Thesis (Ph. D.)--University of Wisconsin--Madison, 1967. / eContent provider-neutral record in process. Description based on print version record.

Thesis (Ph. D.)--Miami University, Dept. of Zoology, 2004. / Title from second page of PDF document. Includes bibliographical references.

Thesis (Ph. D.)--Florida State University, 2006. / Advisor: J. Anthony Stallins, Florida State University, College of Social Sciences, Dept. of Geography. Title and description from dissertation home page (viewed June 7, 2006). Document formatted into pages; contains xiii, 284 pages. Includes bibliographical references.

The present study was designed to provide data bearing directly on the question of the influence of the preschool experience, and specifically, teacher behavior, on pupil social behavior.

archives@tulane.edu / Autism spectrum disorders (ASD) are commonly characterized by abnormal social behaviors. Fragile X syndrome (FXS) is the most common inherited intellectual disability in humans and the most common single-gene cause of ASD symptoms. FXS is caused by the loss or malfunction of the fragile X mental retardation protein (FMRP), an mRNA-binding protein that regulates numerous synaptic proteins, both translationally and through direct protein-protein interactions. One direct-binding target is the large-conductance potassium (BK) channel. BK channels have been shown to be hypoactive in FXS, and represent possible targets for treatment in both general ASD and in FXS specifically. Also, two members of the KCNQ class of voltage-activated potassium channels, KV7.2 and KV7.3, have been identified as FMRP translation targets. Finally, a commonly observed abnormality in the ASD brain is an imbalance in the ratio of excitatory to inhibitory signaling (E/I balance) causing general hyperexcitability in numerous brain areas. One area in which altered E/I balance is often observed is the medial prefrontal cortex (mPFC), which is involved with the processing of social information. Therefore, the goal of this dissertation was to determine if stimulating potassium channel function in the mPFC of Fmr1 KO mice would correct abnormal social behavior. In addition, the possible mechanistic determinants and effects on E/I balance were investigated in WT and Fmr1 KO mice. Infusion of the potassium channel activator, BMS-204352, into the mPFC of KO mice had no effect on social approach behavior, but corrected social novelty impairments as measured by a 3-Chamber Test. Whole-cell patch clamp recordings of pyramidal neurons in layer V of the mPFC revealed no differences in mEPSCs between KO and WT mice, but did reveal higher frequency of mIPSCs in KO mice. Treatment with BMS-204352 resulted in a decrease in mEPSC amplitude in both genotypes, which was blocked by the BK channel antagonist, paxilline. Effects of BMS-204352 treatment on mIPSCs revealed two possible populations of cell types. One population of exhibited a decrease in frequency of mIPSCs, an effect seen in both genotypes. The other population exhibited a slight increase in frequency of mIPSCs, but this was seen only in KO cells. Treatment with paxilline caused a decrease in mIPSC frequency in both genotypes, which was not altered with subsequent BMS-204352 treatment. Pretreatment with the KV7 channel antagonist XE 991 prevented BMS-204352-induced cross-genotype decrease in mIPSC frequency, but did not prevent BMS-204352-induced frequency increase in KO cells. Western blot analyses revealed no changes between genotypes in BK channel expression, but a trend to increased KV7.3 expression in the PFC of KOs compared to WTs. With these data, it was concluded that aberrant activity of potassium channels in the mPFC of KOs mediates some of the social abnormalities observed in the phenotype, that KOs may exhibit increased KV7.3 expression as a potential compensatory mechanism for BK channel dysfunction, and that potassium channels are a promising potential target for future treatment of ASD symptoms / 1 / Ted Sawyer

京都大学 / 0048 / 新制・論文博士 / 博士(理学) / 乙第13323号 / 論理博第1570号 / 新制||理||1663(附属図書館) / 京都大学理学研究科生物科学専攻 / (主査)教授 伊谷 原一, 教授 平田 聡, 教授 幸島 司郎 / 学位規則第4条第2項該当 / Doctor of Science / Kyoto University / DGAM

Individuals with autism spectrum disorder (ASD) demonstrate deficits in social behavior which may hinder them from engaging in social interactions. Results of descriptive analyses suggest that children who engage in prosocial behaviors, such as sharing, likely receive social positive reinforcement from peers in the form of attention. However, functional relations between prosocial behaviors, such as sharing, and their maintaining consequences have yet to be identified. Thus, the purpose of this study was to extend previous research by evaluating the naturally maintaining contingencies associated with sharing in three preschool-aged children with ASD. Functional analyses have traditionally been used to identify the function of maladaptive behavior; however, we extended the same methodological approach to identify functional relations of sharing. Results suggest that sharing was maintained by attention for two participants and was multiply-maintained by both attention and access to tangibles for one participant. These findings indicate that the functional analysis methodology is appropriate to understanding prosocial behaviors. In addition, results advance our understanding of prosocial behavior and may better inform methods of how to functionally teach sharing to individuals with ASD.

Indiana University-Purdue University Indianapolis (IUPUI) / Social processing is the reception, interpretation, and reciprocation of social information and is critical for mental health. The neural structures, circuits, and substrates regulating these complex mechanisms are not well understood. Social processing in the form of social safety learning, as measured by a rat model of social familiarity-induced anxiolysis (SoFiA), was impaired following mild blast traumatic brain injury (mbTBI). Initial findings indicated that mbTBI altered resting state network activity in the orbitofrontal cortex (OFC) and was associated with accumulation of neurotoxin marker, acrolein, in lateral prefrontal cortex (PFC) (including OFC), indicating OFC as a brain region of interest that may contribute to social processing. Measuring GABA and Glutamate-related gene expression in OFC of mbTBI or sham-exposed rat brain revealed specific elevations of metabotropic glutamate receptor type 1 and 5 (mGluR1/5) expression in mbTBI but not sham OFC. Exposure-naïve rats intracranially injected with mGluR1/5 agonist demonstrated attenuated SoFiA, and this coincided with an impairment of social recognition (SR) behavior. Additionally, inactivation of OFC by local intracranial injection of GABAA agonist, muscimol, impaired two different measures of SR in which two conspecifics, or members of the same species, one novel and one familiar, were presented and required discrimination. Novelty seeking, decision-making, memory, and gregariousness were tested in isolation to determine OFC contributions to these specific behavioral contributions to SR test performance. OFC inactivation did not impair novelty seeking, non-social decision-making, or non-social memory as measured by novel object recognition (NOR) test, or gregariousness or social decision-making as measure by social preference (SP) test. When measuring SR behavior via consecutive presentation of two different conspecifics, OFC inactivation did not impact SR. Therefore, OFC is not directly responsible for social recognition, but rather the discrimination or ability to act upon discrimination of two simultaneously present conspecifics. These data suggest a novel role for OFC in high order processing or execution of action based on social information. / 2 years (2021-05-24)

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