the balance of ions on either side of the membrane to become less polarized, or by decreasing the threshold required for the cell to fire an action potential.\n\nIt is important to recognize that the neurotransmitter does not determine if the presynaptic effect on the postsynaptic neuron is either excitatory or inhibitory, but rather the events that follow neurotransmitter binding to the postsynaptic receptor.  In other words, the chemical doesn't determine what happens to the cell, the action of the receptor does.
426295
your dendrites grow and make new connections.
205027
pen and paper - mostly they write it down. \n\nif they don't I'd guess it's called short term memory or working memory (biologically it involves an increase in the efficiency with which nerve impulses pass across synapses. It does not require any protein synthesis or remodeling of the synapse. )
712534
used to change colligative properties of solutions
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Synapse barriers?  I know what a synapse is (simply, space between neurons), but I've never heard of synapse barriers.  There's a neuropsychologist wandering around somewhere on Yahoo Answers who would be the one to ask.
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Jardon B, Bonaventure N. \nCentre de Neurochimie du C.N.R.S. Strasbourg, France.\n\nThe frog horizontal monocular optokinetic nystagmus (OKN) is asymmetrical, the temporal-nasal (T-N) stimulation being the sole stimulation efficient to evoke the reflex, the nasal-temporal (N-T) component being almost absent. Coil recordings showed that, in adult animals, prolonged monocular visual deprivation by unilateral eyelid suture provoked the appearance of the N-T component. The OKN became symmetrical, reacting for both directions of stimulation. Microinjection of either gamma-aminobutyric acid (GABAA) agonist 4,5,6,7-tetrahydroisoxazolo (5,4-C) Pyridin-3-ol (THIP) or muscarinic cholinergic antagonist atropine into the nucleus lentiformis mesencephali, the pretectal mesencephalic structure involved in OKN, transiently abolished the presence of N-T component. This result suggests that the phenomenon of visual plasticity, occurring after a week of monocular deprivation, can be due, at least partially, to reduction in pretectal GABAergic inhibition, and to concomitant activation of cholinergic muscarinic receptors.\n\nPMID: 1584460 [PubMed - indexed for MEDLINE]
888539
its impulse change in momentum
122059
Sure you can. The sense of smell is controlled by brain synapsis just like the ability to see or hear or really any other function of the body. If there is damage to these synapsis then you can lose this ability.
512703
Neurotransmitters transmit impulse from one neuron to the other neuron.It's effect local. On the other hand, neuromodulators have hormone-like effect which can circulate in the bloodstream.For example:Nerve growth factor(NGF)
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Certain antibiotics, particularly aminoglycosides, may compound the effects of neuromuscular blockers, by acting on the sodium channel and thus affect the motor end plate of the neuron and its action potential.