In pregnancy, a 2013 review noted that "nicotine is only 1 of more than 4000 compounds to which the fetus is exposed through maternal smoking. Of these, ∼30 compounds have been associated with adverse health outcomes. Although the exact mechanisms by which nicotine produces adverse fetal effects are unknown, it is likely that hypoxia, undernourishment of the fetus, and direct vasoconstrictor effects on the placental and umbilical vessels all play a role. Nicotine also has been shown to have significant deleterious effects on brain development, including alterations in brain metabolism and neurotransmitter systems and abnormal brain development." It also notes that "abnormalities of newborn neurobehavior, including impaired orientation and autonomic regulation and abnormalities of muscle tone, have been identified in a number of prenatal nicotine exposure studies" and that there is weak data associating fetal nicotine exposure with newborn facial clefts , and that there is no good evidence for newborns suffering nicotine withdrawal from fetal exposure to nicotine. 
New Lower Strength of Auvi-Q Approved for Use in Young Children
Auvi-Q® (epinephrine injection) received FDA approval on November 20, 2017, to treat pediatric patients who weigh between ( pounds) and 25Kg (33 pounds). It is an auto-injector that delivers a smaller dose of epinephrine to block allergic reactions. Because it is designed for use in small children, the injector needle is shorter and the dose is smaller than in other Auvi-Q devices. The new injector has a voice feature that announces each step in the directions for use. Like Auvi-Q and 3mg auto-injectors, the lower dose will be dispensed in cartons containing two devices pre-filled with active drug and one inactive practice device. Detailed instructions are included with each prescription as well. Kaléo, Auvi-Q’s manufacturer, has not released its launch or pricing plans. Prescribing information can be found here .
Damage incurred by traumatic brain injury is believed to be caused in part by mass depolarization leading to excitotoxicity . One way in which progesterone helps to alleviate some of this excitotoxicity is by blocking the voltage-dependent calcium channels that trigger neurotransmitter release.  It does so by manipulating the signaling pathways of transcription factors involved in this release. Another method for reducing the excitotoxicity is by up-regulating the GABA A , a widespread inhibitory neurotransmitter receptor.