Final answer:
Lithium affects neurons by entering through Na+ channels, potentially altering the neuron's electrical properties and affecting neurotransmission. Not all positively charged ions can replace Na+ due to specific ion properties essential for neural functions. Local anesthetics work by blocking these channels, preventing pain signal transmission.
Step-by-step explanation:
Patients suffering from manic-depressive disorders are sometimes treated with lithium, which can move through Na+ channels. These channels are crucial in the process of neurotransmission, involving the movement of ions like Na+ which affects the neuron's response to stimuli through actions such as depolarization and the generation of action potentials.
When lithium enters neurons through the Na+ channels, it can affect the neuron's electrical properties because it is similar in size to Na+, but not identical in function. Specifically, lithium may not be as effective in supporting the repolarization phase of the action potential due to differences in how it is handled inside the cell compared to sodium. This is why any small positively charged ion cannot replace Na+; the specific properties of Na+ are essential for the proper functioning of neural processes.
Ion flow affects the charge inside a neuron compared to the outside by changing the membrane potential, either depolarizing or hyperpolarizing the cell, which is crucial for the transmission of signals. Potassium channel blockers like amiodarone would specifically affect the repolarization phase of the action potential, where K+ channels open to allow K+ out of the cell, returning the membrane potential towards resting levels.
Regarding local anesthetics like lidocaine, their role as Na+ channel blockers makes them effective because they prevent the propagation of action potentials in the neurons that would normally transmit pain signals. This shows the importance of Na+ in the generation and propagation of neural signals.