Neurogenesis In Adults and Effect of Anti-Epileptic Drugs|2023

adult neurogenesis


Lamin B1, a basic component of the nuclear lamina, plays a vital role in brain development, and its role in pathological conditions was detected lately when defects in the gene encoding this protein and its regulators were associated with defects chiefly affecting neurogenesis in the CNS. Results obtained from various experiments indicate that optimal levels of Lamin B1 are key to maintaining neuronal nuclear size and shape. 

Micro-electron arrays, an electrode used in electrophysiology for recording neural signals, are responsive to chemical manipulations, and upon extensive pharmacological modulation, might provide model systems — in the hippocampus — to detect acute pharmacological effects of antiepileptic drugs of neuronal network in vitro, thereby monitoring Neurogenesis secondarily.

This could be worthwhile for investigating the long-term exposure to anticonvulsant compounds in view of developing neuropharmacological/ neurotoxicological analysis for drug screening. Epilepsy treatment is solely dependent on antiepileptic drugs which act primarily to suppress seizure severity and frequency (Mahajan S., 


Neurogenesis, Micro-electron arrays, antiepileptic, Pathological, neuronal network, Epilepsy. 


Neurogenesis is a phenomenon that involves the formation of new neurons in the brain by neural stem cells(NSCs). Investigators have confirmed that neurogenesis occurs in discrete parts of the adult brain as opposed to the embryo’s. This develops primarily in the dentate gyrus (subgranular zone) and the subventricular zone of the lateral ventricle.

The major regulators of adult neurogenesis are growth factors, neurotrophins, cytokines and hormones. In vivo studies have shown that folate plays a critical role in DNA methylation and epigenetic phenomenon with the CNS together with vitamins B-6 and B-12, which is critical for the upkeep of adult neurogenesis. 


Neural stem cells (NSCs) within the embryonic and early postnatal murine brain produce neurons and glia, including astrocytes and oligodendrocytes. The transformation of multipotent and proliferative NSCs to fully differentiated nerve cells is tagged “neurogenesis”. Results prove that the short-term use of antiepileptic prescriptions damage neurons in the immature brain and that the combined use of antiepileptic drugs reduces damage. Neurogenesis in humans wholly begins from gestational week 10 and ends around gestational week 25. 

Antiepileptic drugs (AEDs) communicates with channels, neuronal receptors, metabolic enzymes and transporters within the brain; additionally, they modify bursting properties of neurons, inhibit spread of epileptic activity, and reduce synchronization (Ikonomidou, 2010).

The targets of AEDs are in charge of the regulation and control of processes essential for brain development. Experimental findings on side effects of AEDs within the developing mammalian brain include interference with physiological apoptotic cell death, neurogenesis, cell proliferation and migration, axonal arborization, synaptogenesis, and synaptic plasticity. AEDs are among the foremost rapid causes of fetal malformations, such as neural tube defects, growth retardation, digital anomalies, congenital heart defects, orofacial clefts, developmental delay, and microcephaly. 

Physiological cell death, a process by which cells are deleted from the developing CNS, is a regular phenomenon in the developing brain of mammals. Studies have shown that compounds that are used medically as sedatives, anesthetics, or anticonvulsants can trigger the widespread of apoptotic neurodegeneration throughout the developing brain.

Such compounds include antagonists of NMDA(N-methyl-D-aspartate) receptors: ketamine and laughing gas, agonists of GABAA(Gamma-Amino-Butyric-Acid-A) receptors: barbiturates, benzodiazepines, propofol, and AEDs: sulthiame, phenytoin, vigabatrin, and valproate.

The vulnerable developmental time during which drug-induced neuroapoptosis is recorded in rodents spans the first two weeks of life (Neonatal period). The comparable period in humans stretches from the sixth month of gestation to several years afterwards. Thus, there is an extended period in human development prenatally, during which immature neurons could be prone to committing suicide if exposed to several AEDs(J, C., 2019).

It is conceivable that a disruption of these developmental processes could account for the neurological deficits seen in humans exposed to AEDs prenatally; however, this theory remains highly controversial, because, unfortunately, the aftermath of AEDs in the developing brain has not been systematically analyzed (Chrysanthy, 2019). 

Neurogenesis in the adult hippocampus declines with age, a process that has been compromised in cognitive and emotional impairments; However, the mechanisms underlying this decline have stayed elusive(Gotz, M., 2005). Disruption of neurogenesis and origination of aging‐associated behavioral behaviours occurs due to deletion of the nuclear envelope protein lamin B1 in neural stem or progenitor cells.

It is shown that the age‐related downregulation of lamin B1, one of the nuclear lamins in ANSPCs (adult neural stem or progenitor cells), underlies growth‐related alterations in adult hippocampal neurogenesis. Results relate the excessive levels of lamin B1 in ANSPCs and untimely differentiation, and controlling the maintenance of ANSPCs in the brain; the level of lamin B1 in ANSPCs diminished during aging.

Advanced loss of lamin B1 in ANSPCs progressively promotes neurogenesis but eventually depletes it(Giacomoni, C., 2019). Altogether, results indicate that the reduction in lamin B1 buttresses stem cell aging; this influences the homeostasis of neurogenesis in adults and mood synchronization(Zhang, L., 2018) 

Most times, neurosurgeons identify brain structures and neuronal pathways using a technique known as microelectrode recording. An electrode is passed through regions of the brain, where electrical patterns and linkages are recorded from surrounding brain structures. Micro-electron arrays(MEAs) allow for prompt monitoring of in vivo neurotransmitter activity, and offer atypical temporal and spatial resolution(Mahajani, S. 

The concealed design of the arrays from micro-electron allows for limited tissue damage contrastly to earlier technologies and models; This confers a higher spatial resolution in MEAs,

which facilitates the understudy of microscopic regions of the brain(Edward, C., 2018). Thus far, these arrays have recorded electrophysiological feedback of single neurons within the hippocampus. If this section of the brain is injured, it can result in a patient’s inability to create exceptional new memories. 


The early months of life are the period of maximal vulnerability to injury, during which most of the important steps of neuronal development such as physiologic apoptosis (neuronal pruning) happens. Insertion of micro-electron arrays still poses some threats as with other prosthetic implants, because of the body’s innate response to a foreign object. 

Neurogenesis can be boosted amidst controversies; Fasting, It boosts the development of brain stem cells to mature brain cells. Exercises, especially aerobic activity, have been proven by Havard studies to have a hands-down profound effect on neurogenesis. 

This theory, however, explains in entirety the neural connections and its implicit function in the human brain. Understanding this process on a physiological level will be critically important in reducing the rate of degenerative diseases. 


1. Abdissa, D., Hamba, N., & Gerbi, A. (2020, April 22). Review article on adult neurogenesis in humans. Translational Research in Anatomy. Retrieved October 3, 2021, from 

2. Bedrosian, T. A., Houtman, J., Eguiguren, Mahajani, S. (2021, February 1). “Lamin B1 decline underlies age-related loss of adult hippocampal neurogenesis.” The EMBO journal. Retrieved October 3, 2021, from

3. Colombi, I., Mahajani, S., Frega, M., Gasparini, L., & Chiappalone, M. (1AD, January 1). “Effects of antiepileptic drugs on hippocampal neurons coupled to micro-electrode arrays.” Frontiers. Retrieved October 3, 2021, from 

4. Edwards, C. (2018, April 13). Microelectrode arrays record activity deeper in the brain – verdict medical devices. Medical device Network. Retrieved October 4, 2021, from per-brain/. 

5. Götz, M., & Huttner, W. B. (2005, October 1). The cell biology of neurogenesis. Nature News. Retrieved October 4, 2021, from 

6. Giacomini, C., Lab, M. N., Mahajani, S., Marotta, R., Gasparini, L., “Lamin B1 protein is required for dendrite development in primary mouse cortical neurons.” Molecular Biology of the Cell. Retrieved October 3, 2021, from 

7. Ikonomidou, Chrysanthy. “Prenatal Effects of Antiepileptic Drugs.” Epilepsy Currents, Blackwell Science Inc, Mar. 2010, 

8. J, C., S, L., X, Z., J, C., & F, C. (2009, October). Long-term Antiepileptic Drug Administration during early life inhibits hippocampal neurogenesis in the developing brain. Journal of neuroscience research. Retrieved October 4, 2021, from 

9. Mahajani, S., Giacomini, C., Marinaro, F., De Pietri Tonelli, D., Contestabile, A., & Gasparini, L. (2017, July 7). Lamin B1 levels modulate differentiation into neurons during embryonic corticogenesis. Nature News. Retrieved October 4, 2021, from 

10. Marotta, R., Catelani, T., Pesce, M., Giacomini, C., Mahajani, S., & Laura, G. “Role of lamin B1 in structuring the cell nucleus in eukaryotic cells.” Wiley Online Library. Retrieved October 3, 2021, from 

11. Urbán, Noelia, and François Guillemot. “Neurogenesis in the Embryonic and Adult Brain: Same Regulators, Different Roles.” Frontiers, Frontiers, 1 Jan. 1AD, 

12. Zhang, L., & Zhang, X. (2018, April 5). Factors regulating neurogenesis in the adult dentate gyrus. IntechOpen. Retrieved October 4, 2021, from

Reviewed by: Affia, B. (2021) 

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