Lower potassium levels in the extracellular space cause hyperpolarization of the resting membrane potential. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potential as defined by the Goldman equation. As a result, a greater than normal stimulus is required for depolarization of the membrane to initiate an action potential
An increase in the Na/K ATPase activity
An increase in the number of EPSPs at the neuromuscular junction
A decrease in net K+ efflux
An increase in the number of IPSPs at the neuromuscular junction
A decreased probability of action potential generation
Contraction of intrafusal muscle fibers
Contraction of extrafusal muscle fibers
Increased γ-efferent discharge
Increased activity in group II afferent fibers
Reflex inhibition of motor neurons
Decreased potassium conductance
Spontaneous release of a quantal package of Ach
Increased chloride conductance
Inhibition of the sodium potassium pump
Increased sodium conductance
The inhibition of Na+/K+-ATPase induces a rise in sodium concentration inside cells. This sodium increase induces in its turn an increase in the intracellular calcium concentration, via the sodium-calcium exchanger. The sodium-calcium exchanger is particularly active in myocardium and in smooth vascular muscles. The rise in intracellular calcium increases the force of contraction of the heart and smooth vascular muscles. The inhibition of Na+/K+-ATPase reduces cellular polarization (depolarizing effect).
Decreased intracellular volume
Decreased intracellular sodium concentration
Depolarization of the membrane potential
Increased excitability of nerve cells
Increased intracellular potassium concentration
Repolarization of the action potential is due to efflux of K+ from the cell
Decreasing excitability of the cell
The patient has myasthenia gravis. Giving an acetylcholinesterase inhibitor leaves more acetylcholine in the synaptic cleft to improve symptoms.
Thyroid-stimulating hormone receptor of the thyroid gland is overstimulated by an autoantibody resulting in excess thyroid hormone production, thyroid cell growth, and ultimately fatigue and weakness
Ingestion of a toxin that binds to presynaptic nerve cells and prevents the release of neurotransmitters
Production of antibodies against nACHRs
Production of auto-antibodies against P/Q-type calcium channels at the motor nerve terminals
Oligodendrocytes are the myelinating cells of the CNS. Schwann cells are the myelinating cells of the PNS.
Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and, thus, the release of adrenaline (and noradrenaline) into the bloodstream.
γ-Aminobutyric acid (GABA)
Stimulation of AC or GC induces smooth muscle relaxation. AC and C stimulate cAMP and cGMP-dependent kinases that phosphorylate enzymes that remove Ca2+ from the cytosol leading to decreased contraction. Decreasing K+ permeability or increased Na+ permeability leads to depolarization resulting in contraction. Inhibition of the Ca2+-ATPase favors contraction. No Tn in smooth muscle.
Inhibition of the sarcoplasmic reticulum Ca2+-ATPase
Increased plasma membrane Na+ permeability
Decreased plasma membrane K+ permeability
Decreased affinity of troponin C for Ca2+
Stimulation of adenylate cyclase
Increase in the rate of voltage-dependent changes in K+ permeability
Inhibition of the Na+ –K + pump
Block of voltage-dependent Na+ permeability
Decrease in voltage-dependent Na+ permeability
Decrease in the rate of Na+ inactivation
The membrane potential will become more negative
Sodium conductance will increase
Over time, the membrane will become more excitable
Potassium conductance will increase
The activity of the Na/K pump will decrease
A decrease in the number of postsynaptic neurotransmitter receptors
Impaired skeletal muscle action potential conduction
A decrease in the presynaptic neuron calcium permeability
Impaired α-motoneuron action potential conduction
A decrease in the number of presynaptic neurotransmitter vesicles
Cold delays inactivation of Na+ channels allowing more Na+ to enter the cell. Increased duration does not equal increase membrane potential. No change to capacitance or refractory period. Duration of the AP depends on Na+ not K+.
The duration of the refractory period is increased
The potassium conductance of the membrane is increased
The capacitance of the nerve fiber membrane is increased
The membrane potential becomes more positive
The amount of sodium entering the nerve with each action potential increases
Because the ratio of Na+ to K+channels is low in adult astrocytes, these cells are not capable of regenerative electrical responses such as the action potential.
Astrocytes are predominantly permeable to K+ therefore they help to regulate extracellular K+
Glial membranes have a resting potential more negative than neurons, which makes them more selective to K+
The ratio of Na+ to K+ channels in astrocytes is high in comparison to neurons, making them incapable of producing an action potential.
Inwardly rectifying K+ channels are important in setting the resting potential in glial cells.
Astrocytes diminish neuronal excitability via influx of HCO3- via an electrogenic Na+/HCO3 cotransporter which causes a fall in extracellular pH
In the PNS, a single Schwann cell provides a single myelin segment to a single axon of a myelinated nerve (see Fig. 11-13B). This situation stands in contrast to that in the CNS, where one oligodendrocyte myelinates many axons.
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