title: The effect of early life status epilepticus on ultrasonic vocalizations in mice.
abstract: Infant crying is a series of innate vocal patterns intended to elicit the attention of adult caregivers for fulfillment of specific needs such as pain, hunger, or hypostimulation. It is one of the earliest forms of observable communication. In neonatal rodents, this behavior has recently been investigated as a potential early behavioral marker of neural deficits in neurodevelopmental disorders. However, few studies have examined the effects of seizures on vocalization behavior during the neonatal period. The purpose of this study is to investigate the effect of a single kainate-induced early life seizure on vocalization behavior in mice. This study also investigates the subsequent effect of seizures on two pathways critical for early neural development and epileptogenesis: the phosphoinositide 3-kinase|serine/threonine kinase|mammalian target of rapamycin (PI3K-Akt-mTOR) and canonical (Wingless-Int Wnt) intracellular signaling pathways.
  
  
  
  On postnatal day 10, male and female 129SvEvTac mice received a single intraperitoneal injection of kainic acid (2.5 mg/kg) or vehicle injection. The kainate administration resulted in 1-2 h of status epilepticus. On postnatal days 11 and 12, the quantity and duration of isolation-induced ultrasonic vocalizations were recorded. Western blotting analyses were performed using male and female pups on postnatal day 12.
  
  
  
  There was significant, male-specific suppression in the quantity and total duration of 50-kHz calls on postnatal day 12 following seizures. The hippocampi of male mice on this postnatal day also revealed male-specific changes in the PI3K-Akt-mTOR intracellular signaling pathway, as well as changes in phosphorylated fragile × mental retardation protein.
  
  
  
  These findings demonstrate that early life seizures can disrupt communication behavior in neonatal mice.
authors.affiliation: Department of Psychology and Neuroscience, Baylor University, Waco, Texas, U.S.A.
authors.forename: Conner D
authors.initials: CD
authors.lastname: Reynolds
authors.affiliation: Institute of Biomedical Sciences, Baylor University, Waco, Texas, U.S.A.
authors.forename: Gregory
authors.initials: G
authors.lastname: Smith
authors.affiliation: Department of Psychology and Neuroscience, Baylor University, Waco, Texas, U.S.A.
authors.forename: Taylor
authors.initials: T
authors.lastname: Jefferson
authors.affiliation: Department of Psychology and Neuroscience, Baylor University, Waco, Texas, U.S.A.|Institute of Biomedical Sciences, Baylor University, Waco, Texas, U.S.A.
authors.forename: Joaquin N
authors.initials: JN
authors.lastname: Lugo
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005260:Female; D007608:Kainic Acid / Q000633:toxicity; D008297:Male; D051379:Mice; D051058:Oncogene Protein v-akt / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D012727:Sex Characteristics; D015398:Signal Transduction / Q000502:physiology*; D013226:Status Epilepticus / Q000139:chemically induced / Q000503:physiopathology*; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D014828:Vocalization, Animal / Q000502:physiology*
chemical_list: D018690:Excitatory Amino Acid Agonists; D007608:Kainic Acid; D051058:Oncogene Protein v-akt; D019869:Phosphatidylinositol 3-Kinases; D058570:TOR Serine-Threonine Kinases; C546843:mTOR protein, mouse
keywords: Epilepsy; Isolation-induced vocalizations; Mammalian target of rapamycin; Neurodevelopmental disorder; Phosphoinositide 3-kinase; Ultrasonic vocalization