When neurotransmitters communicate an inhibitory message to the postsynaptic neuron:
Neurotransmitters are released and go into the synaptic cleft.
Neurons aren't able to communicate with each other.
Neurons aren't able to communicate with each other.
Inhibitory neurotransmitters prevent the firing of neurons by binding with certain receptors, causing the influx of chloride ions to hyperpolarize the neuron. When this happens, it requires a much larger excitatory signal to override the inhibitory effects in order to allow the neuron to fire.
That is true. Most stimulants work by binding to excitatory neurotransmitter receptors (such as the case with amphetamines), inducing the release of excitatory neurotransmitters (such as dopamine and norepinephrine, in the case of amphetamines), preventing the breakdown of excitatory neurotransmitters (as in the case of Ritalin, cocaine, etc.), or blocking inhibitory receptors (as in the case of caffeine). When this happens, the brain adjusts by reducing its sensitivity to its own excitatory neurotransmitters...especially in the case of adrenaline (epinephrine), noradrenaline (norepinephrine), and dopamine. So, once the stimulant wears off, the body is not only fatigued again, but is actually MORE sleepy than before...making it very easy to fall asleep.
After neurotransmitters are released in to the synaptic cleft - from the presynaptic neuron, they bind with there specific receptor cites found on the postsynaptic neurons cell membrane. Some neurotransmitters then become inactive by enzymes whiles other simply drift away from the synaptic cleft. Reuptake can also occur where the presynaptic neuron sponges up (or takes back) the remaining neurotransmitters left behind.
The synaptic transmission is where the communication between the terminal button and the dendrite occur. What happens is the impulse moves along the axon and release neurotransmitter from the end plate of the presynaptic neuron and are diffused across the synaptic cleft. This creates a depolarization of the dendrites of the postsynaptic neuron. When that happens the postsynaptic's sodium channels to open and start the action potential. Once the channels are open an enzyme called cholinesterase is released from postsynaptic membrane and it acts to destroy the neurotransmitters. When they are destroyed the sodium channels close and begins recovery.
Neurons aren't able to communicate with each other.
When the action potential (electrochemical signal) reaches the end of the nerve, calcium channels open, causing synaptic vesicles containing neurotransmitters to bind with the neuronal membrane. When this happens, the neurotransmitters are released into the synaptic cleft (process is called exocytosis). Once in the synaptic cleft, they can bind with postsynaptic neuron or muscle cell receptors.
Neurotransmitters can help bring another neuron to the point where it initiates an action potential by binding to postsynaptic receptor sites. If the receptors are the type that allow positively charged ions to flux through the cell membrane, and if this happens on a large enough scale (i.e., multiple sites are hit at once), then the probability of an action potential occurring becomes very high.
Stuff.
As a rule more than one presynaptic action potential is needed to fire the postsynaptic neuron or muscle so that the trigger to initiate an action potential are either many subthreshold local potentials from different sources or from the same neuron received within a short period of time. The first case is called spatial summation and the second case is called temporal summation. Whether a postsynaptic potential (another term for a local potential) is excitatory or inhibitory depends on what ion channels are affected by the transmitter released from the presynaptic vesicles.