Oxytocin receptors in the prefrontal cortex play important roles in short-term social recognition in mice.

We examined the roles of oxytocin (OT) receptors in the prefrontal cortex (PFC) in short- and long-term social recognition and anxiety-related behaviors in mice. Mice injected with high or low doses of an OT receptor antagonist (OTA) or vehicle performed the social recognition test, the open-field test, and the light-dark transition test. In the social recognition test, with three daily trials over three consecutive days, control mice showed short-term recognition of a conspecific on all three days.

The prelimbic cortex but not the anterior cingulate cortex plays an important role in social recognition and social investigation in mice.

The prefrontal cortex (PFC) has been implicated in social cognitive functions and emotional behaviors in rodents. Each subregion (prelimbic cortex, PL; infralimbic cortex; and anterior cingulate cortex, ACC) of the PFC appears to play a different role in social and emotional behaviors. However, previous investigations have produced inconsistent data, and few previous studies directly compared the roles of the PFC subregions using the same experimental paradigm.

Prefrontal cortex is necessary for long-term social recognition memory in mice.

The prefrontal cortex (PFC) plays critical roles in social cognition and emotional regulation in humans and rodents; however, its involvement in social recognition memory in mice remains unclear. Here, we examined the roles of the PFC in short-term and long-term social recognition memory, social motivation, and anxiety-related behavior in C57BL/6J male mice. Sham control and PFC-lesioned mice underwent four different behavioral tests.

Effects of intraperitoneal and intracerebroventricular injections of oxytocin on social and emotional behaviors in pubertal male mice.

Oxytocin plays important roles in the social and emotional behaviors of mammals. In the present study, we examined the effects of intraperitoneal (IP) and intracerebroventricular (ICV) injections of oxytocin on these behaviors in pubertal male mice. Male C57BL/6J mice received IP injection of oxytocin (high-dose group: 1 mg/kg, low-dose group: 0.

Influence of Pre-Weaning Social Isolation on Post-Weaning Emotion Tendency and Mother-Infant Interactions in Infant .

Our previous research using (degus) revealed that preweaning social isolation negatively affected object exploratory behavior. However, it remains unknown how social isolation affects animal psychology and other behaviors. The present study examined the effects of neonatal social isolation on degu emotion and mother-infant interactions before and after weaning.

Pubertal activation of estrogen receptor α in the medial amygdala is essential for the full expression of male social behavior in mice.

Testosterone plays a central role in the facilitation of male-type social behaviors, such as sexual and aggressive behaviors, and the development of their neural bases in male mice. The action of testosterone via estrogen receptor (ER) α, after being aromatized to estradiol, has been suggested to be crucial for the full expression of these behaviors. We previously reported that silencing of ERα in adult male mice with the use of a virally mediated RNAi method in the medial preoptic area (MPOA) greatly reduced sexual behaviors without affecting aggressive behaviors whereas that in the medial amygdala (MeA) had no effect on either behavior.

Effects of Prepubertal or Adult Site-Specific Knockdown of Estrogen Receptor β in the Medial Preoptic Area and Medial Amygdala on Social Behaviors in Male Mice.

Testosterone, after being converted to estradiol in the brain, acts on estrogen receptors (ERα and ERβ) and controls the expression of male-type social behavior. Previous studies in male mice have revealed that ERα expressed in the medial preoptic area (MPOA) and medial amygdala (MeA) are differently involved in the regulation of sexual and aggressive behaviors by testosterone action at the time of testing in adult and/or on brain masculinization process during pubertal period. However, a role played by ERβ in these brain regions still remains unclear.

Sialyltransferase ST3Gal IV deletion protects against temporal lobe epilepsy.

Temporal lobe epilepsy (TLE) often becomes refractory, and patients with TLE show a high incidence of psychiatric symptoms, including anxiety and depression. Therefore, it is necessary to identify molecules that were previously unknown to contribute to epilepsy and its associated disorders. We previously found that the sialyltransferase ST3Gal IV is up-regulated within the neural circuits through which amygdala-kindling stimulation propagates epileptic seizures.

Deep cerebellar nuclei play an important role in two-tone discrimination on delay eyeblink conditioning in C57BL/6 mice.

Previous studies have shown that deep cerebellar nuclei (DCN)-lesioned mice develop conditioned responses (CR) on delay eyeblink conditioning when a salient tone conditioned stimulus (CS) is used, which suggests that the cerebellum potentially plays a role in more complicated cognitive functions. In the present study, we examined the role of DCN in tone frequency discrimination in the delay eyeblink-conditioning paradigm. In the first experiment, DCN-lesioned and sham-operated mice were subjected to standard simple eyeblink conditioning under low-frequency tone CS (LCS: 1 kHz, 80 dB) or high-frequency tone CS (HCS: 10 kHz, 70 dB) conditions.

Differential effects of site-specific knockdown of estrogen receptor α in the medial amygdala, medial pre-optic area, and ventromedial nucleus of the hypothalamus on sexual and aggressive behavior of male mice.

Testosterone is known to play an important role in the regulation of male-type sexual and aggressive behavior. As an aromatised metabolite of testosterone, estradiol-induced activation of estrogen receptor α (ERα) may be crucial for the induction of these behaviors in male mice. However, the importance of ERα expressed in different nuclei for this facilitatory action of testosterone has not been determined.

Amygdala, deep cerebellar nuclei and red nucleus contribute to delay eyeblink conditioning in C57BL /6 mice.

That the cerebellum plays an essential role in delay eyeblink conditioning is well established in the rabbit, but not in the mouse. To elucidate the critical brain structures involved in delay eyeblink conditioning in mice, we examined the roles of the deep cerebellar nuclei (DCN), the amygdala and the red nucleus (RN) through the use of electrolytic lesions and reversible inactivation. All mice received eyeblink training of 50 trials during a daily session in the higher-intensity conditioned stimulus (CS) condition (10 kHz, 70 dB).

The therapeutic potential of human umbilical cord blood-derived mesenchymal stem cells in Alzheimer's disease.

The neuropathological hallmarks of Alzheimer's disease (AD) include the presence of extracellular amyloid-beta peptide (Abeta) in the form of amyloid plaques in the brain parenchyma and neuronal loss. The mechanism associated with neuronal death by amyloid plaques is unclear but oxidative stress and glial activation has been implicated. Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) are being scrutinized as a potential therapeutic tool to prevent various neurodegenerative diseases including AD.

Dual involvement of G-substrate in motor learning revealed by gene deletion.

In this study, we generated mice lacking the gene for G-substrate, a specific substrate for cGMP-dependent protein kinase uniquely located in cerebellar Purkinje cells, and explored their specific functional deficits. G-substrate-deficient Purkinje cells in slices obtained at postnatal weeks (PWs) 10-15 maintained electrophysiological properties essentially similar to those from WT littermates. Conjunction of parallel fiber stimulation and depolarizing pulses induced long-term depression (LTD) normally.

GABAA receptors in deep cerebellar nuclei play important roles in mouse eyeblink conditioning.

The neural circuitry of eyeblink conditioning in rabbits has been studied in detail, however, the basic knowledge of eyeblink conditioning in mice remains limited. In the present study, we examined the role of the deep cerebellar nuclei (DCN) in mice in delay eyeblink conditioning and rotor rod test performance by using the gamma-aminobutyric acidA (GABA(A)) receptor agonist muscimol (MSC) and the GABA(A) receptor antagonist picrotoxin (PTX). Bilateral injections of MSC and PTX into the DCN significantly impaired motor coordination in the rotor rod test, however the performance recovered within 24 h after the injections.

Inducible cAMP early repressor acts as a negative regulator for kindling epileptogenesis and long-term fear memory.

Long-lasting neuronal plasticity as well as long-term memory (LTM) requires de novo synthesis of proteins through dynamic regulation of gene expression. cAMP-responsive element (CRE)-mediated gene transcription occurs in an activity-dependent manner and plays a pivotal role in neuronal plasticity and LTM in a variety of species. To study the physiological role of inducible cAMP early repressor (ICER), a CRE-mediated gene transcription repressor, in neuronal plasticity and LTM, we generated two types of ICER mutant mice: ICER-overexpressing (OE) mice and ICER-specific knock-out (KO) mice.

Role of hippocampal NMDA receptors in trace eyeblink conditioning.

We examined the effects of acute injections of competitive N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonovaleric acid (APV) into the dorsal hippocampus on contextual fear conditioning and classical eyeblink conditioning in C57BL/6 mice. When injected 10 to 40 min before training, APV severely impaired contextual fear conditioning. Thus, APV injection under these conditions was sufficient to suppress hippocampal NMDA receptors.

Mutation of NMDA receptor subunit epsilon 1: effects on audiogenic-like seizures induced by electrical stimulation of the inferior colliculus in mice.

It has been shown that the N-methyl-D-asparate (NMDA) receptor in the inferior colliculus is involved in the induction of audiogenic seizures (AGS). In the present study we examined audiogenic-like seizure susceptibility in GluR epsilon 1 null KO adult mice (n=32) and wild-type adult mice (n=28) by electrically stimulating the inferior colliculus (IC). Threshold current intensities of the GluR epsilon 1 KO mice for wild running, clonic and tonic seizures were higher than those of wild-type mice.

Targeted disruption of the Epm2a gene causes formation of Lafora inclusion bodies, neurodegeneration, ataxia, myoclonus epilepsy and impaired behavioral response in mice.

Mutations in the EPM2A gene encoding a dual-specificity phosphatase (laforin) cause Lafora disease (LD), a progressive and invariably fatal epilepsy with periodic acid-Schiff-positive (PAS+) cytoplasmic inclusions (Lafora bodies) in the central nervous system. To study the pathology of LD and the functions of laforin, we disrupted the Epm2a gene in mice. At two months of age, homozygous null mutants developed widespread degeneration of neurons, most of which occurred in the absence of Lafora bodies.