In the present study, we successfully developed a bioprocess for the rapid production of human neurons using fully controlled stirred tank bioreactors (125 mL).
To study the co-morbid effects of Tat and morphine, we used an in vitro model system of human neurons differentiated from human neural precursor cells isolated from fetal brains.
In addition, similar to our studies with NMDA treatment of human neurons, the HIV protein Tat was used to treat rodent neurons, revealing the upregulation of miR-128a but not miR-21.
Cells exhibited typical electrophysiological features of immature neurons, consistent with the slow maturation of human neurons.
Biologist Gong Chen of the University of Pennsylvania, who was not involved with the research, called it "a remarkable achievement," adding, "it opens the door for many studies on the human brain using human neurons".
Furthermore, we explore whether this cellular system could be used to understand the role of estrogens in human neurons, and present preliminary data in support of this.
Some of these human neurons fire action potentials upon depolarization (Fig. 1G and 1H).
In view of the scarcity of human primary neurons, we used mouse primary neurons to determine the identity of mOatps expressed, to confirm mOatp-mediated MC congener-specific uptake, and to determine MC congener specific inhibition of neuronal PPs.
By inducing astrocytes from hES cells in a chemically defined medium, we could produce human neurons without the use of P-ACM.
To address this issue, and to provide direct information on human neurons, we made use of LUHMES cells.
