Why do negative ions flow into a cell in an inhibitory synapse, even though a neuron has a negative resting potential?

Question

In my spare time I have been reading an introductory Psychology textbook and this question came to my mind after reading about action potentials. I have no previous knowledge in chemistry so if I do need some sort of other knowledge I would appreciate if I could be told what I need to learn in order to understand the physiology of the nervous system better. So Why do negative ions come into a cell during an inhibitory synapse even though a neuron has a negative charged resting potential?

I understand this question might be extremely vague and impossible to answer without previous knowledge of the physiology of the nervous system. Any help would be greatly appreciated.

Answer 1

Short answer
Negative ions can flow against the electrical gradient into the cell, provided their concentration gradient across the cell membrane is large enough.

Background
When an ion channel opens, the resultant ion flow is dependent on two things; the membrane potential (which is indeed negative at rest) and the concentration gradient of the ion.

Consider the activation of a GABA_A receptor. GABA is the principial inhibitory neurotransmitter in the nervous system. GABA opens the associated Cl^- channel on GABA_A receptors.

Using the Nernst equation one can approximate the membrane potential (V_eq) at which an ion is in equilibrium. It mainly depends on the concentration of the ion X outside and inside the cell ([X]_o and [X]_i, respectively).[Cl]_o is approximately 103 mM, and [Cl]_i 4 mM. Hence, there exists a large concentration gradient with lots of it outside the cell.

^{Nernst equation. Source: Physiology Web}

In a neuron, the Nernst potential of Cl^- is around -71 mV. Hence, given that the resting membrane potential is approximately -70 mV for a typical neuron, no Cl^- flux will occur when Cl^- channels open, because the resting membrane potential is equal to the equilibrium potential of Cl^-. However, when a neuron is depolarized by stimulatory neurotransmitters (e.g., glutamate), the membrane potential may be reduced to, say, -60 mV. This is still more negative than the action potential threshold (about -55 mV), but very close to it. So without any inhibition the neuron would be close to firing a spike. However, when GABA is released presynaptically, opening of the Cl^- channels coupled to GABA_A receptors will result in Cl^- influx, because the membrane potential is higher (more positive) than the equilibrium potential of Cl^-. In effect, Cl^- will enter the cell until its equilibrium potential is reached, re-polarizing the neuron back to -70 mV and hence inhibiting it.

Answer 2

I can't add any detail to AliceD's answer, but I can put it in different terms, and perhaps that could be helpful to you.

Yes, Cl^- ions are negatively charged, and the neuron is very often negatively charged. Given only those two facts, yes, you would think Cl^- would not enter the neuron. But there is another key fact: diffusion.

The Cl^- ions feel the force of electrical repulsion, but since they are at body temperature they also feel the force of slamming into each other at very high speeds and bouncing every which way. This "slamming force" tends to spread them out, and that is otherwise known as diffusion. Since there are many more of them outside the neuron than inside (due to active pumping them to that imbalanced state), the force of diffusion tends to drive them inside the neuron--at least as long as it's not too negative in there! If it is too negative, then no, the force of diffusion is not enough to push the Cl^- ions into the neuron, and in fact they may leave the neuron.

What I've written here is, I think, (essentially) equivalent to AliceD's fine answer.