To assess the role of exocytotic release in signaling by monoamines, we have disrupted the neuronal vesicular monoamine transporter 2 (VMAT2) gene. VMAT2-/- mice move little, feed poorly, and die within a few days after birth. Monoamine cell groups and their projections are indistinguishable from those of wild-type littermates, but the brains of mutant mice show a drastic reduction in monoamines. Using midbrain cultures from the mutant animals, amphetamine but not depolarization induces dopamine release. In vivo, amphetamine increases movement, promotes feeding, and prolongs the survival of VMAT2-/- animals, indicating that precise, temporally regulated exocytotic release of monoamine is not required for certain complex behaviors. In addition, the brains of VMAT2 heterozygotes contain substantially lower monoamine levels than those of wild-type littermates, and depolarization induces less dopamine release from heterozygous than from wild-type cultures, suggesting that VMAT2 expression regulates monoamine storage and release.
Two different 19-mer antisense oligodeoxynucleotides complementary to the initial coding regions of dopamine D2 or D3 receptor mRNA were infused unilaterally into the substantia nigra of rats for 3-6 d to suppress synthesis of D2 and/or D3 receptors on substantia nigra dopaminergic neurons, thereby producing specific reductions of D2 and/or D3 receptors. Autoradiographic receptor binding revealed that D2 and D3 antisense oligodeoxynucleotides specifically and significantly reduced D2 or D3 binding in the ipsilateral substantia nigra, respectively, without affecting dopamine receptor binding in the neostriatum. Either D2 or D3 antisense oligodeoxynucleotides greatly attenuated the ability of apomorphine to inhibit dopaminergic neurons in vivo, an effect that was potentiated by simultaneous administration of D2 and D3 antisenses. Despite these effects, neither the rate nor the pattern of spontaneous activity of antisense-treated nigrostriatal neurons differed from those in the control groups. The proportion of antidromic responses consisting of full spikes from antisense-treated rats was significantly greater, and the mean antidromic threshold was significantly lower than in controls, indicating that autoreceptor knockdown increased both somatodendritic and terminal excitability. These data demonstrate that selective reduction of specific dopamine receptor subtypes by antisense infusion can be effected in vivo, and that nigrostriatal neurons express both D2 and D3 autoreceptors at their somatodendritic and axon terminal regions. Although the somatodendritic and terminal autoreceptors modulate dendritic and terminal excitability, respectively, the interaction of endogenously released dopamine with somatodendritic autoreceptors does not appear to exert a significant effect on spontaneous activity in anesthetized rats.
Coastal wetlands are considered as a significant sink for global carbon because their organic-rich soils. Given exposed to shallow water tables, water from groundwater is transported upward to the root zone through capillary rise, thus soil moisture in coastal wetlands is relatively high even when there is no precipitation. We expected that as precipitation occurred, the soils in coastal wetlands might become quickly saturated and lead to the development of anoxic conditions. We further hypothesized that such anoxic conditions might decrease soil respiration by limiting oxygen availability and biological activities of roots and microorganisms. Based on continuous automated soil respiration data collected in a coastal wetland in the Yellow River Delta over 4 years (2012)(2013)(2014)(2015), the results showed that on the annual scale, cumulative soil respiration was 317, 321, 231, and 274 g C m −2 yr -1 for 2012, 2013, 2014, and 2015, respectively, with an average of 286 g C m −2 yr -1 . The rate of soil respiration increased exponentially with soil temperature during each year and its two seasons (growing season and non-growing season). In addition, soil respiration was significantly related to soil moisture during the growing season, but was not affected by soil moisture during the non-growing season. After each precipitation event, soil respiration was significantly negatively correlated with soil moisture under different initial soil water contents. There was a significant positive correlation between changes in soil respiration and changes in soil moisture following precipitation events. Moreover, the increase of soil moisture following precipitation events changed the temperature response of soil respiration. Our study indicated that precipitation events could decrease soil respiration by increasing soil moisture and inducing anoxic conditions in the coastal wetland. Therefore, we speculate that the continuation of decreasing precipitation and increasing temperature trends in the Yellow River Delta may increase soil carbon losses in the coastal wetland due to the increase in soil respiration.
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