BIOL Week 6. Nervous System. Transmission at Synapses

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1 Collin County Community College BIOL 2401 Week 6 Nervous System 1 Transmission at Synapses Synapses are the site of communication between 2 or more neurons. It mediates the transfer of information and it is the place where the signal are transmitted, blocked or modulated. Each neuron in the brain is believed to form about 1000 synaptic endings. With around neurons in the brain, this yields a staggering number of synapses and possible pathways for impulses to travel. 2 1

2 Synapses Definitions The neuron that sends the signal = pre-synaptic neuron The neuron receiving the signal = post-synaptic neuron If the signal travels from axon to dendrite = axodendritic synapse If the signal goes from axon to cell body = axosomatic synapse If signal travels from axon to axon = axoaxonic synapse 3 SYNAPSES There are two types of Synaptic transmission 1. Electrical Synapses arriving impulse forces ions to flow through gap junctions that connect to adjacent cells electrical disturbance depolarizes the post- synaptic cell they result in fast transmission and capable to synchronize the activity of interconnecting cells 4 2

3 SYNAPSES 2. Chemical Synapses This synapse is characterized by a synaptic cleft which separates the two neurons ( ~ nm).. So there is no physical connections Impulses cannot jump this cleft. That's why the organization across a synapse is such that the presymaptic neuron terminal contains vesicles with neurotransmitters ( the chemical signal) and the postsynaptic neuron membrane contains the receptor proteins for this messenger 5 SYNAPSES In a chemical synapse, the presynaptic impulse which is ionic in nature, is converted to a chemical signal (neurotransmitters) that crosses the cleft and influence the chemically gated ion channels in the postsynaptic neuron, and consequently the membrane potential in that area. 6 3

4 ACTIONS AT A SYNAPSE 1. Action potential, moving along axon s voltage-gated Na + and K + channels, arrives at terminal. Ca ++ 2 AXON 1 2. Action potential opens voltage-gated Ca ++ channels Ca ++ influx triggers neurotransmitter release into the synaptic cleft. DENDRITE 4 4. The binding of neurotransmitters to receptor proteins in the postsynaptic membrane is linked to an alteration in its ion permeability. 7 ACTIONS AT POSTSYNAPTIC END The function of the neurotransmitters is to bind to a specific receptor on the postsynaptic membrane Those receptors are chemically gated ion channels. The neurotransmitter is thus the chemical that will bind to an ion channel and result in a certain action. This action can be a local depolarization ; if this is the case we are dealing with the creation of graded potentials. This action can however be a local hyperpolarization ; if this is the case we are preventing the creation of graded potentials. 8 4

5 EPSP versus IPSP Excitatory PostSynaptic Potential (EPSP) Is a depolarization created in the Postsynaptic membrane. It increases the possibility of having an A.P. in the axon of this neuron Inhibitory PostSynaptic Potential (IPSP) Is a hyperpolarization created in the Postsynaptic membrane. It decreases the possibility of having an A.P. in the axon of this neuron 9 EPSP versus IPSP An excitatory postsynaptic potential (EPSP) is a graded depolarization that moves the membrane potential closer to the threshold for firing an action potential (excitement). 10 5

6 EPSP Neurons versus IPSP An inhibitory postsynaptic potential (IPSP) is a graded hyperpolarization that moves the membrane potential further from the threshold for firing an action potential (inhibition). 11 EPSP versus IPSP Graded depolarizations are typically the result of the inward movement of Na + (but can result from Ca ++ influx and/or decreased K + efflux). Graded hyperpolarizations are typically the result of the outward movement of K + (but can result from decreased Na + influx). 12 6

7 Signal Integration Neurons receive as many as 200,000 terminals. Effect on initial membrane segment reflects an integration of all activity at that time. It is an integration and summming up of all EPSP s and IPSP s! 13 Signal Integration Threshold refers to the minimum graded depolarization that initiates the cyclic activity of the voltage-gated Na + and K + channels, resulting in the initiation of an action potential. The membrane potential of a real neuron typically undergoes many EPSPs (A) and IPSPs (B), since it constantly receives excitatory and inhibitory input from the axons terminals that reach it. 14 7

8 NEURONAL COMMUNICATION Two types of signal summation Temporal Summation Spatial Summation 15 NEURONAL COMMUNICATION Temporal Summation The same neuron fires quickly in succession The result is more N.T. released and thus a bigger graded potential The same neuron releases always the same N.T., thus the effect is always similar 16 8

9 NEURONAL COMMUNICATION Spatial Summation Different neurons fire in quick in succession or at the same time The result is more N.T. in the synaptic cleft Each neuron releases it s own N.T.; the effect is not always similar 17 Temporal versus Spatial Summation Panel 1: Panel 2: Panel 3: Panel 4: Panel 5: Two distinct, non-overlapping, graded depolarizations. Two overlapping graded depolarizations demonstrate temporal summation. Distinct actions of stimulating neurons A and B demonstrate spatial summation. A and B are stimulated enough to cause a suprathreshold graded depolarization, so an action potential results. Neuron C causes a graded hyperpolarization; A and C effects 18 add, cancel each other out. 9

10 Graded potentials decay as they move over distance. Threshold is reached A.P. will start in axon Distance from stimulus Where v.g. channels start 19 Cholinergic Synapses These are synapses that use Acetylcholine (ACh) as Neurotransmitters They are the oldest studied and the best known They are present in the Neuromuscular Junction (NMJ), CNS, and PNS. ACh in the NMJ always results in an EPSP in the postsynaptic membrane because it opens chemically gated Na+ channels 20 10

11 Terminating the Signal at the Synapse At every synapse, the signal that started the events has to be terminated If not, we would have continuous stimulation For example, at a NMJ, this would mean a continuous contraction of the skeletal muscle involved. What we want is one signal ( EPSP above threshold) = one contraction Termination mechanisms Neutrotransmitter becomes degraded by specific enzymes Neurotransmitter diffuses out of the synapse area Neurotransmitter is taken up be glial cells or by pre-synaptic membrane (axon itslef) 21 Termination of the NT effect Re-uptake for recycling by the axon terminals (requires specific transporters) Diffusion out of synaptic cleft Breakdown by specific membranes located on postsynaptic membrane 22 11

12 AcetylCholine-Esterase AcetylCholine Esterase (AChesterase) is a specific enzyme found on the postsynaptic membranes of cholinergic synapses It functions to break down ACh into Acetate and Choline Thus, from the moment ACh is releases in the synaptic cleft, it is already being broken down The axon then takes up the choline part and recycles it back into Ach within the NT vesicles 23 AcetylCholine-Esterase Acetate Choline 24 12

13 Cholinergic Synapses 25 Modulation of Neurotransmitter Release Modulation of N.T. release refers to changing the amount of N.T. released into the synaptic cleft. The more (less) N.T. released that causes EPSP s, the higher (lower) the probability of an A.P. The reverse holds true for N.T. that result in IPSP s 26 13

14 Modulation of Neurotransmitter Release Facilitation A neuron that is brought closer to threshold is said to be facilitated. The higher the degree of facilitation, the less additional stimuli needed to trigger an A.P. Examples Nicotine : stimulates ACh receptors Caffeine : lowers the threshold for stimulation 27 Modulation of Neurotransmitter Release Presynaptic Inhibition A neuron that for example causes an IPSP at the presynaptic membrane Or a neuron that releases a NT (Example is GABA) at the presynaptic membrane that in turn closes v.g. Ca++ channels Both situation will result in less Ca++ influx in the axon terminal and hence less exocytosis of NT vesicles! 28 14

15 Modulation of Neurotransmitter Release Presynaptic Facilitation A neuron that for example causes a prolonged opening of v.g. Ca++ channels ( action of seretonin at some synapses) In this situation more Ca++ influx occurs into the axon terminal and hence more exocytosis of NT vesicles! 29 Examples of Neurotransmitters AcetylCholine (Ach) Blocks Ach receptors and causes paralysis in muscles 30 15

16 Examples of Neurotransmitters Biogenic Amines These are N.T. derived from amino acids The following are derived from Tyrosine Also known as the catecholamines Epinephrine = adrenaline Dopamine is an important brain N.T. 31 Amino Acids Examples of Neurotransmitters 32 16

17 Heavy metal poisoning Neuronal Afflictions results in damage to neuroglia and demyelination mercury, lead arsenic are the major ones Multiple Sclerosis results demyelination of neurons in brain, spinal cord believed to be a defect of the immune system Tay Sachs Disease genetic abnormality that results in a build-up of gangliosides in lysosomes of neurons Results in destructions of neurons; children die at early age. 33 Tetrodotoxin (TTX) found in Pufferfish (fugu) and some salamanders very potent v.g. Na + channel blocker Neuro-Toxins Saxitoxin found in some marine microorganisms (dinoflagellates) some are responsible for red tide in seas eating contaminated shellfish can result in paralytic shellfish poisoning (mechanism is similar as TTX) 34 17

18 Neuro-Toxins Nerve gases and Insecticides Inhibit the function of ACh-esterase Results in maintained contractions of muscles such as diaphragm (person can t exhale anymore) Atropine Competes with ACh for binding sites on receptor tubocurare Prevents binding of ACh to its receptor 35 18