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Lecture 15

BIOL 1030 Lecture 15: Lecture 15
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Department
Biological Sciences
Course
BIOL 1030
Professor
Scott Kevin
Semester
Winter

Description
Lecture 15 o Action potentials propagate down the neuron. Myelination speeds up that process and refractory ensures that this propagation occurs in a single direction. o The signal has now reached the presynaptic terminals and now needs to communicate with the next neuron (cell-cell communication). o The pre and postsynaptic cells are physically separated by a gap known as a synapse (the space itself is known as the synaptic cleft). o Electrical signals cannot jump physical gaps and so the electrical signal (which is in the form of a depolarization – charge “flipping”) needs to be converted to a chemical signal. o Chemical signals are in the form of neurotransmitters which are released by the presynaptic neuron and diffuse across the synaptic cleft and reach the plasma membrane of the postsynaptic cell. o Now the voltage-gated calcium (Ca ) channels become involved (as they are not involved in the actual action potential). They are present only in the presynaptic terminals. o The wave of depolarization travels down the length of the neuron. The membrane of the presynaptic terminal becomes depolarized and become positive on the inside of the cell. o This flip of charge is the key to activate (opens) the voltage gated calcium channels. o Calcium is much more concentrated on the outside than the inside and so will flood into the presynaptic neuron through those channels. o Calcium is important as it is involved in the movement of the vesicles containing neurotransmitters. o Vesicles of neurotransmitters are “just sitting around” at a resting state. Calcium causes them to move to the end (plasma membrane) of the presynaptic terminals. This is known as calcium-dependent trafficking. o The vesicles fuse with the plasma membrane and release their contents into the synaptic cleft. o Theydiffuse to the postsynaptic cell where there are ligand-gated channels on the plasma membrane of the postsynaptic cell. In which case the ligands are the neurotransmitters. o There are two important neurotransmitters for the situation studied. They aren’t the only two. o One neuron will only produce one neurotransmitter. o Acetylcholine (Ach) is one type of neurotransmitter, if a neuron produces Ach then it will not produce any other neurotransmitter. o There are ligand-gated sodiumchannels on the plasma membrane of the postsynaptic cell (like the ones found on a nociceptor), however, they are only specific to acetylcholine. o Onlyacetylcholinewill open them.When Achis boundto the channel, it opens and sodium is free to move into the cell. o This causes small depolarizations in the postsynaptic cell as there is generally not a lot of sodium entering the cell (subthreshold stimulus). It would then return to resting state. o If the acetylcholine release occurs a short time after the first release this can build onto the depolarizations. o Collectively these depolarizations caused by acetylcholine are known as EPSPs (excitatory postsynaptic potential). Depolarizations makes the neuron closer to threshold so is referred to as excitatory. o A second important neurotransmitter is GABA. On the postsynaptic cell are ligand-gated chlorine (Cl ) channels which opens when the ligand GABA is bound to the channel. o That allows chloride to move down its concentration gradient (into the cell). This makes the cell more negative – referred to as a hyperpolarization – this decreases the membrane potential. o Afterthestimulusisgone –thecellreturnstoitsrestingmembranepotential –andsimilarly this stimulus can be built upon. o These hyperpolarizations created by the influx of chlorine ions are deemed IPSPs (inhibitory postsynaptic potential). Makes the cell’s potential further from threshold. o Any one cell is receiving stimuli from hundreds of presynaptic neurons. A single presynaptic neuron is never strong enough to stimulate the postsynaptic cell enough to reach threshold. o Theirsignals can add up. Someofthese presynapticneurons will beinhibitory (releasing GABA) and others will be excitatory (releasing acetylcholine). o When these signals are adding/taken in at the same time – this is referred to as summation – which refersto theaddition of all thenextchargedifferences inducedbythepresynaptic neurons (all the hyper and depolarizations from GABA and Ach respectively). o If the summation is enough for the membrane potential to reach threshold, an action potential will result. o One form of summation is known as temporal summation – which is repeated signaling over time. o For example – inhibitory signal → delay(returns to resting due to delay). Excitatorysignal → delay (returns to resting). o Gradual “up and down,” if there are enough positive signals (EPSPs) to outweigh the negative signals (IPSPs) – an action potential will be reached. Adding over time. o Analogy – your mom telling to clean up your room over and over. Might not do it the first time, over time if she tells you constantly you get tired of her nagging and do it – temporal summation. o With spatial summation, it involves many neurons stimulating a postsynaptic cell at the same time. For example – 10 EPSPs and 2 IPSPs at the same time (the EPSPs outweigh and cause a large increase in membrane potential). o Firingoccursat different parts ofthe target cell.The net effects of excitatoryandinhibitory stimuli will determine what occurs at the postsynaptic cell with spacial summation. o With respect to the reflex arch, ligand-gated sodium channels at the nociceptors are involved in the detection of a stimulus. This generates an action potential that propagates down the sensory neuron. o This leads to the release of neurotransmitters at the presynaptic terminals of the sensory neuron that stimulate the next postsynaptic cell (an interneuron in the spinal cord in the case for a reflex arch). o At the interneuron, this presynaptic stimulation is always excitatory (Ach). Sensory neurons are always excitatory. o The same events as above will again occur in the interneuron. The interneuron synapses to a motor neuron and it also always induces an excitatory signal. o This occurs again within the motor neuron and the motor neurons are also all excitatory as they synapse to a target organ (muscle). o Similar events occur at the target organ; however, it does not generate an action potential, it will instead contract. o Presynaptic terminals of the motor neuron synapse with the muscle cells – referred to as a neuromuscular synapse (the muscle cells contain bundles of myofibrils). The myofibrils are wrapped in the blue sarcoplasmic reticulum. o Acetylcholineis released into thesynaptic cleft at themusclecell.Attheplasmamembrane of the muscle cells are ligand-gated sodium channels. Ach binds → sodium rushes into the muscle cells → the muscle cells are depolarized (same as with postsynaptic neurons). o The plasma membrane of the muscle cells form deep invaginations known as T-tubules which make physical contact with the sarcoplasmic reticulum around the myofibrils inside the muscle cell. o The sarcoplasmic reticulum is the endoplasmic reticulum of a muscle fibre. Its main role in muscle contraction is the storage of calcium ions. There is a much larger concentration of calcium ions in the sarcoplasmic reticulum than in the cytosol of the muscle cell. o There is also a greater concentration of calcium ions in the outside interstitial fluid than in the cytosol. o Calcium is vital in the co
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