HGF, GABA and Autism severity

Correlation Between Hepatocyte Growth Factor (HGF) and Gamma-Aminobutyric Acid (GABA) Plasma Levels in Autistic Children.



There is much support for the role of Gamma-Aminobutyric acid (GABA) in the etiology of autism. Recent research has shown that hepatocyte growth factor (HGF) modulates GABAergic inhibition and seizure susceptibility.

This study was designed to determine and correlate plasma levels of HGF, GABA, as well as symptom severity, in autistic children and neurotypical controls.

Plasma from 48 autistic children and 29 neurotypical controls was assessed for HGF and GABA concentration using ELISAs.

Symptom severity was assessed in these autistic individuals and compared to HGF and GABA concentrations.

We previously reported that autistic children had significantly decreased levels of HGF.

In this study, the same autistic children had significantly increased plasma levels of GABA (P = 0.002) and decreased HGF levels correlated with these increased GABA levels (r = 0.3; P = 0.05).

High GABA levels correlated with

increasing hyperactivity (r = 0.6; P = 0.0007)

and impulsivity severity (r = 0.5; P = 0.007),

tip toeing severity (r = 0.35; P = 0.03),

light sensitivity (r = 0.4; P = 0.02), and

tactile sensitivity (r = 0.4; P = 0.01).

HGF levels did not correlate significantly with any symptom severity.

These results suggest an association between HGF and GABA levels and suggest that plasma GABA levels are related to symptom severity in autistic children.


Further Readings of Interest


Exercise, Resilience , Anxiety and GABA : Implications for Autism


Wiki –

In 2007, an excitatory GABAergic system was described in the airway epithelium. The system activates following exposure to allergens and may participate in the mechanisms of asthma.[28] GABAergic systems have also been found in the testis[29] and in the eye lens.[30]

Inhibitory role for GABA in autoimmune inflammation


GABA, the principal inhibitory neurotransmitter in the adult brain, has a parallel inhibitory role in the immune system.

We demonstrate that immune cells synthesize GABA and have the machinery for GABA catabolism. Antigen-presenting cells (APCs) express functional GABA receptors and respond electrophysiologically to GABA.

Thus, the immune system harbors all of the necessary constituents for GABA signaling, and GABA itself may function as a paracrine or autocrine factor.

These observations led us to ask further whether manipulation of the GABA pathway influences an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE).

Increasing GABAergic activity ameliorates ongoing paralysis in EAE via inhibition of inflammation. GABAergic agents act directly on APCs, decreasing MAPK signals and diminishing subsequent adaptive inflammatory responses to myelin proteins.

This entry was posted in Allergy, Asthma, Autism, co-morbid, Depression, diabetes, Immune System, Inflammation, Neurology, Physiology, Schizophrenia. Bookmark the permalink.

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