The Effect of Drugs, Toxins, and Other Molecules on Synapse and Synapse Transmission.
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The effect of drugs, toxins, and other molecules on synapse and synapse transmission.
The synapse is the small gap separating two neurons, the presynaptic neuron (neuron that carries the impulse to the synapse,) and postsynaptic neuron (neuron that carries the impulse away from the synapse.) It separates the axon terminals of the presynaptic neuron from the postsynaptic neuron. The synapse is made of three major parts: a presynaptic neuron, a postsynaptic neuron, and a synaptic cleft. The presynaptic neuron contains the neurotransmitters, mitochondria, endoplasmic reticulum, and other cell organelles. The postsynaptic neuron contains receptor sites for the neurotransmitters in the presynaptic neuron. The synaptic cleft is the space between the presynaptic and postsynaptic neuron.
The arrival of an action potential normally causes the release of neurotransmitters from the presynaptic neuron. The action potential travels down to the axon terminal of the presynaptic neuron. Each axon terminal becomes swollen forming a presynaptic knob. There is a depolarisation of the presynaptic membrane resulting from the action potential. This depolarisation causes an increase in the permeability to sodium and calcium ions. The presynaptic knob is then filled with membrane-bound vesicles; each filled with a neurotransmitter. Calcium ions then flood into the presynaptic knob by diffusion. The influx of calcium ions triggers the exocytosis of the synaptic vesicles. The neurotransmitters are then released into the synaptic cleft. The neurotransmitters travel across the synaptic cleft towards the receptors by diffusion.
There are two main categories of transmissions, excitatory transmissions and inhibitory transmissions. Excitatory transmissions occur when the neurotransmitter at a synapse depolarises the postsynaptic membrane. Chemically regulated channels are the receptors where the neurotransmitters bind to at the postsynaptic membrane. Inhibitory transmissions occur when the neurotransmitter at a synapse hyperpolarises the postsynaptic membrane, which causes the transmembrane potential to be beyond from the threshold. The threshold is the transmembrane potential where an action potential begins. This increased membrane potential is called an inhibitory postsynaptic potential (IPSP). It is inhibitory, because now there must be a stronger depolarisation in order for the membrane potential to return to the threshold.
Cholinergic transmissions are a type of excitatory transmission. The cholinergic transmission involves the release of the neurotransmitter, acetylcholine (ACh). Below are the steps involved in a cholinergic transmission:
Step 1: The action potential travels down to the axon terminal of the presynaptic neuron. Each axon terminal becomes swollen, forming a postsynaptic knob. There is a depolarisation of the presynaptic membrane as a result from the action potential. This depolarisation causes and increases in the permeability to sodium and calcium ions. The presynaptic knob is then filled with membrane-bound vesicles; each filled with ACh. Calcium ions then flood into the presynaptic knob by diffusion.
Step 2: The influx of calcium ions triggers the exocytosis of the synaptic vesicles. ACh is then released into the synaptic cleft. The ACh molecules diffuse across the synaptic cleft towards and attaches to the receptors of the postsynaptic membrane.
Step 3: The release of ACh stops shortly as calcium ions are quickly removed from the cytoplasm. Chemically regulated channels are the ACh receptors at the postsynaptic membrane. The ACh molecules then bind to these receptors, resulting in increased sodium permeability, which reduces the membrane potential. This reduced membrane potential is called an excitatory postsynaptic potential, (EPSP.) The EPSP produced by one cholinergic transmission isnt enough to reach the threshold of the postsynaptic neuron. When the EPSP produced isnt enough to reach the threshold of the neuron, the neuron is called a facilitated neuron. Many EPSPs created in a series, added together, can reach the threshold of the neuron. The series of EPSPs added together is the process of summation. If the threshold is reached, then an action potential is generated. There is a synaptic delay within the arrival of stimuli at the presynaptic knob and the result of the stimuli on the postsynaptic membrane. This delay is about 0.2 to 0.5 milliseconds long. The synaptic delay is a result of the increased concentration of calcium ions and the release of the ACh.
Step 4: Acetylcholinesterase (AChE) breaks down all of the ACh in the synaptic cleft and removes it from the postsynaptic ending. The AChE does this by hydrolyzing the ACh molecules into acetate and choline. The presynaptic knob then absorbs the choline from the synaptic cleft. The choline molecules are used to remake ACh. When ACh molecules are recycled, the recycling and transport mechanisms may not be able to keep up with the neurotransmitter. This results in synaptic fatigue, where the synapse is inactive until ACh is replenished.
Above is an explanation about the synapse and the transmission of synapse, below is the description of the effects of drugs and toxins on synaptic transmissions. Most drugs that affect the nervous system do so by influencing the transmission of nerve impulses across synapse. Drugs may affect the release of the neuron transmitter; others modify the effect that the neurotransmitters have on the postsynaptic membrane.
Medical drugs have different effects on synapses and the nervous system overall. Morphine, a pain killer, binds to (enkephalin) receptors, which are receptors involved in transmitting pain signals back to the brain. The morphine hyperpolarises the postsynaptic membrane, which prevents the (enkephalins) receptor from transmitting pain, signals. Novocaine, an anesthetic, affects ACh at synapses, because it reduces sodium permeability