Comparison of protective effects of electroacupuncture and moxibustion at Zusanli(ST 36)on perinatal nicotine exposure-induced lung phenotype in rat offspring

Objective:To compare the effects of electroacupuncture(EA)and moxibustion at Zusanli(ST 36)on the lung phenotype of rat offspring exposed to nicotine during the perinatal period.Methods:Pregnant Sprague-Dawley rats were randomly divided into 4 groups:the control group(saline only),the model group(nicotine only),the EA group(nicotine+EA at ST 36 acupoints bilaterally),and the moxibustion group(nicotine+moxibustion at ST 36 acupoints bilaterally).n=6 rats per group.On postnatal day 21,the body weight,lung weight,and pulmonary function were determined and lung morphometry was performed.Peroxisome proliferator-activated receptor gamma andβ-catenin levels in the lung tissue of offspring were also determined.Results:Perinatal nicotine exposure(PNE)results in decreased body and lung weights of offspring rats,abnormal lung tissue morphology,and significantly altered pulmonary function,showing an increase in total airway resistance and a decrease in tidal volume,minute ventilation,total airway compliance,and peak expiratory flow.Bilateral EA at ST 36 acupoints could block all of these perinatal nicotine-induced effects.Although moxibustion also had protective effects in nicotine-induced offspring lungs,some of these effects did not reach statistical significance,e.g.,protection against the upregulation ofβ-catenin,the downregulation of PPARγsignaling,and the increase in peak expiratory flow.Conclusion:Maternal EA at ST 36 blocked the PNE-induced changes in key developmental signaling pathways,prevented the PNE-induced changes in lung morphology,and protected pulmonary function.Moxibustion at ST 36 showed similar but weaker protective effects against the PNE-induced changes in the exposed offspring.It is important to note that the mechanism underlying the protective effects of moxibustion at ST 36 may be different from those of EA at ST 36,and further research is needed to understand these differences.

Prenatal nicotine alters development of the laterodorsal tegmentum:Possible role for attention-deficit/hyperactivity disorder and drug dependence

As we cycle between the states of wakefulness and sleep,a bilateral cholinergic nucleus in the pontine brain stem,the laterodorsal tegmentum(LDT),plays a critical role in controlling salience processing,attention,behavioral arousal,and electrophysiological signatures of the sub-and microstates of sleep.Disorders involving abnormal alterations in behavioral and motivated states,such as drug dependence,likely involve dysfunctions in LDT signaling.In addition,as the LDT exhibits connectivity with the thalamus and mesocortical circuits,as well as receives direct,excitatory input from the prefrontal cortex,a role for the LDT in cognitive symptoms characterizing attention-deficit/hyperactivity disorder(ADHD)including impulsivity,inflexibility,and dysfunctions of attention is suggested.Prenatal nicotine exposure(PNE)is associated with a higher risk for later life development of drug dependence and ADHD,suggesting alteration in development of brain regions involved in these behaviors.PNE has been shown to alter glutamate and cholinergic signaling within the LDT.As glutamate and acetylcholine are major excitatory mediators,these alterations would likely alter excitatory output to target regions in limbic motivational circuits and to thalamic and cortical networks mediating executive control.Further,PNE alters neuronal development and transmission within prefrontal cortex and limbic areas that send input to the LDT,which would compound effects of differential processing within the PNE LDT.When taken together,alterations in signaling in the LDT are likely to play a role in negative behavioral outcomes seen in PNE individuals,including a heightened risk of drug dependence and ADHD behaviors.