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.
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.
Excitatory neurotransmitters increase the likelihood of a neuron firing an action potential, while inhibitory neurotransmitters decrease this likelihood. Excitatory neurotransmitters typically depolarize the neuron, making it more likely to reach its firing threshold, while inhibitory neurotransmitters hyperpolarize the neuron, making it less likely to fire. This balance of excitatory and inhibitory neurotransmission is crucial for maintaining proper brain function.
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.
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 an impulse arrives at a synapse, neurotransmitters are released from the presynaptic neuron into the synaptic cleft. The neurotransmitters then bind to receptors on the postsynaptic neuron, leading to changes in the postsynaptic neuron's membrane potential. This can either excite or inhibit the postsynaptic neuron, influencing whether or not an action potential will be generated.
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.
The nerve impulse triggers the release of neurotransmitters from the presynaptic neuron. These neurotransmitters diffuse across the synaptic cleft and bind to receptors on the postsynaptic neuron, causing ion channels to open and leading to generation of a new nerve impulse in the postsynaptic neuron.