The potential use of push-pull polyenes and polyynes for second harmonic generation has been compared on the basis of hyperpolarizabilities computed for a large number of model systems of the type D(HC=CH),A and D ( m C ) , A (n = 2-8, and D = NH2, Br, or I; A = NO2 or CN). Geometries optimized at the AM1 level were used in a CI calculation including single and pair excitations involving up to 193 configurations. The sum-over-states expression was used to obtain the j3 values. While the trends in the computed j3 are the same for the two series of compounds, the values are generally smaller and increase less rapidly with increasing n for the polyynes. The results are interpreted in terms of the nature of the lowest excited states which contribute to j 3 in these systems. Mixing of in-plane and out-of-plane u-u* excited configurations reduces the contribution of the lower excited states to j3. Push-pull polyynes with higher j3 values than the corresponding polyenes can be designed by the combined use of donor and acceptor groups such as I (or Br) and C N which can interact with both sets of orthogonal T MOs.
Reactive astrogliosis is a common pathological hallmark of central nervous system (CNS) injury, infection, and neurodegeneration, where reactive astrocytes can be protective or detrimental to normal brain functions. Currently, the mechanisms regulating neuroprotective astrocytes and the extent of neuroprotection are poorly understood. Here, we report that conditional deletion of serum response factor (SRF) in adult astrocytes causes reactive-like hypertrophic astrocytes throughout the mouse brain. TheseSrfGFAP-ERCKO astrocytes do not affect neuron survival, synapse numbers, synaptic plasticity or learning and memory. However, the brains ofSrfknockout mice exhibited neuroprotection against kainic-acid induced excitotoxic cell death. Relevant to human neurodegenerative diseases,SrfGFAP-ERCKO astrocytes abrogate nigral dopaminergic neuron death and reduce β-amyloid plaques in mouse models of Parkinson’s and Alzheimer’s disease, respectively. Taken together, these findings establish SRF as a key molecular switch for the generation of reactive astrocytes with neuroprotective functions that attenuate neuronal injury in the setting of neurodegenerative diseases.
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