section_path: Mechanism/Neurocircuitry in mammals
section_name: Neurocircuitry in mammals
paragraph_text: Neurocircuitry in mammals
  
  The brain structures that are the center of most neurobiological events associated with fear are the two amygdalae, located behind the pituitary gland. Each amygdala is part of a circuitry of fear learning. They are essential for proper adaptation to stress and specific modulation of emotional learning memory. In the presence of a threatening stimulus, the amygdalae generate the secretion of hormones that influence fear and aggression. Once a response to the stimulus in the form of fear or aggression commences, the amygdalae may elicit the release of hormones into the body to put the person into a state of alertness, in which they are ready to move, run, fight, etc. This defensive response is generally referred to in physiology as the fight-or-flight response regulated by the hypothalamus, part of the limbic system. Once the person is in safe mode, meaning that there are no longer any potential threats surrounding them, the amygdalae will send this information to the medial prefrontal cortex (mPFC) where it is stored for similar future situations, which is known as memory consolidation.
  
  Some of the hormones involved during the state of fight-or-flight include epinephrine, which regulates heart rate and metabolism as well as dilating blood vessels and air passages, norepinephrine increasing heart rate, blood flow to skeletal muscles and the release of glucose from energy stores, and cortisol which increases blood sugar, increases circulating neutrophilic leukocytes, calcium amongst other things.
  
  After a situation which incites fear occurs, the amygdalae and hippocampus record the event through synaptic plasticity. The stimulation to the hippocampus will cause the individual to remember many details surrounding the situation. Plasticity and memory formation in the amygdala are generated by activation of the neurons in the region. Experimental data supports the notion that synaptic plasticity of the neurons leading to the lateral amygdalae occurs with fear conditioning. In some cases, this forms permanent fear responses such as post-traumatic stress disorder (PTSD) or a phobia. MRI and fMRI scans have shown that the amygdalae in individuals diagnosed with such disorders including bipolar or panic disorder are larger and wired for a higher level of fear.
  
  Pathogens can suppress amygdala activity. Rats infected with the toxoplasmosis parasite become less fearful of cats, sometimes even seeking out their urine-marked areas. This behavior often leads to them being eaten by cats. The parasite then reproduces within the body of the cat. There is evidence that the parasite concentrates itself in the amygdala of infected rats. In a separate experiment, rats with lesions in the amygdala did not express fear or anxiety towards unwanted stimuli. These rats pulled on levers supplying food that sometimes sent out electrical shocks. While they learned to avoid pressing on them, they did not distance themselves from these shock-inducing levers.
  
  Several brain structures other than the amygdalae have also been observed to be activated when individuals are presented with fearful vs. neutral faces, namely the occipito cerebellar regions including the fusiform gyrus and the inferior parietal / superior temporal gyri. Fearful eyes, brows and mouth seem to separately reproduce these brain responses. Scientists from Zurich studies show that the hormone oxytocin related to stress and sex reduces activity in your brain fear center.