[Neurotransmission in developmental disorders].
Attention deficit/hyperactivity disorder (AD/HD) is a heterogeneous developmental disorder with an etiology that is not fully understood. AD/HD has been considered to occur due to a disturbance in cathecholaminergic neurotransmission, with particular emphasis on dopamine. The neurotransmission of dopamine in subcortical regions such as the basal ganglia and limbic areas is synaptic; on the other hand, dopamine neurotransmission in the frontal cortex is quite different, because there are very few dopamine transporters (DAT) in the frontal cortex that allow dopamine to diffuse away from the dopamine synapse ("volume transmission"). It is now clear that noradrenergic neurons play a key regulatory role in dopaminergic function in the frontal cortex. Furthermore, serotonergic neurons exert an inhibitory effect on midbrain dopamine cell bodies, and they have an influence on dopamine release in terminal regions. There is accumulating neurobiological evidence pointing toward a role of the serotonin system in AD/HD. The etiology of autism spectrum disorders (ASD) is still unclear, but information from genetics, neuropathology, brain imaging, and basic neuroscience has provided insights into the understanding of this developmental disorder. In addition to abnormal circuitry in specific limbic and neocortical areas of the cerebral cortex, impairments in brainstem, cerebellar, thalamic, and basal ganglia connections have been reported. Numerous studies have pointed to abnormalities in serotonin and glutamate neurotransmission. Three important aspects involved in the pathophysiology of ASD have been proposed. The first is cell migration, the second is unbalanced excitatory-inhibitory networks, and the third is synapse formation and pruning, the key factors being reelin, neurexin, and neuroligin. Serotonin is considered to play an important role in all of these aspects of the pathophysiology of ASD. Finally, I would like to emphasize that it is crucial in the field of child neurology medical examination and treatment should be based on the basic neuroscience, always taking "neurons" into consideration.
Takeuchi
Yoshihiro
Y
Department of Pediatrics, Shiga University of Medical Science, Otsu, Shiga. takeuchi@belle.shiga-med.ac.jp
D000818:Animals; D001289:Attention Deficit Disorder with Hyperactivity / Q000209:etiology / Q000503:physiopathology*; D001321:Autistic Disorder / Q000209:etiology / Q000503:physiopathology*; D001921:Brain / Q000502:physiology; D015816:Cell Adhesion Molecules, Neuronal; D004298:Dopamine / Q000502:physiology*; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D009638:Norepinephrine / Q000502:physiology; D000091042:Reelin Protein; D012701:Serotonin / Q000502:physiology; D009435:Synaptic Transmission
D015816:Cell Adhesion Molecules, Neuronal; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D000091042:Reelin Protein; C098004:neuroligin 3; D012701:Serotonin; D018698:Glutamic Acid; C000717127:RELN protein, human; D004298:Dopamine; D009638:Norepinephrine