Biochemistry Online: An Approach Based on Chemical Logic

Biochemistry Online

CHAPTER 9 - SIGNAL TRANSDUCTION

B:  NEURAL SIGNALING

BIOCHEMISTRY - DR. JAKUBOWSKI

 06/10/14

Learning Goals/Objectives for Chapter 9B:
After class and this reading, students will be able to

  • describe how a transmembrane ion gradient and nongated/gated membrane ion channels specific for given ions can give rise to a transmembrane electric potential across membranes
  • given ion concentrations and the electrical potential across a membrane, predict likely changes in the membrane potential and ion concentrations on the opening of specific channnels;
  • use the Goldman equation to predict transmembrane electrical potentials;
  • state difference between the communication across the neuromuscular junction and a synapse between two neurons;
  • state the difference between nongated and gated ion channels;
  • describe different ways to open/close gated ion channels
  • describe the immediate changes in the muscle cells when acetylcholine is released into the neuromuscular junction
  • describe the roles of stimulatory neurotransmitter receptors, voltage-gated Na+and K+ channels and the Na/K-ATPase  in the activation of a neuron;
  • explain the mechanism for selectivity of K+ over the smaller Na+ ion in the K+ channel;
  • briefly explain how membrane protein channels can be gated open by changes in transmembrane potential;

B2. Transmembrane Potentials

Several questions arise about the distribution of ions and the magnitude of the transmembrane potential.

  1. How are the ion gradients established?
  2. How does the transmembrane ion distribution contribute to the membrane potential?
  3. How can the resting electrochemical potential and the ion distribution be maintained?

The answer to these questions will be illustrated using studies on two types of brain cells, glial cells (which function as protectors, scavengers, and feeder for brain neurons) and neurons. Both types of cells have transmembrane potentials.

Glial Cells

1. The transmembrane ion gradients for ions can be established by different mechanisms.  One uses ion-specific ATPases (P-type ion transporters), such as we discussed with the Na/K ATPase. This transporter ejects 3 sodium ions from the inside of the cell for every 2 potassium ions it transports in, all against a concentration gradient.  Since it is an electrogenic antiporter, it helps generate the potential.  Additionally, specific ion channels also contribute (as described below) to the transmembrane gradients and potentials. 
2. The harder question is how the ion distribution contribute to the membrane potential.  Two things must occur for a membrane potential to exist:  First, there must be a concentration gradient of charged ions (for example, sodium, potassium, or chloride) across the membrane.  Second, the membrane must be differentially permeable to different ions.   If the membrane were completely impermeable to ions, then no movement of ions across the membrane could occur, and no membrane potential would arise.   If, however, membranes are differentially permeable to the ions, an electrical potential across the membrane can arise.   Remember, synthetic bilayers are quite impermeable to ions, given the hydrophobicity of the internal part of the bilayer. Likewise it is quite impermeable to glucose. It turn out that glial cells appear to have only a non-gated potassium channel, which allows the outward flow of potassium ions down the concentration gradient. The inside will then have a net negative charge since impermeable anions remain. The chemical potential gradient causes this outward flow of potassium ions. As more ions leave, the inside gets more negative, and a transmembrane potential develops which resists further efflux of potassium. Eventually they balance, and the net efflux of potassium stops. The resting transmembrane potential reaches -75 mV which is exactly the value obtained from the equations we will derive below. Since glial cells appear to only express a nongated potassium channel, their resting potential is equal to the potassium equilibrium potential.  

Figure:  Visualizing the transmembrane potential in K+ loaded vesicles + a nongated K+ channel.

(Note:  above figure has mistake.  Cl- ion , assuming that is not permeable, will not change across the membrane at equilibrium.)

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