Neonicotinoids have become the most widely used class of insecticides world-wide. Although numerous studies have documented neonicotinoid toxicity in bees and other insects, the effects of exposure during early development in mammals remain largely unexplored. We assessed the effects of the neonicotinoid imidacloprid (IMI) in adult male and female mice after in utero and early postnatal exposure. Pregnant mice were infused with IMI (0.5 mg/kg/day) from gestational day 4 to the end of nursing at postnatal day 21. The young adult offspring were studied in a series of biochemical and behavioral tests. To assess reproducibility, the behavioral analyses were conducted in three separate studies using multiple exposed litters. Exposure to IMI reduced fecundity, and in adult offspring, decreased body weight in male but not female pups. Offspring from IMI-treated mothers displayed lower triglycerides, elevated motor activity, enhanced social dominance, reduced depressive-like behavior, and a diminution in social aggression compared to vehicle treated controls. Low levels of IMI were detected in the brains and livers of the treated mothers, while trace levels were detected in some offspring. Our results demonstrate that transient exposure to a neonicotinoid over the early developmental period induces long-lasting changes in behavior and brain function in mice.

Object: Entrapment of the superior cluneal nerve (SCN) in an osteofibrous tunnel in the space surrounded by the iliac crest and the thoracolumbar fascia is a cause of low-back pain (LBP). Several anatomical and surgical reports describe SCN entrapment as a cause of LBP, and a recent clinical study reported that patients with suspected SCN disorder constitute approximately 10% of the patients suffering from LBP and/or leg symptoms. However, a detailed anatomical study of SCN entrapment is rare. The purpose of this study was to investigate the courses of SCN branches and to ascertain the frequency of SCN entrapment. Methods: Branches of the SCN were dissected in 109 usable specimens (54 on the right side and 55 on the left side) obtained in 59 formalin-preserved cadavers (average age at death 84.8 years old). All branches were exposed at the points where they perforated the thoracolumbar fascia. The presence or absence of an osteofibrous tunnel was ascertained and, if present, the entrapment of the branches in the tunnel was determined. Results: Of 109 specimens, 61 (56%) had at least 1 branch running through an osteofibrous tunnel. Forty-two medial (39%), 30 intermediate (28%), and 14 lateral (13%) SCN branches passed through such a tunnel. Of these, only 2 medial branches had obvious entrapment in an osteofibrous tunnel. There were several patterns for the SCN course through the tunnel: medial branch only (n = 25), intermediate branch only (n = 11), lateral branch only (n = 4), medial and intermediate branches (n = 11), medial and lateral branches (n = 2), intermediate and lateral branches (n = 4), and all branches (n = 4). Conclusions: Several anatomical variations of the running patterns of SCN branches were detected. Entrapment was seen only in the medial branches. Although obvious entrapment of the SCN is rare, it may cause LBP.

Neonicotinoids such as acetamiprid (ACE) belong to a new and widely used single class of pesticides. Neonicotinoids mimic the chemical structure of nicotine and share agonist activity with the nicotine acetylcholine receptor (nAchR). Neonicotinoids are widely considered to be safe in humans; however, they have recently been implicated in a number of human health disorders. A wide range of musculoskeletal and neuromuscular disorders associated with high doses of neonicotinoids administered to animals have also been reported. Consequently, we used a mouse model to investigate the response of the central nervous system to ACE treatment. Our results show that exposure to ACE-containing water for three or seven days (decuple and centuple of no observable adverse effect level (NOAEL)/day) caused a decrease in body weight in 10-week old A/JJmsSlc (A/J) mice. However, the treatments did not affect brain histology or expression of CD34. ACE concentrations were significantly higher in the midbrain of ACE-treated mice than that of the normal and vehicle groups. Expression levels of α7, α4, and β2 nAChRs were found to be low in the olfactory bulb and midbrain of normal mice. Furthermore, in the experimental group (centuple ACE-containing water for seven days), β2 nAChR expression decreased in many brain regions. Information regarding the amount of accumulated ACE and expression levels of the acetylcholine receptor in each region of the brain is important for understanding any clinical symptoms that may be associated with ACE exposure.