Postanoxic encephalopathy refers to a rare condition in which a patient who has experienced insufficient blood flow and oxygen to the brain, make a complete clinical recovery. This is seen in patients who go into a state of unconsciousness, as result of a sudden malfunction in the heart that causes it to stop beating. This is known as cardiac arrest. The only treatment that has provided a benefit to this illness is known as therapeutic hypothermia. This is the reduction of core body temperature, for patients who do not regain consciousness after the return of circulation, following cardiac arrest. This hypothermia is used in the hopes of avoiding further damage by preserving remaining energy levels in the body. By preserving these energy levels, it provides a healthy internal state of our neurons, which maintain membrane voltage and regular cellular processes.

In relation to postanoxic encephalopathy, the purpose of this study conducted by Irina I. Stoyanova et al., (2016), was to study the damage of areas in the brain, caused by low oxygen levels, responsible for connecting brain regions to each other. The brain region responsible for this connection is called the synapse. To test the effect of oxygen deprivation in the brain, the experimenter used the culture of neurons, and tested the effects of ghrelin as a treatment. Ghrelin is a hormone responsible for hunger. To put this experiment to test, the brains of five rat pups were removed and placed in a gelatinous substance, which is made up of nutrients called growth mediums. This growth medium ensures that brain cells do not die, which is vital for the conduction of this experiment. After restoring the brain cells, the experimenter must go through the different layers of the brain, and extract the cells required for this experiment. These cells then undergo oxygen deprivation for 6 hours, followed by a 3 hour period to recover in an environment that contained normal oxygen levels. After the recovery stage, half the brain cells were treated with ghrelin for 24 hours, while the other half were not. To investigate the results this experiment had on synapses in the brain, a common laboratory technique was used that anatomically visualizes the location of a specific protein or antigen in cells. This technique is referred to as immunochemistry.

The results of the study found that oxygen deprived brain cells, resulted in a massive decline in the number of synapses in the brain. Without these synapses, the brain regions cannot communicate with one another, and therefore cannot function properly. However, the decline in synapses was selective according to neuronal size. It was found that large and small sized neurons were more vulnerable to synaptic damage than medium sized neurons. Therefore, the medium sized neurons did not show sensitivity to oxygen deprivation. With this being said, the density of the synapse was increased in brain cells that were treated with ghrelin, compared to the non-treated cells. As a result of this, it can be concluded that ghrelin has a strong impact in the recovery of synapses, in brain cells that have undergone oxygen deprivation. Thus, providing increasing support for the possibility that ghrelin can be used as a therapeutic measure in the treatment of postanoxic encephalopathy.

Citation:

Stoyanova, I., Hofmeijer, I., Putten, J., & Feber, M. (2016). Acyl Ghrelin Improves Synapse Recovery in an In
Vitro Model of Postanoxic Encephalopathy. Molecular Neurobiology, 53(9), 6136-6143.