Alcohol and nicotine reduce cell proliferation and enhance apoptosis in dentate gyrus

Jang, Mi Hyeon; Shin, Min Chul; Jung, Sae Bin; Lee, Taeck Hyun; Bahn, Geon Ho; Kwon, Yunhee Kim; Kim, Ee Hwa; Kim, Sang Hoon

doi:10.1097/00001756-200208270-00004

Cited by 84 publications

(55 citation statements)

References 22 publications

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“…This finding supports suggestions by Jang et al [49] that 3 days of nicotine exposure in adolescent male rats induced a 110% increase in active caspase-3 from the dentate gyrus.…”

Section: Discussionsupporting

confidence: 92%

Nicotine-induced memory impairment by increasing brain oxidative stress

Hrițcu

Ciobîcă²,

Gorgan

2009

Open Life Sciences

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Male Wistar rats were subjected to chronic nicotine treatment (0.3 mg/kg; 7 continuous days) and their memory performance was studied by means of Y-maze and multi-trial passive avoidance tasks. Nicotine significantly decreased spontaneous alternation in Y-maze task and step-through-latency in the multi-trial passive avoidance task, suggesting effects on both short-term memory and long-term memory, respectively. In addition, nicotine induced neuronal apoptosis, DNA fragmentation, reduced antioxidant enzymes activity, and increased production of lipid peroxidation and reactive oxygen species, suggesting pro-oxidant activity. Our results provide further support that nicotine-induced memory impairment is due to an increase in brain oxidative stress in rats.

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“…This finding supports suggestions by Jang et al [49] that 3 days of nicotine exposure in adolescent male rats induced a 110% increase in active caspase-3 from the dentate gyrus.…”

Section: Discussionsupporting

confidence: 92%

Nicotine-induced memory impairment by increasing brain oxidative stress

Hrițcu

Ciobîcă²,

Gorgan

2009

Open Life Sciences

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“…Our own work showed that a single, acute dose of alcohol (5 g/kg by gavage) inhibited cell proliferation by around 40% as examined with BrdU labeling. Jang et al (2002b), as mentioned earlier, had also shown a similar decrease with three days of single injections at 4 g/kg (i.p.) and reported that alcohol dose dependently decreases cell proliferation even at a dose of 0.5 g/kg (i.p., once a day for 3 days) in adolescent rats.…”

Section: Alcohol Inhibition Of Adult Neurogenesis: Different Mechanissupporting

confidence: 78%

Alcohol and adult neurogenesis: Roles in neurodegeneration and recovery in chronic alcoholism

2006

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The concept of "structural plasticity" has emerged as a potential mechanism in neurodegenerative and psychiatric diseases such as drug abuse, depression, and dementia. Chronic alcoholism is a progressive neurodegenerative disease while the person continues to abuse alcohol, though clinical and imaging studies show that some recovery may occur with abstinence. The neural plasticity observed in chronic alcoholism coupled with conflicting reports on alcohol-induced hippocampal neuropathology make this disease ripe for reconsideration in terms of the phenomenon of adult neurogenesis. This review describes opposing neurogenic processes that occur with alcohol intoxication and abstinence following alcohol dependence and how these opposing events relate to neurodegeneration and recovery from chronic alcoholism.

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“…It has been shown previously that in vivo nicotine exposure reduces proliferation in the DG, but not in the SVZ (10,11). In light of these reports, the data obtained here with chronic nicotine administration starting after the proliferation phase suggest that once differentiation has started, the survival of DG cells is no longer affected by nAChR activity.…”

Section: Discussionsupporting

confidence: 61%

“…In vitro activation of the latter by low doses of nicotine has been shown to lead to apoptotic cell death of undifferentiated primary and immortalized progenitor cells from the dentate gyrus (DG), the other main region of neurogenesis in the mature brain (9). In accordance with these results, in vivo chronic nicotine exposure in adult rats was shown to reduce proliferation in the DG (10,11). Interestingly, nicotine exposure had no effect on proliferation in the SVZ, suggesting that nAChRs might not be involved in adult OB neurogenesis.…”

mentioning

confidence: 69%

Nicotinic receptors regulate the survival of newborn neurons in the adult olfactory bulb

Mechawar

Saghatelyan

Grailhe

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Cholinergic axons and nicotinic receptors are abundant in all layers of the olfactory bulb (OB), the main region of newborn neuron integration in the adult brain. Here, we report that the OB granule cell layer in mice lacking the predominant form of brain highaffinity nicotinic acetylcholine receptors (␤ 2 ؊/؊ mice) displayed nearly 50% more newborn neurons and significantly fewer apoptotic cells than did ␤2 ؉/؉ mice. Conversely, in vivo chronic nicotine exposure significantly decreased the number of newborn granule cells in ␤2 ؉/؉ but not ␤2 ؊/؊ adult mice, confirming that the survival of newborn neurons can be controlled by the activation of ␤2-containing nicotinic acetylcholine receptors. Unexpectedly, investigating the behavioral consequence of an increased number of granule cells in ␤2 ؊/؊ mice revealed that these animals have a less robust short-term olfactory memory than their wild-type counterparts. Taken together, these results provide evidence that highaffinity nicotinic receptors are involved in the maturation of adult OB local circuits. They also indicate that an increase in the number of granule cells does not necessarily correlate with better olfactory performance and further highlight the importance of cholinergic afferents for olfactory processing.T hroughout adulthood, the olfactory bulb (OB) is furnished with a constant supply of neuroblasts originating from the subventricular zone (SVZ) and rostral migratory stream (RMS) (1, 2). These cells first migrate tangentially along the RMS before migrating radially in the OB and differentiating into functional inhibitory granule or periglomerular cells (3), a process that takes 3-4 weeks to complete (4, 5). Within the bulb, the activity of these cells can be strongly modulated, via muscarinic (mAChRs) and nicotinic (nAChRs) acetylcholine receptors (6), by the dense cholinergic innervation pervading all OB layers (7).The family of nAChRs is composed of heteromeric and homomeric pentamers forming gated ion channels. The main nAChRs in the brain are composed of ␣ 4 and ␤ 2 subunits (high affinity for nicotine) or of ␣ 7 subunits only (high affinity for ␣-bungarotoxin) (8). In vitro activation of the latter by low doses of nicotine has been shown to lead to apoptotic cell death of undifferentiated primary and immortalized progenitor cells from the dentate gyrus (DG), the other main region of neurogenesis in the mature brain (9). In accordance with these results, in vivo chronic nicotine exposure in adult rats was shown to reduce proliferation in the DG (10, 11). Interestingly, nicotine exposure had no effect on proliferation in the SVZ, suggesting that nAChRs might not be involved in adult OB neurogenesis. However, given the strong expression of high-affinity nAChRs in the OB (12, 13), a study on the involvement of these receptors in events downstream to SVZ proliferation was warranted. In this context, we undertook a study of OB neurogenesis in ␤ 2 Ϫ/Ϫ and ␤ 2 ϩ/ϩ mice subjected or not subjected to chronic nicotine exposure and report here that ␤ 2 -conta...

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Alcohol and nicotine reduce cell proliferation and enhance apoptosis in dentate gyrus

Cited by 84 publications

References 22 publications

Nicotine-induced memory impairment by increasing brain oxidative stress

Nicotine-induced memory impairment by increasing brain oxidative stress

Alcohol and adult neurogenesis: Roles in neurodegeneration and recovery in chronic alcoholism

Nicotinic receptors regulate the survival of newborn neurons in the adult olfactory bulb

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