Chemical Synapse

The end of the axon spread into some shorter fibers that have swellings on the ends called synaptic knobs. The synaptic knob has a number of little saclike structures in it called synaptic vesicles. Inside the synaptic vesicles are chemicals hung in fluid, which are molecules of substances called neurotransmitters which are inside a neuron and are going to transmit a message. Neurotransmitter are released into the synapse from synaptic vesicles. The neurotransmitter molecules bind to receptor sites on the releasing neuron and the second neuron or glands or even muscles causing a reaction.

An action potential travels down the axon of the presynaptic neuron; once the action potential reaches the axon terminal synaptic vesicles migrate toward the synapse. They then release neurotransmitters into the synaptic cleft. The

The neurotransmitter is released from vesicles from a pre-synaptic neurone and diffuses across the synapse, which is a gap between two neurones, and travels to the post synaptic neurone. Serotonin binds to reuptake channels on the presynaptic neurone, from which it was released, and is transported back so that it can be stored and reused.

That signal may be strong enough to pass the axon hillock and to then open the ion channels that grant positively charged ions to enter into the cell (Ingersoll, year). Those positively charged ions continue to assist the electrical signal. The electrical signal goes down the axon to the terminal button. When a charge of acceptable force gets to the terminal button, the cell “fires.” From there, the synaptic vesicle comes together with the terminal button wall. This lets the neurotransmitter molecules exit the neuron.

In the brain, neurons communicate between each other and with target cells via a great numbers of chemicals they release, so called neurotransmitters. A signal in the brain is sent from a presynaptic neuron to a postsynaptic cell through synaptic transmission, allowing the brain to process information in a rapid way. (Südhof, Starke and Boehm, 2008)

A. Depolarization; excitatory postsynaptic potential. Sodium would depolarize the membrane and increase the likelihood that the post synaptic neuron would fire an action potential.

It plays a significant role in many neurological functions, including brain plasticity (4), learning and memory (5), and induction of pain (6). Poor or excess release of glutamate can cause serious neurodevelopmental and neurodegenerative disorders such as autism (7-9), epilepsy (7, 10-13), schizophrenia (14), Alzheimer’s disease (14-17) and Parkinson’s disease (18, 19). Physiologically, glutamate is released from pre-synaptic vesicles into neuronal synapses in response to action potential. The concentration of glutamate within the vesicles is reported to be ~100 mmol/L (20). The action potential firing mechanism primarily involves the movement of cations (Ca2+, Na+ and K+) across the neuronal membrane. Two voltage-gated ion-channels located in the axon permit active transport of K+ and Na+, into and out of the cells (20). This ion exchange creates a potential difference of -70 mV (resting potential) through the neuronal membrane. Sudden depolarisation or action potential occurs when potential drops, allowing Na+ to flood into the cells. Action potential is terminated to restore the resting potential of the membrane. Ca2+ channels open to allow the transport of Ca2+ (2). This ultimately causes glutamate to be released from its vesicle into the area between presynaptic membrane and postsynaptic membrane of the subsequent neuron. Through this electrochemical signal

The dendrites pick up the signal and activate the neuron's action potential that shoots an electric charge down the axon to its terminals and towards neighboring neurons. Neurotransmitters are stored in vesicles inside the terminal button of the axon; the vesicles are transported to the edge of the button and the neurotransmitters released into the synaptic gap. In the synapse, neurotransmitters can bind with a receptor site on the next neuron if the receptor site is the right type and is vacant. This is often described by a lock and key analogy, in that the neurotransmitters (like keys) can only fit into certain receptor sites (like

The communication between neurons advances through a series of steps. First, the presynaptic neuron delivers an action potential down its axon until it loses its myelin sheath and divides into many branches called buttons or synaptic knobs. (Zillmer, 2008, p. 105) Between the two neurons is a space called the synaptic cleft. This is the space where neurotransmitters are sent before being received by the postsynaptic neuron.

When an action potential races along the axon of a neuron, activating sodium and potassium channels in a wave, it eventually comes down to the presynaptic terminal, and activates the VGCC channels to release calcium into the neurons cytoplasm. This flow of positively-charged calcium ions causes the synaptic vesicles to fuse with the cell membrane and release their chemical messengers. It’s these neurotransmitters that act like couriers diffusing across the synaptic cleft and binding to receptor sites on the post synaptic

An electrical impulse carrying a neuronal message is called an action potential. During action potential, the neural membrane allows a net positive inflow of ions into the cell and negatively charged ions out of the cell. This causes a voltage change in the neuronal membrane which is also known as depolarization. Ions that participate in establishing an action potential are sodium, potassium, calcium and chloride. In a normal brain, hyper excitability of neurons is achieved by different inhibitory mechanisms.

As soon as the electrical signal reaches the end of the axon, mechanism of chemical alteration initiates. First, calcium ion spurt into the axon terminal, leading to the release of neurotransmitters “molecules released neurons which carries information to the adjacent cell”. Next, inside the axon terminal, neurotransmitter molecules are stored inside a membrane sac called vesicle. Finally, the neurotransmitter molecule is then discharged in synapse space to be delivered to post synaptic neuron.

It is the electrical events that are conducted along the entire length of the nerve cell's axon. At threshold potential, special sodium channels called voltage-gated channels are triggered to rapidly open,at that time, so too are the potassium voltage gated channels triggered to open (they open very slowly). When opened this allows a large amount of sodium ions to rapidly enter the cell down their concentration gradients, this results in a rapid depolarisation. Once a key maximum potential is reached usually about plus 30 millivolts the voltage gated sodium channels close. The depolarisation stops. Focusing on the potassium channels now, by the time the action potential peak is reached these channels are fully opened. And now a large amount of potassium ions move out of the cell down their concentration gradient. The removal of positive charges results in the membrane potential becoming more negative known as repolarisation. The cell nown returns to its resting values the potassium channels are triggered to close but they close slowly resulting in hyperpolarization. Finally the potassium voltage gated channels close and hyperpolarization stops and the membrane potential returns to rest. This all happens within two

At the end of a neuron, there is a small gap that separates one neuron with another, thus making two neurons not directly in contact with each other. Therefore when an electrical impulse reaches one end of the neuron, the impulse triggers the release of a chemical neurotransmitter before the impulse is able to be passed on to the next neuron. From here the released chemical neurotransmitters diffuse across the synapse which separates the two neurones apart, and once the neurotransmitter has successfully diffused across it then binds onto the receptor molecules found on next neuron.

Synaptic transmission is trigger by calcium influx through voltage gated calcium channels (VGCCs). VGCCs open in response to membrane depolarization cause, in most cases, by action potentials propagating through a nerve ending. Once inside the terminal, calcium diffuses and binds to a calcium-sensing protein called synaptotagmin I, which acts as the trigger for vesicle fusion with the pre-synaptic active zone. The basic mechanisms of synaptic transmission have been extensively described in the past 70 years, but the finest details of how neurotransmitters are released in response to action potentials remain unclear. Recent work indicates that at Schaffer collateral synapses neurotransmitter release is triggered by opening of one single calcium