14.1 Neuronal signaling and action potentials

Neurons are the building blocks of our nervous system, transmitting electrical signals through action potentials. These signals allow our brains to process information and control our bodies. Understanding how neurons work is crucial for grasping the complexities of brain function.

Action potentials are like electrical waves that travel along neurons, triggered by changes in ion concentrations. These waves are the basis for neural communication, enabling our brains to process sensory input, control movement, and form memories. Let's dive into the fascinating world of neuronal signaling!

Neuronal membrane properties

Composition and selective permeability

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• Neuronal membranes are composed of a lipid bilayer with embedded proteins, including ion channels and pumps, which regulate the flow of ions across the membrane
• The lipid bilayer is selectively permeable, allowing certain ions and molecules to pass through while restricting others
  • This selective permeability creates a concentration gradient and electrical potential difference across the membrane
  • The main ions involved in neuronal signaling are sodium (Na+), potassium (K+), calcium (Ca2+), and chloride (Cl-)

Ion channels and resting membrane potential

• Ion channels are transmembrane proteins that form pores allowing specific ions to pass through the membrane
  • They can be gated by voltage, ligands, or mechanical stimuli
  • Examples of ion channels include voltage-gated sodium channels, voltage-gated potassium channels, and ligand-gated channels (AMPA, NMDA)
• The resting membrane potential of a neuron is typically around -70 mV
  • This potential is maintained by the Na+/K+ ATPase pump and the selective permeability of the membrane to K+ ions
  • The Na+/K+ ATPase pump actively transports Na+ out of the cell and K+ into the cell, establishing concentration gradients

Action potential generation

Initiation and rising phase

• Action potentials are brief, all-or-none electrical signals that propagate along the axon of a neuron, enabling communication between neurons
• The generation of an action potential involves the opening and closing of voltage-gated sodium and potassium channels in a specific sequence
  • When the membrane potential reaches a threshold value (around -55 mV), voltage-gated sodium channels open, allowing a rapid influx of Na+ ions
  • This influx causes the membrane potential to depolarize rapidly, known as the rising phase of the action potential

Falling phase and refractory period

• The depolarization triggers the opening of voltage-gated potassium channels, leading to an efflux of K+ ions
  • This efflux repolarizes the membrane potential, known as the falling phase of the action potential
• After the action potential, there is a brief refractory period during which the neuron cannot generate another action potential
  • This refractory period ensures unidirectional propagation of the action potential along the axon
• Action potentials propagate along the axon through local currents that depolarize adjacent regions of the membrane
  • This depolarization triggers the opening of voltage-gated sodium channels and generates a new action potential
• Myelination of the axon by Schwann cells or oligodendrocytes increases the speed of action potential propagation through saltatory conduction

Voltage-gated channels and excitability

Role in action potential generation

• Voltage-gated ion channels are crucial for regulating neuronal excitability and generating action potentials
• The activation and inactivation kinetics of voltage-gated sodium and potassium channels determine the shape and duration of the action potential
  • Voltage-gated sodium channels rapidly activate and inactivate, contributing to the rising and falling phases of the action potential
  • Voltage-gated potassium channels activate more slowly, contributing to the repolarization and hyperpolarization of the membrane potential

Influence on neuronal firing patterns

• The density and distribution of voltage-gated ion channels along the axon and dendrites influence the neuron's excitability and firing patterns
  • A higher density of voltage-gated sodium channels can lower the action potential threshold and increase excitability
  • The presence of voltage-gated potassium channels can modulate the firing frequency and adapt the neuron's response to sustained input
• Mutations or dysfunction of voltage-gated ion channels can lead to neurological disorders
  • Examples include epilepsy, migraine, and certain types of ataxia
• Neurotoxins, such as tetrodotoxin (TTX) and saxitoxin (STX), specifically target voltage-gated sodium channels, blocking action potential generation and propagation

Neuronal signal integration

Synaptic inputs and postsynaptic potentials

• Neurons receive and integrate multiple synaptic inputs from other neurons, which can be excitatory or inhibitory
• Excitatory postsynaptic potentials (EPSPs) depolarize the membrane potential, bringing the neuron closer to the action potential threshold
  • EPSPs are generated by the opening of ligand-gated ion channels, such as AMPA and NMDA receptors, in response to neurotransmitter binding (glutamate)
• Inhibitory postsynaptic potentials (IPSPs) hyperpolarize the membrane potential, making it more difficult to reach the threshold
  • IPSPs are generated by the opening of ligand-gated ion channels, such as GABAA receptors, in response to neurotransmitter binding (GABA)

Spatiotemporal integration and dendritic computation

• The soma and dendrites of a neuron act as a spatiotemporal integrator, summing up the EPSPs and IPSPs received from multiple synapses
• The passive electrical properties of the neuronal membrane, such as membrane resistance and capacitance, influence the spread and summation of synaptic potentials
  • Higher membrane resistance allows synaptic potentials to spread further along the dendrites
  • Membrane capacitance acts as a low-pass filter, attenuating high-frequency synaptic inputs
• Active dendritic processes, mediated by voltage-gated ion channels and synaptic receptors, can amplify or attenuate synaptic inputs
  • Dendritic spikes, generated by voltage-gated sodium and calcium channels, can boost the impact of synaptic inputs and contribute to neuronal computation
• The timing and location of synaptic inputs on the dendritic tree can affect the integration and processing of signals
  • Synaptic plasticity, such as long-term potentiation (LTP) and long-term depression (LTD), can modulate the strength of synaptic connections based on the timing of pre- and postsynaptic activity
  • Dendritic computation enables individual neurons to perform complex operations, such as coincidence detection and pattern recognition