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.
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.
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.
When the action potential reaches the axon terminals, it triggers the release of neurotransmitters from synaptic vesicles into the synaptic cleft. These neurotransmitters bind to receptors on the postsynaptic neuron's membrane, leading to the generation of a new action potential in that neuron if the signal is strong enough. This process allows for communication between neurons, effectively completing the circuit and transmitting signals throughout the nervous system.
The electrical impulse causes chemicals called neurotransmitters to be released from the axon terminals of the pre-synaptic neuron which diffuseacross the synaptic cleft and fit into receptors on the post-synaptic neuron.In an excitatory synapse, the presence of the neurotransmitters in the receptors of ligand-gated ion pores cause those pores to open and allow sodium ions into the post-synaptic neuron, which results in an electrotonic signal being conducted down the dendrite and soma to the axon hillock, which may initiate an action potential in the axon if enough signals are summed up at the axon hillock to reach a trigger value.
Neurons aren't able to communicate with each other.
Neurotransmitters bind to specific receptors on the postsynaptic neuron, leading to changes in the membrane potential and potentially causing depolarization. If the depolarization reaches a threshold, it triggers the opening of voltage-gated ion channels, allowing sodium ions to flow into the cell, generating an action potential. This electrical signal then propagates along the neuron's axon to transmit information to other neurons.