|
Neurotransmitter release at a synapse is initiated by the arrival of an action potential in the axon terminal. As the action potential spreads through the axon terminal it triggers the opening of a population of voltage-gated Ca2+ channels. With an extracellular Ca2+ of 1.8 mM and an intracellular concentration of 100 nM there is clearly a concentration gradient that encourages the flow of Ca2+ into the axon terminal. So as soon as the voltage-gated Ca2+ channels open, Ca2+ rushes into the axon terminal down its concentration gradient. The consequent increase in intracellular Ca2+ concentration triggers the migration of synaptic vesicles and their subsequent fusion with the presynaptic membrane. The vesicle membrane then breaks down and the neurotransmitters is exocytosed into the synaptic cleft. The neurotransmitter then diffuses across the synaptic cleft and binds to its receptors on the postsynaptic membrane. |
 |
The binding of the neurotransmitter to their receptors initiates a diverse range of effects in the postsynaptic neurone. To a large extent the nature of these effects is determined by the type of receptor to which the neurotransmitter binds. There are two major classes of receptors and these are dealt with in the subsequent modules of this lesson.
The duration of effects of the neurotransmitter is restricted by a number of mechanisms that act to remove it from the synaptic cleft and therefore limits its actions on postsynaptic receptors:
Diffusion
The most common mechanism that limits the duration of a neurotransmitter is simply diffusion of the chemical out of the cleft and into the extracellular space surrounding the synapse. Because the receptors are restricted to the postsynaptic membrane, the neurotransmitter no longer has any effect.
Reuptake
Many neurotransmitters are recycled back into the axon terminal, repackaged and used again. This recycling process is enabled by the presence of specific transporters in the membrane of the axon terminal.
Enzymatic Degradation
Some neurotransmitters broken down by enzymes located within the synaptic cleft. For example acetylcholine is broken down by the enzyme acetylcholinesterase into choline and acetate and consequently inactivated.
Because both reuptake and enzymatic degradation reduce the effective concentration of the neurotransmitter in the synaptic cleft, manipulation of these systems can have quite dramatic effects on the efficacy of synaptic transmission. For example the powerful psychotropic drug cocaine blocks the membrane transporter responsible for the reuptake of the neurotransmitter dopamine. The psychoactive and addictive nature of cocaine are believed to be a direct consequence of the increased dopamine concentration in the synaptic cleft as a result.
Although the individual molecular events involved in chemical synaptic transmission occur fairly quickly, collectively these constitutes a small but significant delay between the action potential arriving in the axon terminal and the effects of the neurotransmitter be manifest in the postsynaptic neurone.
The sum of the times that it takes for Ca2+ channel opening, Ca2+ diffusion, synaptic vesicle migration, exocytosis, diffusion and binding of the neurotransmitter and the changes produced in the postsynaptic neurone contribute to a synaptic delay of approximately 0.5 ms.
Thus synaptic transmission in chemical synapses is significantly slower than that observed in electrical synapses. Whilst this is not an issue for mono- and disynaptic pathways involved in reflexes and sensory pathways, it does mean that neural processes that involve many synaptic interactions (e.g. memory) do require a little more processing time.