Glial cell abnormalities in major psychiatric disorders: the evidence and implications

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

“…Recent studies have shown that glucocorticoid treatment inhibits NG2-positive cell proliferation in the adult rat hippocampus (Alonso, 2000;Wennström et al, 2006), whereas electroconvulsive seizure treatment reverses this effect (Wennström et al, 2006). The functional significance of these observations is not clear, but recent theories suggest that glial cell dysfunction may contribute to the pathogenesis of affective disorders (Coyle and Schwarcz, 2000;Cotter et al, 2001b). Moreover, there is experimental evidence indicating that stress and antidepressant treatment can induce changes in structural plasticity of astrocytes and NG2-positive glia (Czéh et al, 2006;Wennström et al, 2006).…”

“…Moreover, there is experimental evidence indicating that stress and antidepressant treatment can induce changes in structural plasticity of astrocytes and NG2-positive glia (Czéh et al, 2006;Wennström et al, 2006). The majority of the post mortem histopathological studies on glial reduction in frontolimbic structures have not identified which populations of glial cells are reduced, but there is an indication of the involvement of both astrocytes and oligodendrocytes (Cotter et al, 2001b;Rajkowska, 2003).…”

Neurogenic hypothesis and psychiatric disorders

“…Though some other controversial results have also shown, these results have given the possible relationship between the morphological changes of the amygdala and the pathophysiologic development of autism. Mercadante et al [99] [110,111] Growth factors: 1) Brain-derived neurotrophic factor (BDNF) [31] 2) Vascular endothelial growth factor (VEGF) [41] 3) Insulin-like growth factor 1 (IGF1) [41] Neurotransmitters: 1) GABA [36] 2) Serotonin [37] 3) Glutamate/NMDA receptor [38] 4) Dopamine and acetylcholine [39] -Decrease in number of Ki-67 +ve cells in schizophrenia patients [26] Intracellular molecules: 1) Disrupted in Schizophrenia 1 (DISC1) [75] 2) Neuronal PAS domain protein 3 (NPAS3) [85] 3) Neuregulin 1 (NRG1) [ [99,103] have further suggested that the new immature-neurons newly produced in the amygdala may be helpful in increasing the ability to learn from new experiences via modulation of the gamma-aminobutyric acid (GABA) as patients with autism were found to have alteration on the GABAergic system. However, further investigations are needed as this is a new etiologic hypothesis of autism.…”

“…Another example has shown that chronic stress could decrease cell proliferation in the medial prefrontal cortex which cause abnormal decrease in glial cells number [110]. According to some of the human studies, the decrease in the number of glial cells in the prefrontal cortex can trigger the development of various mood disorders [110,111]. Also, there was a study that found the reduction in glial density in the anterior cingulated cortex may be related to the major depressive disorder [111].…”

“…According to some of the human studies, the decrease in the number of glial cells in the prefrontal cortex can trigger the development of various mood disorders [110,111]. Also, there was a study that found the reduction in glial density in the anterior cingulated cortex may be related to the major depressive disorder [111]. Glial cells have been previously suggested to retain the ability to renew in adult brains [110] and they have been shown to have important roles such as: regulating the process of synaptogenesis, adjusting the cerebral flow and also lying very close to the neurons and the blood vessels for mediating the process of neurogenesis and angiogenesis [111].…”