الفهرس 
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Abstract
Autism spectrum disorders (ASD) constitute a group of neurodevelopmental disorders, with a population prevalence of approximately 0.5–1.5 %. ASDs are more common in males than in females, with a gender ratio of approximately 4:1.
ASD are characterized by impaired communication, significant reduction in social interaction, and repetitive and stereotyped behavior. It is highly heritable however, genomic alterations, environmental and epigenetic factors may also increase the risk of developing autism or autistic traits
Regardless of the origins of autism, abnormal patterns of synaptic connectivity are thought to be at the core of the autistic disorder. Indeed, many of the genes associated with high risk for autism and those increasing susceptibility are directly, or indirectly, involved in axon guidance, neuronal signaling, and synaptic homeostasis. Therefore, along with an early diagnosis, the prevention and correction of the abnormal connectivity and the modulation of the synaptic function are the main goals of current and future treatment. Emerging evidence suggests that this pathway critically involves impairments in particular aspects of inhibitory gamma-amino butyric acid (GABA) neurotransmission.
Calcium is required for high affinity binding to GABA. Zinc ions are concentrated in the central nervous system and regulate GABA (A) receptors, which are pivotal mediators of inhibitory synaptic neurotransmission. Due to the concerted and intertwined activity of GABAergic and glutamatergic neurotransmission, even small net deviances could affect the excitation-inhibition balance in the autistic brain. Such an imbalance would reduce the ratio signal to noise of the sensory and procedural information in mild cases (14) and, in the extreme ones, it could lead to epilepsy. The presence of paroxystic activity in the electroencephalogram (EEG) of approximately 68% of autistic people. These gradual alterations of the EEG traces suggest that aberrant electrical activity in the autistic brain is expressed as a continuum and it may be present even in cases of autism with normal EEG recordings.
The aim of this study is to evaluate the role of GABA receptors, glutamate and zinc in the pathogenesis of autism. This will help us to specify more drugs which act as direct agonists at the GABA receptor for more selective and effective treatment.
Our study included 80 children who were categorized into 2 groups: group I: included forty autistic children. Their age ranged between 3-6 years old. All cases were diagnosed with autism according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) (APA, 1994), Autism Diagnostic Interview- Revised (ADI-R) (Rutter, 2003) and Childhood Autism Rating Scale (CARS) (Schopler et al, 1988). All cases were attended to the Outpatient Clinic for ”Autistic Children” at the Medical Research Center of Excellence, National Research Center from 2014 till 2016.
group II: forty children with age and sex matched healthy non autistic children were enrolled as controls. Their age ranged between 3-6 years old.
Determination of Serum GABA A & B receptors using, Gamma-aminobyuteric acid (GABA) A & B receptors ELISA Kits Determination of serum Glutamate in whole blood using Mass Spectrometry/ Mass Spectrometry (MS/MS).
Determination of serum zinc by atomic absorption spectrometry method.
Determination of serum calcium level by colorimetric method.
Determination of serum potassium level by flame photometry.
Our results revealed that the autistic children had significantly lower levels of GABA A receptors, GABA B receptors, ZINC, Calcium, and Potassium. However there was a significantly higher level of glutamate among the two groups.
On the other hand our results also revealed that Comparison between the levels of Zinc and the severity of autism among: mild, moderate and severe cases showed that the mean values of Zinc were significantly lower in the cases with severe degree of autism. The rest of the GABA receptors A & B, Glutamate,K, and Ca showed no significant statistical difference.
Regarding the correlation between the ADI-R domains and the levels of the GABA Receptors (A&B), Glutamate, Zinc, K, and Ca among the autistic cases, our results showed there was a positive significant correlation between GABA B receptors; Zinc and Repetitive behavior domain, while no correlation was found between the domains and GABA A receptors, Glutamate, K, and Ca.
As for the correlation between the levels of both GABA (A) receptors and GABA (B) receptors among the cases, our results showed there was significant positive correlation between the levels of them.
When we compared between the levels of the GABA receptors (A & B), Glutamate, Zinc, K, and Ca among cases with abnormal EEG and those with normal recording, showed no statistical difference.