The amygdala is an almond-shaped nucleus located deep and medially within the temporal lobe and is thought to play a crucial role in the regulation of emotional processes. GABAergic neurotransmission inhibits the amygdala and prevents us from generating inappropriate emotional and behavioral responses.
Central amygdala (CeA) neurons that produce corticotropin-releasing factor (CRF) regulate anxiety and fear learning. These CeACRF neurons release GABA and several neuropeptides predicted to play important yet opposing roles in these behaviors.
The amygdala is a key player in the processing of fear. This brain area is prominently modulated by the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT).
High concentrations of GABA and GABAa receptors are found in the limbic system, an area of the brain where personal feelings and emotional memories are generated and stored.
GABA is known for producing a calming effect. It's thought to play a major role in controlling anxiety, stress and fear. Decreased GABA levels are associated with several neurological and mental health conditions, as well as other medical conditions.
Inhibitory neurons in the CeL
Arguably the best-studied inhibitory neurons in the amygdala anxiety circuitry are the PKCδ+ neurons of the CeL, which are believed to form a monosynaptic connection with PAG-projecting neurons of the CeM56,61.
GABA-B receptors are present as autoreceptors that inhibit GABA release or heteroreceptors that reduce the release of glutamate, norepinephrine, serotonin, or dopamine.
The most important function of GABA is in our brain. When GABA levels get too low, it's difficult for the body to relax after a stress-induced neurotransmitter release. Low GABA activity leads to anxiety, depression, insomnia, and mood disorders. GABA is a natural brain relaxant that makes us feel good.
GABA plays an important role in behavior, cognition, and the body's response to stress. Research suggests that GABA helps to control fear and anxiety when neurons become overexcited. Lower-than-normal levels of GABA in the brain have been linked to schizophrenia, depression, anxiety, and sleep disorders.
Fearful stimuli including fearful faces, fear inducing images, and fear conditioned cues, have been found to activate amygdala in several brain imaging studies using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) [3–5].
Corticotropin-releasing hormone (CRH) is one of the cell groups (neuropeptides) richly expressed in the central nucleus of the amygdala and in the lateral BNST, and therefore is of special interest, as it is tied to all of these behavioral and autonomic events (see below).
A lack of GABA leaves your central nervous system with too many neuronal signals and causes conditions like epilepsy, seizures or mood disorders. Meanwhile, too much GABA means not enough brain activity and can lead to hypersomnia or daytime sleepiness.
Research shows that Gamma-aminobutyric acid (GABA) may play a key role in protecting against depression and anxiety. A review published in the journal Neuropharmacology concluded that people with anxiety and depression are more likely to have low levels of GABA.
GABA and Mental Health
This can lead to too little GABA, which may play a role in disorders related to brain function and mood, including schizophrenia, autism, depression, and anxiety.
GABA release into the synaptic cleft is stimulated by depolarization of presynaptic neurons. GABA diffuses across the cleft to the target receptors on the postsynaptic surface. The action of GABA at the synapse is terminated by reuptake into both presynaptic nerve terminals and surrounding glial cells.
While generally inhibitory in the adult brain, GABAA receptor activation is excitatory under certain conditions in which the GABA reversal potential is shifted positive due to intracellular Cl− accumulation, such as during early postnatal development and brain injury.
When GABA molecules or GABA-like compounds bind to the receptor and activate it, this channel temporarily opens and allows the passage of negatively charged molecules (i.e., ions), such as chloride ions (Cl−), to pass from the cell's exterior to its interior. This ion flow decreases the cell's excitability.
Prefrontal Cortex: ↑ The control center of the brain that controls thoughts and actions. Its main job is to control the emotional responses to stress by regulating the amygdala.
As soon as you recognize fear, your amygdala (small organ in the middle of your brain) goes to work. It alerts your nervous system, which sets your body's fear response into motion. Stress hormones like cortisol and adrenaline are released.
The amygdala is the part of the brain responsible for this reaction. When a person feels stressed or afraid, the amygdala releases stress hormones that prepare the body to fight the threat or flee from the danger. Common emotions that trigger this response include fear, anger, anxiety, and aggression.
Gamma-aminobutyric acid (GABA) is a major inhibitory neurotransmitter in the forebrain structures, and the GABAergic system has been found to have roles in attentional and learning processes, recognition of aversive stimuli, and regulation of emotion and behavior.
Too much GABA can cause an increase in anxiety, a shortness of breath, numbness around the mouth and tingling in the extremities. When you start taking GABA you might experience drowsiness or lightheadedness (so don't take it before driving), and in some individuals, skin hives or a rash may appear.
Low GABA function is proposed to be an inherited biological marker of vulnerability for development of mood disorders. Environmental factors, including stress and excessive alcohol use, may increase GABA, causing symptoms of depression or mania.