Electromagnetic field exposure to the nervous system can cause neurological changes. The effects of extremely low-frequency electromagnetic fields, such as second-generation and third-generation radiation, have been studied in most studies. The current study aimed to explore fourth-generation cellular phone radiation on hippocampal morphology and behavior in mice. Swiss albino male mice (n = 30) were randomly categorized into 3 groups; control, 40 min, and 60 min exposure to 2400 MHz radiofrequency electromagnetic radiation (RF-EMR) daily for 60 days. The control mice were housed in the same environments but were not exposed to anything. Anxiety-like behaviors were tested using the elevated plus-maze. For histological and stereological examination, the brain was dissected from the cranial cavity. On Cresyl violet stained brain slices, the number of pyramidal neurons in the cornu ammonis of the hippocampus were counted. In exposed mice compared to control mice, a significant increase in anxiety-like behavior has been observed. Histological observations have shown many black and dark blue cytoplasmic cells with shrunken morphology degenerative alterations in the neuronal hippocampus in the radiation exposed mice. In the RF-EMR mouse hippocampus, stereological analyses revealed a significant decrease in pyramidal and granule neurons compared to controls. Our findings suggest that 2400-MHz RF-EMR cell phone radiation affects the structural integrity of the hippocampus, which would lead to behavioral changes such as anxiety. However, it alerts us to the possible long-term detrimental effects of exposure to RF-EMR.

Huntingtin-associated protein 1 (HAP1) is an essential component of the stigmoid body (STB) and known as a possible neuroprotective interactor with causative proteins for Huntington's disease, spinal and bulbar muscular atrophy, spinocerebellar ataxia type 17 (SCA17), and Joubert syndrome. To clarify what other causative molecules HAP1/STB could interact with, we cloned normal causative genes for several neural disorders from human brain RNA library and evaluated their subcellular interaction with HAP1/STB by immunocytochemistry and immunoprecipitation after cotransfection into Neuro2a cells. The results clearly showed that HAP1/STB interacts with the normal ataxin-3 through Josephin domain and polyglutamine-expanded mutants derived from SCA3 as well. The findings suggest that HAP1/STB could modify the physiological function of normal ataxin-3 and pathogenesis of SCA3 attributable to the mutant ataxin-3.

• This study is the first to examine HAP1-expression in dorsal root ganglia (DRG). • HAP1 is highly co-expressed with the markers of nociceptive/proprioceptive neurons. • HAP1 is completely lacking in the touch-sensitive DRG neurons. • HAP1 may play an important role in modulating nociceptive/proprioceptive functions. • It will be of great interest to clarify the pathophysiological role of HAP1 in DRG.