Neuron Resting Potential and Channels

Membrane Channels and Resting Potential

Sodium ions use channels in the membrane to move down their concentration gradient.
The permeability of the membrane to different ions is crucial for establishing the resting membrane potential.

Lead channels facilitate sodium movement.
More "doors" (channels) allow faster ion movement. For example, 100 doors for 1000 people means a 1:10 door-to-people ratio, enabling quick exit/entry.

As the cell interior becomes more negative:
- Potassium exit rate decreases.
- Sodium entry rate increases.
Equilibrium is reached when the rate of potassium leaving equals the rate of sodium entering (a one-to-one ratio).
Around negative 70 mV, these rates become approximately equal.

Resting membrane potential is achieved when there's an even exchange of positive ions.
For every positive ion exiting, one enters, resulting in no net change in membrane potential.
Negative 70 mV is the standard resting membrane potential when considering all ions.
At -70 mV, potassium continues to actively leave the cell; it doesn't stop.

Equilibrium potential for sodium is +60 mV.
Sodium-potassium pumps maintain ion concentrations, preventing membrane potential disruption.
These pumps, using primary active transport, are embedded in the neuron membrane.
- They move sodium out against its concentration gradient (from low to high concentration).
- They move potassium in against its concentration gradient (from low to high concentration).
A change in membrane potential in one area (e.g., -70 mV) doesn't automatically affect other areas of the membrane.

The axon of a presynaptic neuron (neuron number one) triggers vesicles to release neurotransmitters via exocytosis.
These are excitatory neurotransmitters.
Neurotransmitters bind to receptors, causing them to open.

Receptors can be thought of as gated channels that open when a specific neurotransmitter (ligand) binds to them.
Ligand-gated sodium channels are closed until a ligand binds.
If a neuron's dendrite is at -70 mV, excitatory neurotransmitters released into the synaptic cleft can bind to and open sodium channels on the dendrite of another neuron.

Neurons maintain an ideal environment for sodium influx.
Excitatory neurotransmitters function by binding to receptors (sodium channels) on other cells.
This binding causes ligand-gated sodium channels to open on the postsynaptic neuron's dendrites.