Neuroanatomy Overview

Changes in membrane potential that travel down the axon of a neuron, allowing the nervous system to transmit information.

The minimum level of depolarization required to trigger an action potential.

The characteristic of an action potential where its amplitude remains the same regardless of the strength of the stimulus.

The intensity of a stimulus is encoded in the frequency of action potentials, not their amplitude.

Proteins that actively transport ions across the cell membrane against their concentration gradients.

Proteins that allow specific ions to move passively across the cell membrane, following their concentration gradients.

The difference in electrical potential between the inside and outside of a cell at rest. It is typically around -70mV in neurons due to the selective permeability of potassium.

The movement of potassium ions (K+) out of the cell through leak channels, leading to a negative charge inside the cell.

Synapses are the junctions between neurons where communication occurs. They can be either chemical or electrical.

Chemical synapses use neurotransmitters (NTs) to transmit signals across the synaptic cleft. They are slower, require energy, and provide complex communication.

Electrical synapses are faster and require less energy than chemical synapses. They allow direct electrical current flow between neurons, but lack complexity.

Synaptic plasticity refers to the ability of synapses to change their strength over time, either short-term or long-term. These changes are crucial for learning and memory.

Short-term plasticity refers to changes in synaptic strength that last for milliseconds to minutes. It involves mostly presynaptic changes, like altered neurotransmitter release.

Long-term plasticity refers to changes in synaptic strength that persist for longer than hours. It involves both pre- and post-synaptic changes and is linked to learning and memory.

Long-term potentiation (LTP) is a type of long-term plasticity where synapses become stronger with repeated stimulation. It is often associated with learning and memory.

The process of LTP involves a complex cascade of events, including the activation of NMDA and AMPA receptors, increased calcium levels, and changes in gene expression.

Axon guidance cues that are non-diffusible and interact directly with receptors on the growth cone. Examples include semaphorins and ephrins.

Axon guidance cues that diffuse through the environment and bind to receptors on the growth cone. They include netrin, slit and semaphorins.

A type of contact-mediated axon guidance cue that can either attract or repel axons, depending on the specific ephrin and Eph receptor involved.

A specific type of diffusible cue that acts as a chemoattractant, guiding axons towards their target by binding to DCC receptors.

A specific type of diffusible cue that acts as a chemorepellent, guiding axons away from their target by binding to Robo receptors.

The process by which growing axons change direction in response to cues in their environment, such as contact-mediated or diffusible cues.

Factors secreted by target cells that are essential for the survival, growth, and differentiation of neurons.

The relationship between neurons and their target cells, where the target cells provide crucial factors for the survival of the neuron.

The movement of ions within the cytoplasm and across the membrane in response to local depolarization. It spreads the depolarization passively to neighboring areas, reducing the voltage difference and bringing them closer to threshold. It's fast but decays with distance.

The process of regenerating the action potential by opening voltage-gated Na+ channels in neighboring segments. This ensures the signal doesn't fade and can travel long distances.

The period after depolarization where Na+ channels are inactivated, preventing the action potential from moving backward. This ensures unidirectional signal transmission.

The mechanism by which the action potential jumps between the Nodes of Ranvier in myelinated axons, greatly increasing conduction speed. This occurs because myelin insulates the axon, allowing for faster passive current flow.

The process by which the positive charge inside the axon from Na+ influx triggers nearby voltage-gated Na+ channels to open, leading to the propagation of the action potential along the axon.

Small molecule neurotransmitters are stored in vesicles in the axon. Upon release, they become precursors and are recycled back into the cell, where they are converted back into the neurotransmitter. This process involves enzymes synthesized in the soma and transported along the axon.

The process by which an action potential triggers the release of neurotransmitters. This occurs through the opening of Ca2+ channels at the presynaptic terminal, allowing Ca2+ to enter and trigger the fusion of vesicles containing neurotransmitters with the membrane.

Substances that bind to and activate receptors. Examples include acetylcholine, glutamate, and GABA.

A method used to measure the flow of ions through individual ion channels in a cell membrane.

This technique allows you to study the ion channel activity in its natural environment within the cell membrane.

This configuration measures the total flow of ions through all the channels in the cell membrane.

This configuration allows you to study the intracellular side of an ion channel, giving you control over the cell's interior.

This configuration allows you to study the extracellular side of an ion channel, exposing it to the outside environment.

This technique allows for measuring ion currents while maintaining the cell membrane's integrity, using a special type of pipette.

The rate at which ions move through a channel.

Mechanisms that control the opening and closing of ion channels.

Glutamate binds to both AMPA and NMDA receptors on the postsynaptic neuron, but only AMPA receptors are active initially due to the NMDA receptor being blocked by magnesium.

When a presynaptic neuron releases a lot of glutamate, and the postsynaptic neuron is simultaneously depolarized, the magnesium block on the NMDA receptor is removed, allowing calcium and sodium to enter the postsynaptic neuron.

The influx of calcium activates signaling pathways that lead to the insertion of more AMPA receptors into the synapse and structural changes like new dendritic spines, making the postsynaptic neuron more responsive to glutamate.

After LTP, the same amount of glutamate release from the presynaptic neuron will elicit a larger response in the postsynaptic neuron, indicating a strengthened synapse.

LTP only occurs in the specific pathway that receives the high-frequency stimulation (tetanus) and not in adjacent, unstimulated pathways.

A weakly stimulated synapse can undergo LTP if it is active at the same time as a strongly stimulated synapse on the same postsynaptic neuron.

Depolarization caused by the strong stimulus spreads across the neuron, opening NMDA receptors at the weakly stimulated synapse. This allows calcium influx and triggers LTP at the weaker synapse.