Hyperpolarization (biology)

Voltage gated ion channels respond to changes in the membrane potential. Voltage gated potassium, chloride and sodium channels are key components in the generation of the action potential as well as hyper-polarization. These channels work by selecting an ion based on electrostatic attraction or repulsion allowing the ion to bind to the channel. This releases the water molecule attached to the channel and the ion is passed through the pore. Voltage gated sodium channels open in response to a stimulus and close again. This means the channel either is open or not, there is no part way open. Sometimes the channel closes but is able to be reopened right away, known as channel gating, or it can be closed without being able to be reopened right away, known as channel inactivation. At resting potential, both the voltage gated sodium and potassium channels are closed but as the cell membrane becomes depolarized the voltage gated sodium channels begin to open up and the neuron begins to depolarize, creating a current feedback loop known as the Hodgkin cycle. ==Experimental technique==

Hyperpolarization is a change in membrane potential. Neuroscientists measure it using a technique known as patch clamping that allows them to record ion currents passing through individual channels. This is done using a glass micropipette, also called a patch pipette, with a 1 micrometer diameter. There is a small patch that contains a few ion channels and the rest is sealed off, making this the point of entry for the current. Using an amplifier and a voltage clamp, which is an electronic feedback circuit, allows the experimenter to maintain the membrane potential at a fixed point and the voltage clamp then measures tiny changes in current flow. The membrane currents giving rise to hyperpolarization are either an increase in outward current or a decrease in inward current. ==Examples==

GABA receptors are commonly known to downregulate neuronal activity by various means. • GABAA can induce hyperpolarization through an influx of Cl– ions. GABAA itself is a chloride ion channel. This process of hyperpolarization is highly dependent on which direction Cl– flows. If Cl– travels into the cell, the flow of ions increases the voltage gradient. If Cl– flows out of the cell, the voltage gradient will decrease. • GABAB induces hyperpolarization through K+ ion influx into the neuron. Unlike GABAA, GABAB is a G-Protein Coupled Receptor that activates potassium channels via Protein Kinase A (PKA) activation. Potassium typically has a higher concentration inside the cell, while sodium typically has a higher concentration outside. When potassium channels open, K+ ions flow out of the cell and cause the cell's internal potential to become more negative. GABAB activation of PKA also leads to Ca channel inactivation in presynaptic neurons. This likely leads to inhibited synaptic transmission. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels have been identified as channels that mediate hyperpolarization. They were initially discovered in pacemaker cells of the heart. These channels are controlled by cAMP, and activated by a hyperpolarized membrane. They allow the flow of Na+ and K+ ions, typically leading to a slight depolarization. == References ==