How The Neurotransmitter GABA Works For Anxiety In The Brain

Hello, I’m Dr. Carlo Carandang, and I’m a psychiatrist. Today I will talk about how GABA works for anxiety. GABA is an inhibitory neurotransmitter in the central nervous system (CNS). So we know that when you have anxiety, you have overactive fear circuits which are centered on the amygdala. So here is the amygdala, and this is the fear center of the brain. When you have anxiety, the amygdala is hyperactive, in addition to the connected fear circuit. So when you have anxiety, you have an overactive amygdala and overactive fear circuits.

These GABA neurons actually connect to the amygdala. So here’s a GABA neuron, and it connects to the amygdala via these connections which are called the synapse. The synapse between neurons is how neurons connect to one another, and they connect to one another via these neurotransmitters. Neurotransmitters are molecules which travel from one neuron to another neuron, and they basically cross this empty space between them to communicate with each other. So we do know that GABA is inhibitory- so when GABA is released into the synapse, they bind to the postsynaptic GABA receptors here on the amygdala. When GABA binds to these receptors it actually inhibits the amygdala and it slows down the hyperactivity of the amygdala- therefore it reduces anxiety.

I’m going to explain in detail about GABA neurotransmission , about how this whole process starts and ends with GABA being released and anxiety being reduced- please refer to the video presentation above. So again this is the GABA neuron and this is the amygdala. So the GABA neuron actually projects to the amygdala and it communicates via the synapse. In the GABA neuron there are GABA neurotransmitters in these vesicles, so these vesicles then release their contents into the synapse when the neuron is stimulated (has an action potential propagated down the axon). So GABA is released from the vesicles into the synapse and GABA then travels across the synapse, binds to the GABA receptors, and this in turn opens up these ion channels that are attached to these receptors. When the ion channel opens up, it lets chloride in, so when chloride is let in, it actually inhibits the neurotransmission postsynaptically. So in essence, when GABA binds the GABA receptor and the chloride ion channel is open, then it basically inhibits the neurotransmission in the amygdala and therefore it reduces the hyperactivity. GABA is then recycled by being reabsorbed by what’s called a GABA reuptake pump, which is similar to other neurotransmitter reuptake pumps that we have studied, such as the serotonin reuptake pump.

So GABA has a reuptake pump to recycle GABA from the synapse into the presynaptic neuron. We do know that there are some drugs and oral supplements that block the reuptake of GABA and thereby effectively increases the GABA concentration in the synapse, and subsequently there’s more binding of GABA to these postsynaptic receptors. What happens is you have more opening of ion channels and this increases the inhibition of the amygdala. This results in decreased anxiety, as the hyperactivity is reduced from the increase in GABA from the drug or the supplement that you took.

As an example of what blocks the GABA reuptake pump, here is an herbal supplement for anxiety called passion flower. So we know that passion flower actually works by blocking the reuptake of GABA by binding to the GABA reuptake pump. We also know that there are other medications that can affect GABA neurotransmission, such as benzodiazepines. Benzodiazepines bind to a different part of the GABA receptor postsynaptically, and what it does is it actually enhances GABA neurotransmission. So when you have both GABA and you have a benzodiazepine binding to the GABA receptor at the same time, it actually increases the hole of the ion channel even more, allowing for more chloride ions to pass through and therefore facilitates the inhibition postsynaptically. So what GABA and benzodiazepines do together is that they further inhibit the amygdala and therefore it reduces anxiety. So that’s how benzodiazepines work, because it binds to a different part of the GABA receptor. However, benzodiazepines are not effective if the GABA neurotransmitter were not present (hypothetical case). So bear in mind that for benzodiazepines to work, the GABA neurotransmitter needs to be present (again, this is just a hypothetical case, to illustrate how benzodiazepines work in concert with GABA to reduce anxiety).

In summary, GABA is an inhibitory neurotransmitter. So when you have GABA binding to the GABA receptor, it opens up the chloride ion channel and it inhibits the activity of the amygdala, resulting in decreased anxiety. For more information and help on GABA and anxiety, please visit the rest of AnxietyBoss.com.

Thank you for listening, I’m Dr. Carlo Carandang.