anxiety when their neurons lacked growth hormone receptors, or agents mediating chemicals acting on and the physiological response of neurons.
Specifically, these receptors were found to be lacking in a group of somatostatin-expressing neurons, which inhibit an anxiety response by releasing the protein constituent somatostatin.
While there is growing evidence around the role of hormones in regulating neurological processes, including their influence on one's vulnerability to neuropsychiatric disorders, the researchers said the regulatory mechanism in neurons associated with such disorders had not yet been discovered.
«We demonstrated that (growth hormone) changes the synapses (or interconnections of neurons) and structurally alters the neurons that secrete somatostatin,» said Jose Donato Junior, a professor at the university's Biomedical Sciences Institute and last author of the study published in the Journal of Neuroscience.
Further, the scientists found that the lack of growth hormones in somatostatin-releasing neurons in both male and female mice decreased «fear memory», characteristic of post-traumatic stress disorder. This meant a reduced capacity to form fear memory, they said.
The findings offering a «possible chemical explanation for neuropsychiatric disorders» could contribute towards developing a new class of anxiety-relieving, or anxiolytic, drugs, they said.
Located at the base of the brain, the master gland of the endocrine system, the pituitary gland, is responsible for releasing the growth hormone in the bloodstream, promoting tissue growth throughout the body.