Cell-specific plasticity associated with integrative memory of triple sensory signals in the barrel cortex.

Neuronal plasticity occurs in associative memory. Associative memory cells are recruited for the integration and storage of associated signals. The coordinated refinements and interactions of associative memory cells including glutamatergic and GABAergic neurons remain elusive, which we have examined in a mouse model of associative learning. Paired olfaction, tail and whisker stimulations lead to odorant-induced and tail-induced whisker motions alongside whisker-induced whisker motion. In mice that show this cross-modal associative memory, barrel cortical glutamatergic and GABAergic neurons are recruited to encode the newly learned odor and tail signals alongside the innate whisker signal. These glutamatergic neurons are functionally upregulated, and GABAergic neurons are refined in a homeostatic manner. The mutual innervations between these glutamatergic and GABAergic neurons are upregulated. Therefore, the co-activations of sensory cortices by pairing the input signals recruit their glutamatergic and GABAergic neurons to be associative memory cells, which undergo coordinated refinement among glutamatergic and GABAergic neurons as well as homeostatic plasticity among subcellular compartments in order to drive these cells toward the optimal state for the integrative storage of associated signals.

Glucocorticoid Induces Incoordination between Glutamatergic and GABAergic Neurons in the Amygdala.

BACKGROUND: Stressful life leads to mood disorders. Chronic mild stress is presumably major etiology for depression, and acute severe stress leads to anxiety. These stressful situations may impair hypothalamus-pituitary-adrenal axis and in turn induce synapse dysfunction. However, it remains elusive how the stress hormones mess up subcellular compartments and interactions between excitatory and inhibitory neurons, which we have investigated in mouse amygdala, a structure related to emotional states. METHODS AND RESULTS: Dexamethasone was chronically given by intraperitoneal injection once a day for one week or was acutely washed into the brain slices. The neuronal spikes and synaptic transmission were recorded by whole-cell patching in amygdala neurons of brain slices. The chronic or acute administration of dexamethasone downregulates glutamate release as well as upregulates GABA release and GABAergic neuron spiking. The chronic administration of dexamethasone also enhances the responsiveness of GABA receptors. CONCLUSION: The upregulation of GABAergic neurons and the downregulation of glutamatergic neurons by glucocorticoid impair their balance in the amygdala, which leads to emotional disorders during stress.

[Pharmacokinetic and Tissue Distribution Study of Ephedrae Herba and Herbal Pair of Ephedrae Herba-Atractylodis Macrocephalae Rhizoma in Rats].

OBJECTIVE: Five kinds of Ephedra alkaloids (NME, NMP, E, PE and ME) in Ephedrae Herba extracts and Ephedrae Herba-Atractylodis Macrocephalae Rhizoma herbal pair extracts of plasma pharmacokinetic and tissue distribution study in rats were carried out, to discuss the changes of Ephedrae Herba compatibility with Atractylodis Macrocephalae Rhizoma before and after METHODS: HPLC- MS method was used and the condition was as flollows: ZORBAX SB-C18 column (100 mm x 2.1 mm, 3.5 µm), column temperature of 35 °C, mobile phase of ACE-0.1% formic solution in gradient elution mode, flow rate at 0.4 mL/min; MRM positive ion detection mode. RESULTS: The distribution trends of Ephedra alkaloids were changing in plasma and tissues of rats after Ephedrae Herba compati- bility with Atractylodis Macrocephalae Rhizoma. CONCLUSION: Ephedrae Herba compatibility with Atractylodis Macrocephalae Rhizoma may increase drug efficacy and reduce the toxicity of Ephedra alkaloids at the same time.