Extracellular recording is an accessible technique used in animals and humans to study the brain physiology and pathology. As the number of recording channels and their density grows it is natural to ask how much improvement the additional channels bring in and how we can optimally use the new capabilities for monitoring the brain. Here we show that for any given distribution of electrodes we can establish exactly what information about current sources in the brain can be recovered and what information is strictly unobservable. We demonstrate this in the general setting of previously proposed kernel Current Source Density method and illustrate it with simplified examples as well as using evoked potentials from the barrel cortex obtained with a Neuropixels probe and with compatible model data. We show that with conceptual separation of the estimation space from experimental setup one can recover sources not accessible to standard methods.
The α-Ca /calmodulin-dependent protein kinase II (αCaMKII), a key regulator of the glutamatergic synapse, has been implicated in many psychiatric disorders characterized by social impairments. Here we tested whether autophosphorylation of αCaMKII at threonine 286, which prolongs the activity of the enzyme, affects social behaviors in mice. We observed that autophosphorylation-deficient (αCaMKII-T286A) mutant female mice showed abnormal social behaviors characterized by decreased social preference and interest in conspecifics of the same sex, as compared to their wild-type littermates. Moreover, we developed a mathematical approach to analyze social interactions in group-housed mice in the automated IntelliCages. Using this approach we observed that αCaMKII-T286A mutants show decreased levels of social interactions in a social group, as compared with WT mice. WT mice increased the frequency of close social interactions when learning about the location of the food reward. This phenomenon was absent in the mutants. Overall, our data indicates that autophosphorylation of αCaMKII affects social interactions.
Background and Purpose: The therapeutic effects of fluoxetine are believed to be due to increasing neuronal plasticity and reversing some learning deficits. Nevertheless, a growing amount of evidence shows adverse effects of this drug on cognition and some forms of neuronal plasticity.Experimental Approach: To study the effects of chronic fluoxetine treatment, we combine an automated assessment of motivation and learning in mice with an investigation of neuronal plasticity in the central amygdala and basolateral amygdala. We use immunohistochemistry to visualize neuronal types and perineuronal nets, along with DI staining to assess dendritic spine morphology. Gel zymography is used to test fluoxetine's impact on matrix metalloproteinase-9, an enzyme involved in synaptic plasticity.Key Results: We show that chronic fluoxetine treatment in non-stressed mice increases perineuronal nets-dependent plasticity in the basolateral amygdala, while impairing MMP-9-dependent plasticity in the central amygdala. Further, we illustrate how the latter contributes to anhedonia and deficits of reward learning. Behavioural impairments are accompanied by alterations in morphology of dendritic spines in the central amygdala towards an immature state, most likely reflecting animals' inability to adapt. We strengthen the link between the adverse effects of fluoxetine and its influence on MMP-9 by showing that behaviour of MMP-9 knockout animals remains unaffected by the drug. Conclusion and Implications: Chronic fluoxetine treatment differentially affects various forms of neuronal plasticity, possibly explaining its opposing effects on brain and behaviour. These findings are of immediate clinical relevance since reported side effects of fluoxetine pose a potential threat to patients.
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