Synaptic Transmission + Inhibition (SAQ)

Synaptic transmission involves the arrival of an action potential at the pre-synaptic ending, triggering Ca2+ voltage-gated channels to open. This causes vesicles containing neurotransmitters to fuse to the membrane and release neurotransmitters into the synaptic cleft. The neurotransmitters then diffuse across the synaptic cleft and bind to receptors on the post-synaptic membrane, causing the action potential to continue in the post-synaptic nerve. Inhibition involves the regulation of the post-synaptic potential through the sum of excitatory post-synaptic potentials (EPSPs) and inhibitory post-synaptic potentials (IPSPs), which generate depolarization and hyperpolarization, respectively.

The three different types of removal of neurotransmitters at the synaptic cleft include uptake into astrocytes or pre-synaptic nerve, breakdown of neurotransmitters by releasing enzymes into the synaptic cleft, and diffusion out at the synaptic cleft into the surroundings or blood vessels.

Reversal potentials are the point at which the ionic flux changes direction and are determined by the membrane potential. In the endplate, the membrane potential determines the direction of the movement of ions. For example, if the membrane potential is more negative, more Na+ will move in than K+ moving out when the channel is open (inward current), and if the membrane potential is more positive, more K+ will move out than Na+ moving in when the channel is open (outward current).

EPSPs (excitatory post-synaptic potentials) and IPSPs (inhibitory post-synaptic potentials) sum to generate depolarization and hyperpolarization, respectively, and their sum regulates the post-synaptic potential.

An example of synaptic modulation is the knee jerk reflex, which is made up of the excitation of the quad muscle and the inhibition of hamstring, caused by feed-forward inhibition from a sensory neuron.

1. Action potential arrives at pre-synaptic ending, triggering Ca2+ voltage-gated channels to open. 2. Ca2+ floods into the ending, causing vesicles containing neurotransmitter to fuse to the membrane. 3. Neurotransmitters diffuse across the synaptic cleft and bind to receptors on the post-synaptic membrane, causing the action potential to continue in the post-synaptic nerve.

1. Uptake into astrocytes or pre-synaptic nerve. 2. Breakdown of neurotransmitter by releasing enzymes into the synaptic cleft. 3. Diffusion out at the synaptic cleft into surroundings or blood vessels.

The reversal potential determines the direction of the movement of ions. For example, at the endplate, if the membrane potential of the axon is more negative, then more Na+ will move in than K+ moving out once the channel is open (inward current). If the membrane potential is more positive, then more K+ will move out than Na+ moving in when the channel is open (outward current). The reversal potential is the point at which the ionic flux changes direction.

EPSPs are excitatory post-synaptic potentials that sum to generate depolarization, while IPSPs are inhibitory post-synaptic potentials that sum to generate hyperpolarization. The sum of EPSPs and IPSPs regulates the post-synaptic potential.

The knee jerk reflex is composed of excitation of the quad muscle and inhibition of the hamstring, which is caused by feed-forward inhibition from the sensory neuron. This reflex illustrates the coordination of excitatory and inhibitory post-synaptic potentials in the nervous system.

The text does not provide information on the two types of synaptic modulation.

Ca2+ influx triggers the fusion of vesicles containing neurotransmitters to the pre-synaptic membrane, allowing the release of neurotransmitters into the synaptic cleft to bind to receptors on the post-synaptic membrane.

The text does not provide information on the role of astrocytes in the removal of neurotransmitters at the synaptic cleft.