Post-Synaptic Potentials & Integration | Neuroscience Basics

Resting membrane potential is approximately -70 mV, with inside negative relative to outside. This arises from ion concentration gradients maintained by the sodium-potassium pump (3 Na+ out, 2 K+ in per ATP) and leak channels. Potassium leak channels allow passive diffusion of K+ out, contributing to negativity. Sodium leak channels permit small Na+ entry. These gradients create the electrochemical foundation for neuronal excitability and action potential generation.

Resting membrane potential is the electrical charge difference across the cell membrane at rest, with the inside negative and outside positive. The primary ions involved are sodium (Na+) as the main extracellular cation, potassium (K+) as the main intracellular cation, chloride (Cl-) as the main extracellular anion, and proteins/phosphate as main intracellular anions. The membrane is 50-70 times more permeable to potassium than sodium, allowing potassium to leak out and create the negative interior. The sodium-potassium pump (Na+/K+ ATPase) maintains this gradient by pumping 3 Na+ out and 2 K+ in for each ATP consumed, contributing approximately 93% to the resting potential.

The resting membrane potential is approximately -70 mV, meaning the inside is slightly negative relative to the outside. This voltage arises from ion concentration gradients: sodium is higher outside, potassium is higher inside, and negatively charged proteins remain inside. Cell membranes are selectively permeable to ions, requiring channels for passage. Permeability depends on channel number and ion size. The electrochemical gradient combines chemical concentration forces and electrical potential forces. For potassium-only cells, equilibrium potential is -90 mV. In neurons, slight sodium permeability shifts this to -70 mV. The sodium-potassium pump maintains this by actively transporting 3 Na+ out and 2 K+ in per cycle, counteracting natural ion leakage. Potassium slowly leaks out while sodium slowly leaks in, causing the membrane potential to drift toward zero if not corrected.

Electrochemical gradients occur when charged ions move across selectively permeable membranes, creating both concentration and electrical forces; in cells with high internal potassium concentration and potassium-selective channels, potassium ions diffuse out, leaving behind negative charges and establishing a resting membrane potential of approximately -70 mV, which is the equilibrium potential where the electrical force exactly balances the concentration-driven force.

The mechanism of synaptic transmission involves several key steps: (1) Action potentials travel down the axon to the axon terminal, (2) Neurotransmitters are synthesized and packaged into synaptic vesicles, (3) Vesicles fuse with the presynaptic membrane and release neurotransmitters into the synaptic cleft, (4) Neurotransmitters bind to specific receptors on the postsynaptic membrane, (5) This binding triggers ion channel opening (such as sodium ion influx), (6) The ion influx generates new action potentials in the postsynaptic neuron. This entire process represents paracrine signaling where the presynaptic neuron releases chemical signals that act on the neighboring postsynaptic neuron.

Synaptic transmission involves three main steps: (1) An action potential in the presynaptic neuron stimulates calcium channels to open, causing calcium ions to flow into the cytoplasm; (2) Calcium ions trigger vesicles containing neurotransmitter molecules to release from the presynaptic neuron into the synaptic cleft; (3) Neurotransmitters diffuse across the synaptic cleft and bind to receptors on the postsynaptic neuron's membrane, causing depolarization and generating a new action potential in the receiving neuron.

The complete mechanism of synaptic transmission involves: (1) nerve impulse arrival at axon terminal, (2) opening of voltage-gated calcium channels, (3) calcium influx triggering vesicle fusion, (4) neurotransmitter release into synaptic cleft, (5) neurotransmitter binding to postsynaptic receptors, (6) receptor activation opening ion channels, (7) ion influx causing depolarization, and (8) generation of new nerve impulse.

Synaptic transmission involves action potentials arriving at presynaptic terminals, calcium influx triggering vesicle fusion and neurotransmitter release, neurotransmitters binding to postsynaptic receptors, and postsynaptic membrane potential changes. Synaptic vesicles contain neurotransmitters and are stored in the presynaptic terminal. When calcium enters, vesicles move to the membrane and fuse, releasing contents into the synaptic cleft. Acetylcholine is an excitatory neurotransmitter that binds to postsynaptic receptors and opens sodium channels, depolarizing the postsynaptic cell. Acetylcholine receptors are ligand-gated ion channels composed of five subunits with a binding site and pore.

Neurotransmitter release is triggered when calcium ions enter the presynaptic neuron, causing vesicle contraction and exocytosis. Vesicles containing neurotransmitters move to the synaptic membrane and release their contents into the synaptic cleft. Since neurotransmitters are hydrophilic, they cannot cross the lipid bilayer and must be released outside the cell. After release, neurotransmitters bind to specific receptors on the postsynaptic membrane. These receptors are highly specific proteins that recognize only particular neurotransmitters. Binding triggers intracellular signaling cascades that can either excite or inhibit the postsynaptic cell, depending on the receptor type.

An action potential is a rapid change in membrane potential caused by ion channels opening and closing, allowing ions to move in and out of the cell. The four phases include resting state at -70mV, depolarization crossing zero to become positive, repolarization becoming negative again, and reset. Threshold is the critical membrane potential (typically -50 to -60mV) that must be reached for an action potential to occur. Action potentials follow an all-or-nothing principle: if threshold is not reached, no action potential occurs and the cell returns to resting state. This ensures reliable neural signaling without partial responses.

Action potential is a rapid change in membrane potential that occurs when a neuron is stimulated. It consists of several phases: resting stage (-90 mV), depolarization (rising to +35 mV), repolarization (returning to negative values), and hyperpolarization (dropping below resting value). For an action potential to occur, the membrane potential must reach the threshold (approximately -65 mV in large neurons). If the resting potential is close to the threshold (e.g., -70 mV), a small stimulus can trigger an action potential. If the resting potential is far from the threshold, a stronger stimulus is needed. This is called the 'all-or-none' principle. The threshold is the membrane potential level required to trigger an action potential.

An action potential is a rapid, temporary change in membrane potential that travels along the neuron. The threshold is the membrane potential that must be reached for an action potential to occur, approximately -55 mV. When the membrane potential reaches this threshold, voltage-gated sodium channels open rapidly, causing a rapid influx of sodium ions and the generation of an action potential. The all-or-nothing principle states that once the threshold is reached, an action potential will occur with the same amplitude regardless of how much the threshold was exceeded. Subthreshold stimulation (not reaching threshold) causes only small changes in membrane potential without generating an action potential. The action potential has several phases: (1) Resting potential (-70 mV), (2) Depolarization (membrane potential becomes less negative), (3) Repolarization (membrane potential returns to negative), and (4) Hyperpolarization (membrane potential becomes more negative than resting).

Action potentials are rapid alterations in membrane potential of excitable cells (neurons and cardiac muscle), varying from negative to positive and back. The resting membrane potential has a negative interior and positive exterior, with different cells having different resting potentials (-60 to -90 mV). Action potentials consist of three phases: depolarization (Na+ entry through voltage-gated channels), repolarization (K+ exit), and hyperpolarization (slow K+ channel closure). The refractory period prevents immediate re-firing: absolute refractory period makes new action potentials impossible regardless of stimulus strength, while relative refractory period allows action potentials only with stronger-than-normal stimuli. Action potentials only occur when membrane potential reaches a threshold level (around -55 mV). The all-or-nothing principle states that once threshold is reached, an action potential will propagate fully along the axon and cannot be stopped or reduced in amplitude.

Action potential has four phases: depolarization (membrane becomes less negative), repolarization (returns toward resting), hyperpolarization (becomes more negative than resting), and return to resting. Action potentials are generated only when membrane potential reaches threshold (-55 mV). If depolarization does not reach threshold, no action potential is generated. Action potentials follow the all-or-nothing principle: once threshold is reached, they are generated with full amplitude regardless of stimulus strength. This ensures reliable signal transmission.