Neurons are the primary cells responsible for transmitting electrical and chemical signals, making them the fundamental units of the nervous system. Their unique structure supports complex communication among different parts of the body.

Dendrites are specialized structures that act like antennae, picking up signals from other neurons. Their extensive branching increases the surface area for receiving information, making them key to neural communication.

An action potential is a rapid electrical change that travels along a neuron's membrane to propagate a signal. It is initiated when the neuron reaches a threshold, allowing for quick and efficient communication.

The cerebellum plays a crucial role in motor control, ensuring smooth, coordinated movements and maintaining balance. Its function is essential for performing precise and controlled physical activities.

The synapse is the junction between neurons where the transmission of chemical signals occurs through neurotransmitters. This specialized gap is critical for inter-neuronal communication in the nervous system.

The rough endoplasmic reticulum, studded with ribosomes, is essential for synthesizing proteins that support neuronal structure and function. This protein production is vital for cell maintenance and repair.

Dopamine is a key neurotransmitter in the brain's reward circuitry, often linked to feelings of pleasure and motivation. Its release reinforces behaviors that are essential for survival, making it central to reward processing.

GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter that helps regulate neural activity by dampening excessive signals. Its function is critical for maintaining a balance between excitation and inhibition in the brain.

Myelin sheaths insulate axons, allowing electrical impulses to travel faster along the neuron. This process, known as saltatory conduction, greatly increases the speed and efficiency of signal transmission.

The prefrontal cortex is integral to complex thought processes, including decision-making, planning, and problem solving. Its development and connectivity are essential for advanced cognitive functions.

Long-term potentiation (LTP) is a lasting enhancement in signal transmission between neurons resulting from repeated stimulation. It is a cellular mechanism underlying learning and memory formation.

During depolarization, sodium ions rapidly enter the neuron, causing a change in the membrane potential that leads to an action potential. This influx is essential for the propagation of electrical signals along the axon.

The blood-brain barrier is a highly selective barrier that prevents harmful substances in the bloodstream from entering the brain. Its integrity is critical for maintaining the stable environment required for proper neuronal function.

The axon hillock is the trigger zone of a neuron, where the summation of electrical signals occurs. Its high density of voltage-gated sodium channels makes it the ideal site for initiating an action potential.

Oligodendrocytes are the glial cells that form myelin sheaths around axons in the central nervous system, enhancing the speed of electrical transmission. In contrast, Schwann cells perform a similar function in the peripheral nervous system.

Astrocytes play a supportive role by managing the levels of neurotransmitters in the synaptic space and contributing to the maintenance of the blood-brain barrier. This regulation is critical for both protecting neurons and modulating synaptic communication.

After an action potential, voltage-gated sodium channels enter an inactivated state for a short period, contributing to the refractory period. This temporary inactivation prevents the neuron from firing again too soon, ensuring proper signal timing.

Long-term synaptic plasticity, such as long-term potentiation, involves the activation of NMDA receptors which allows calcium ions to enter the neuron. This influx initiates intracellular pathways that lead to protein synthesis and structural changes at the synapse, ensuring lasting modifications.

In Alzheimer's disease, beta-amyloid plaques form due to protein misfolding and aggregation, which disrupts normal synaptic communication. This interference in neuronal signaling contributes to the cognitive decline associated with the disease.

The brain's stability relies on a fine balance between excitatory and inhibitory signals, which prevents overexcitation that can lead to disorders such as seizures. This equilibrium is essential for proper information processing and maintaining overall neural network function.