[Music] and this video will talk about synapses between neurons there are several types of relationships between the input to a synapse and output but the common types of neuron neuron relationship is many to one meaning one neuron takes input from several neurons creating several synaptic regions it is very important to know that synaptic connections are mainly on a cell body or in a dendritic membranes the places where we see ligand gated channels we will see how an action potential transmits from one neuron to another first let me zoom here a single dendritic synaptic point the action potential comes and depolarizes the presynaptic membrane the vesicles release their content into the synaptic cleft suppose it releases acetylcholine this neurotransmitter binds with its receptor and opens channels increasing sodium and potassium conductance because the net force on sodium is greater than net force on potassium the main current flowing is sodium influx sodium influx depolarize the postsynaptic membrane let's suppose from negative 72 zero millivolt to value approximately halfway between the equilibrium potentials for sodium and potassium it is very important to know that at negative 10 millivolts we have the threshold potential when we reach the threshold potential the current travels along the dendritic and cell body membranes up to the axon hillock it is important to know that at dendrites as well as at neuronal body the current flow cannot initiate an action potential because here we do not have fast voltage-gated sodium channels the only region near to the dendrites where we do have a high density of voltage-gated sodium channels is an axon hillock let me zoom here the membrane of the axon hillock when a current flows up to the axon hillock it takes the membrane potential from its resting state up to the threshold potential as a consequence the voltage-gated sodium channels open up and we get a sodium influx and this sodium influx initiates an action potential this action potential further transmits forward along the axon another important point is that the closer the synapse is to the axon hillock the greater its influence in determining whether an action potential is generated in other words out of these two synapses the second one has greater chains to generate an action potential because it is closer to the axon hillock another important point understand is that in these synapses an action potential in a presynaptic cell is insufficient to produce an action potential in a postsynaptic cell instead many presynaptic cells converge on the postsynaptic cell these inputs are made and the sum of the inputs determines whether the postsynaptic cell will fire an action potential in this part of the video we will talk about the differences between the excitatory postsynaptic potential and inhibitory postsynaptic potential first let's talk about excitatory postsynaptic potential when a presynaptic membrane depolarizes let's suppose it releases glutamate and excitatory neurotransmitter glutamate attaches to its receptor in a postsynaptic membrane and opens non selectively permeable channels for sodium and potassium because of the net force sodium influx dominates over potassium efflux the sodium influx let suppose make the membrane potential less negative perhaps to negative 60 millivolts these 10 millivolts of depolarization is called excitatory postsynaptic potential excitatory postsynaptic potential brings the membrane potential close to the threshold potential which is at negative 10 millivolts this excitatory postsynaptic potential increases the excitability of the postsynaptic neuron making the neuron more likely to fire an action potential it is important to note that excited to repost synaptic potential is a similar to the endplate potential found at the neuromuscular junction and also some mates to reach the threshold and generate an action potential in addition to glutamate excitatory neurotransmitters include acetylcholine and aspartate second let's talk about inhibitory postsynaptic potential when a presynaptic membrane depolarizes suppose it releases an inhibitory neurotransmitter gaba in a synaptic cleft gabber attaches to its receptor in a postsynaptic membrane and opens chloride ion channels a type of ligand gated channel because the membrane potential in the postsynaptic membrane is Nega 70 millivolts and a chloride equilibrium potential is negative 90 millivolts we get a net force on chloride directed inward please note chloride is negatively charged ion this chloride influx hyperpolarizes the postsynaptic cell toward its equilibrium potential suppose from negative 70 to negative 85 millivolts this 15 millivolts of hyper polarization is referred to as inhibitory postsynaptic potential inhibitory postsynaptic potential takes the membrane potential away from threshold this it decreases the excitability of the postsynaptic neuron making the neuron further from firing and action potential in addition of gaba inhibitory neurotransmitters include glycine now let's recap and sum up what we have looked at in this section and add some points which are important for clinical purposes first let's talk about decreased neuronal excitability connection and increased neuronal excitability or conduction clinical signs of decreased neuronal excitability and conduction could include weakness ataxia hyperreflexia paralysis and sensory deficit the causes of decreased neuronal excitability include ion disturbances that include hypokalemia chronic hyperkalemia and hypercalcemia a second possible cause of decreased neuronal excitability and conduction includes loss of neurons demyelination as in case of guillain-barre a amyotrophic lateral scoliosis and normal physical aging the third cause of decreased neuronal excitability and conduction includes toxins and drugs like local anesthetics like cane drugs and toxins like tetrodotoxin and saxitoxin the neuromuscular Junction disorders drugs and toxins also decrease the excitability in neuromuscular Junction because of decreased excitability in neuromuscular Junction include depolarizing muscular nicotinic receptor blockers nondepolarizing muscular nicotinic receptor blockers the diseases like lambert-eaton syndrome myasthenia gravis and botulinum toxin next let's talk about increasing neuronal excitability or conduction clinical signs of increasing neuronal excitability and conduction could include hyperreflexia spasms muscle fasciculation cad knee tremors paresthesias and convulsions the causes of increased neuronal excitability and conduction include ion disturbances in a case of acute hyperkalemia and hypocalcemia we have already explained the mechanisms loss of neurons demyelination in a case of multiple sclerosis third toxins like Sigma toxin and batrachotoxin the neuromuscular junction disorders drugs and toxins also increase the excitability in neuromuscular Junction because of increased excitability in neuromuscular Junction include acetylcholine esterase inhibitors and lateral toxin you