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Neuropsychopharmacology. 2006 March 22; [Epub ahead of print]

Paz R, Barsness B, Martenson T, Tanner D, Allan AM.

[1] Department of Neurosciences, University of New Mexico, Albuquerque, NM, USA [2] Departamento de Psiquiatria y Neurociencias, Universidad Diego Portales, Portales, Chile [3] Instituto Psiquiatrico Dr Jose Horwitz Barak, Santiago de Chile, Chile.

Prenatal nicotine exposure (PNE) has been associated with increased prevalence of attention deficit hyperactivity disorder (ADHD), major depressive disorder (MDD) and substance abuse in exposed children and adolescents. Whether these syndromes are caused by nicotine exposure, or genetic and psychosocial adversities associated with maternal smoking is not completely clear. Animal models suggest a direct impact of PNE. However, the fact that nicotine is forcefully administrated in these paradigms raises some questions about the specificity of these findings.

Pregnant C57BI/6J mice were allowed to choose drinking saccharin/nicotine solutions or pure water. Controls could choose saccharin solutions or pure water. Offspring were tested in spontaneous locomotion, fear-associated learning (trace conditioning), addictive (conditioned place preference), and depression-like (learned helplessness) behaviors.

There was no significant difference in weight or pup number between the prenatal treatment groups. A significant effect of PNE was observed on spontaneous locomotion, preference for a cocaine-associated place, and latency to escape in the learned helplessness paradigm.

Surprisingly, PNE mice exhibited an increased learning of trace-conditioned fear-associated cues. The hyperlocomotive behavior reported in animal models of PNE is not likely an artifact of forceful nicotine administration. The increased prevalence of ADHD, MDD and substance abuse observed in PNE children and adolescents is probably caused by direct behavioral teratogenic effects of PNE. The role of PNE as a risk factor of syndromes associated to increased learning of fear-associated cues such as post-traumatic stress disorder (PTSD) warrants further evaluation.

Neuropsychopharmacology advance online publication, 22 March 2006; doi:10.1038/sj.npp.1301066.

PMID: 16554741 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16554741

Nicotine Babies

As seen in studies such as the one above there is increasing alarm among toxicologists and pharmacologists that "NICOTINE" is "THE" major player when it comes to inflicting permanent damage upon the fetus. It seems as though each new nicotine study raises more issues that it settles.

We know that nicotine interacts with still developing fetal acetylcholine receptors causing a host of still developing neuro-circuits in multiple still developing brain regions to attempt to function before development is complete. The result is the birth of a mind that was never allowed to experience normal development, the birth of a "Nicotine Baby."

The only way to show you where nicotine harm science stands in this particular area is to share the author's discussion that normally comes at the end of a full-text copy of these studies. As you read the following discussion keep in mind that other researchers are studying and documenting other aspects of the nicotine harm equation.

John (Gold x6)

"Similar to rat-models of PNE, increased spontaneous locomotion was observed in adult mice exposed to nicotine during intrauterine and early neonatal stages of neural development." "This finding indicates that the hyperactive behavior that has been observed in rats that were exposed to nicotine prenatally using forced-administration paradigms is not likely the result of an interaction between the stress reaction potentially caused by forced nicotine administration to pregnant mothers and prenatal nicotine exposure. Thus, together with clinical and epidemiological studies showing an increased prevalence of ADHD in children born from mothers voluntarily consuming nicotine, our findings indicate that intrauterine brain exposure to nicotine by itself is a risk factor for the emergence of hyperlocomotive behaviors in exposed subjects. Even though we cannot rule out subtle effects of nicotine on placental or brain vascular integrity, which may indirectly impair brain development, it seems more likely that the abnormal behavior observed in PNE mice was caused by the pathological activation of acetylcholine nicotinic receptors AchNR) during early stages of brain development (Slotkin, 1998; Slotkin, 2004). Consistent with this interpretation, a recent study suggests that the normal activation of AchNR located in cortico-thalamic terminals plays a critical role in the development of neural circuits involved in the regulation of normal fear-associated learning (King et al, 2003). In this study, knocking-out the b2 subunit of these receptors in neonatal, but not adult, mice resulted in increased learning of a fear-associated learning task known as passive avoidance. Paralleling these findings, we found that PNE mice exhibited increased learning of fear-associated cues. Since blunted presynaptic cholinergic activity has been described in PNE rats (Navarro et al, 1989; Zahalka et al, 1992), the surprising improvement in the learning of fearconditioned cues observed in PNE mice might be the result of blunted presynaptic cholinergic activity during early stages of brain development. Consistent with this interpretation, increased learning of passive avoidance was also reported in PNE rats in another study (Genedani et al, 1983). These findings raise the intriguing possibility that the risk of developing neuropsychiatric syndromes associated with augmented learning of fear associated cues such as post-traumatic stress disorder (PTSD) might be increased in individuals who were exposed to nicotine prenatally. Consistent with this hypothesis, a recent study found an increased prevalence of ADHD in patients with PTSD (Adler et al, 2004). Thus, it is possible that some subtypes of PTSD, coexisting or being preceded by ADHD, may share common neurodevelopmental origins with this condition, one of them being, perhaps, PNE. Future clinical and epidemiological studies may explore this hypothesis.

In the current study, PNE mice also displayed an increased latency to escape in the learned helplessness paradigm. To the best of our knowledge this is the first study to show a behavioral pattern suggesting a vulnerability to develop depressive-like responses in PNE animals. Together with epidemiological studies reporting an increased prevalence of MDD in PNE children and adolescents (Fergusson et al, 1998; Wu and Anthony, 1999) our study suggest that abnormal activation of AchNR during prenatal and early neonatal stages of brain development may affect the maturation of brain circuits critical for mood regulation during adulthood. Consistent with this hypothesis, PNE rats have been shown to have decreased cortical binding of [H3] paroxetine, a well known marker of the functional integrity of the serotonergic system (Xu et al). Likewise, increased 5HT-2 and 5HT-1A receptor binding were also recently reported in the cerebral cortex of these animals (Slotkin et al, 2005). A recent epidemiologicgenetic study strongly suggests that the functional state of the serotonergic system may play a critical role as modulator of the risk of developing depressive episodes during life-stress situations in vulnerable subjects (Caspi et al, 2003). Likewise, a growing body of experimental evidence indicates that the functional state of the serotonergic system during early stages of neural development plays an enduring role in shaping the way that animals may face stress situations later in life (Gross et al, 2002; Ansorge et al, 2004; Sibille and Lewis, 2006). Thus, the abnormalities reported in the serotonergic system in PNE rats, and the increased latency to escape following an inescapable stress experience observed in PNE mice, suggest that a causal link could be mediating the association observed between PNE and MDD in epidemiological studies. Future studies exploring the mechanisms involved in this interesting phenomenon are warranted. An increased preference for a place previously associated with cocaine was also observed in PNE mice. Since clinical and epidemiological studies have reported high rates of substance abuse problems in PNE children and adolescents (Fergusson et al, 1998), our results suggest that a direct causal link may also underlie this association. Overall the variety of behavioral abnormalities observed in adult mice whose brains were exposed to nicotine during prenatal and early neonatal stages of neural development stresses the clinical relevance of developing aggressive strategies to identify and treat pregnant women addicted or abusing tobacco (Slotkin, 1998, 2004). From the clinical neuroscience point of view, uncovering the molecular and cellular mechanisms, as well as the precise brain circuits involved in the generation of these neurodevelopmentally induced abnormalities in PNE mice may shed some light about the causes of disabling neuropsychiatric conditions.

Copyright © 2006 by the American College of Neuropsychopharmacology

http://www.nature.com/npp/index.html

As evidenced by the study abstract immediately above, nicotine is a super toxin (that drop for drop is more potent than diamond back rattlesnake venom) that actually destroys brain grey matter. In the below article Dr. DeNoble shows 7th graders what nicotine has done to a smoker's brain. Feeling an urge to again put nicotine into your brain? Imagine the damage nictotine has done to your brain being shown to students. Picture the amount of nicotine entering the bloodstream after smoking a single cigarette (about 1mg) being sufficient to kill a 1 pound rat. How many rats could we have killed each and every day? If it destroys them why wouldn't it slowly do the same to us? Still just one rule ... no nicotine today, Never Take Another Puff, Dip or Chew! John (Gold x7)

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Whistle-blower warns
kids about tobacco

by Molly Priddy

Wednesday, April 25, 2007

Dr. Victor DeNoble laughed in delight Monday afternoon as a health class of C.R. Anderson 7th graders took out camera phones to photograph the monkey brain he was holding.

DeNoble, a former research scientist for tobacco giant Philip Morris, used two different samples to show the effects of nicotine on the brain. He is known as the first whistleblower of the tobacco industry and was in Helena to speak at the Montana Tobacco Use Prevention Program's annual conference at the Great Northern Best Western Hotel.
His harrowing tale of corporate coverups and bullying fascinated his adolescent audience. The beginning of the story has DeNoble in a secret laboratory in Virginia funded by Philip Morris from 1980 to 1984. The original purpose for his research was to find a new chemical to put in cigarettes that would be healthier for the human heart.
However, DeNoble used his laboratory to study the effects of nicotine on the brain and central nervous system. They first tested the brains of rats, then of a monkey and, finally, the brain of a human.
At this point in the lecture, two brains were produced for the students to see. There were twitters of excitement as he walked around, showing them up close. One belonged to a monkey addicted to nicotine; the other belonged to a man who died of cancer. Both brains were physically changed due to nicotine use. According to DeNoble, the tobacco company constantly told him to ignore the brain research and focus on the heart.
Eventually the lab staff came up with a solution for the heart problems that accompanied smoking, he said. They developed a cigarette that contained a newly created chemical and filter system that would decrease cancerous toxins by 80 percent and be healthier for the cardiac system.
This cigarette was never released. DeNoble said that he was taken into the corporate offices and told his new design would not be for sale. The company would be vulnerable to lawsuits if a safer cigarette was on the market and would lose money on their other brands, he was told. DeNoble was then given a copy of the secrecy agreement he had signed at the beginning of his employment and fired.
He said he was able to retain some of the pictures from the laboratory and managed to work his way around the secrecy agreement to tell the truth about cigarettes. In 1994, a judge ordered him to answer questions under oath and, in the same year, Congress released him from his secrecy contract. His testimony against the company resulted in expensive repercussions and investigations into the tobacco industry.
His story certainly caught the attention of young Montanans on Monday. DeNoble pointed out that the average age people begin smoking is 12 and, if they start that early, they will most likely smoke for the next 42 years. He told them that it is not only a health risk but will cost anywhere from $75,000 to $150,000.
"If you make it to 18 without trying cigarettes, you have an 80-percent chance of never smoking. If you make it to 21, there's a 95-percent chance you will never smoke," he said.
At the end of his presentation, DeNoble told the 7th graders to go to college and stay educated. Along with not smoking, he said attending college is one of the best ways to take care of yourself.