A structure of the brain cell that is like a tiny antenna was earlier considered to be an area of lesser importance.
However, researchers believe the vestige that was once considered to be useless holds an important role in the brain development region of mammals.
The impairment of antennae results in brain wiring defects that has roots similar to schizophrenia, autism and other related disorders.
Scientists at the UNC School of medicine conducted experiments by having the wiring defects restored through these antenna structures.
These antenna structures are known as primary cilia.
Author Eva Anton, professor of physiology and cell biology, says, “Primary cilium on the neuronal structure of the brain environment results in refinement and formation of successful circuits in the development of the brain.”
These findings shed light on the increasing number of individuals with cilium-related genetic mutations that often endi up showing autism-related behaviors.
The study further reveals different cellular pathways which modify the brain circuits that are associated with schizophrenia and autism, among other related brain disorders.
In the study, Eva and her colleagues observed the role the primary cilium played in the later developmental stages of inhibitory interneurons.
The interneurons modulate other neuronal activities that help the other brain circuits to perform efficiently.
Nevertheless, the existing defects in interneuron signalling are being observed in schizophrenia and autism-related disorders.
Autism individuals are further seen to suffer from ARL13B mutations and other related intellectual disabilities.
The researchers further conducted lab tests on newborn mice by deleting ARL13B genes. The deletions were seen to cause defects in the abilities of interneurons to form the right link with other related excitatory neurons.
Further, the researchers observed that mutations in ARL13B in patients resulted in causing similar effects. The experiments were seen to confirm the abnormal influence of interneurons on the circuits of the brain where they were seen to be connected.
These actions resulted in other circuits being misbalanced in similarity with genetic models of schizophrenia and autism. It was further observed that the prima cilia of the defective interneurons were missing the somatostatin receptor3.
Interestingly, the group found a way to artificially force the expressions of these missing receptors from the depleted interneurons. The researchers believe in this way, one can prevent abnormal growth of interneurons.
Further, the inflow of brain signals in the interneurons is seen to be of prime importance for the healthy development of the neuron.
The results of the study conclude that restoration of such signals in the early life of an individual might be therapeutic.
Dr. Eva Anton further says, “These mutations, even after they have affected patients in their early stages of embryonic development, a possible fix to the problem can still be expected and addressed.”
Nevertheless, Eva adds that the approach can lead to broader impacts in the way one can expect the circuit malformations to be corrected. The doctor says, a further in-depth study is required as there are many existing neuropsychiatric conditions that can be linked to the disrupted connectivity of interneurons.