Problem Inclusive leadership models have been introduced to represent a shift from traditional leadership approaches. However, missing from these models are principles of social justice and forward-thinking outcomes for building human relations. An examination of the detrimental consequences of exclusion is needed to realize the benefits of inclusion. Solution The Deconstructing Exclusion for Inclusive Leadership model, a framework for practice, is offered as a practical guide for deconstructing exclusionary practices and building positive, healthy human relations. The model is supported by affective behaviors and traits and cognitive competencies that inclusive leaders need to discourage exclusion and advocate for more inclusive relationships and social justice outcomes. Stakeholders Leaders, managers, practitioners, human resource development scholars, researchers, and educators.

Problem Theoretical and practical frameworks delineating the individual and relational needs inherent to creating perceptions of belongingness in the workplace are absent in Human Resources Development (HRD) literature. For inclusive leadership practitioners, the literature itself lacks direct mentioning of belonging, causing the awareness around the concept to be problematic. Without a clear understanding of factors that influence perceptions of belonging, leaders lack direction in building inclusive workplaces and reaping the beneficial business outcomes these have the potential to bring, including increased employee engagement, performance, and innovation. Solution The Individual and Relational Belongingness (IRB) model is introduced to explore and define the unique needs that are vital for individual to perceive a sense of belongingness in the workplace across individual, relational, personal, and organizational dimensions. Stakeholders Organizational and Human Resources Development scholar practitioners benefit from understanding the nuanced and complex needs that drive perceptions of belongingness, since these bring additional context to the scholarship and practice of inclusive leadership.

GNAO1 encodes Gαo, a heterotrimeric G protein alpha subunit in the Gi/o family. Gαo, the most abundant membrane protein in the brain, mediates downstream signaling pathways by itself, or via regulating free Gβγ subunits. To determine the role of Gαo protein in regulating synaptic transmission, we use electrophysiology to study cerebellar molecular layer interneuron ‐ Purkinje cell synaptic transmission in a haploinsufficient loss‐of‐function (LOF) Gnao1 mouse model, manifest with movement abnormalities and enhanced seizure susceptibility. We hypothesize that a LOF Gαo protein will increase GABA release through presynaptic Gαo ‐ coupled receptors. Inhibitory post synaptic currents (IPSCs) and excitatory post synaptic currents (EPSCs) were recorded using standard patch clamp techniques. Spontaneous IPSCs (sIPSCs) were isolated with glutamatergic receptor inhibitors CNQX and AP‐5. Spontaneous EPSCs (sEPSCs) were isolated with the GABAergic receptor inhibitor bicuculline. Miniature PSCs were isolated with the additional perfusion of tetrodotoxin. Cerebellar molecular layer inhibitory neurons were labeled with the Kit‐eGFP method and observed under an inverted epifluorescence microscope. Gαo and Gβ protein expression levels from flash‐frozen mouse brain tissues were determined using Western Blot. Instead of increase, we observe a significant reduction in both sIPSC (40%) and mIPSC (75%) frequency but not amplitude in the Gnao1 mutant mouse model. Both frequency and amplitude of sEPSCs and mEPSCs remain unchanged. On Western blots, levels of Gαo were reduced by about half, as expected, while Gβ levels were unchanged from control. To determine whether this reduction is due to the loss of cerebellar inhibitory interneuron populations, we compare cerebellar interneuron number in the cerebellar molecular layer between Gnao1 mutant mice and their wildtype littermate control. There is a modest reduction (13%) in interneuron number of cerebellar molecular layer in the Gnao1 mutant mouse. The observed reduction in IPSC frequency is not related to Gαo ‐ coupled GABAergic receptors. Also, the modest change in cerebellar interneuron counts does not seem to account for the marked reduction in IPSC frequency. These observations, and the reduced Gαo expression in brain with the normal levels of Gβ, strongly support that a model with a haploinsufficient LOF Gnao1 mutant mainly functions through receptor‐independent regulation of free Gβγ subunits to suppress inhibitory neurotransmitter release in Gnao1 mutant cerebellum.

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