A new feedback on climate change from the hydrological cycle

An intensification of the hydrological cycle is a likely consequence of global warming. But changes in the hydrological cycle could affect sea-surface temperature by modifying diffusive ocean heat transports. We investigate this mechanism by studying a coupled general circulation model sensitivity experiment in which the hydrological cycle is artificially amplified. We find that the amplified hydrological cycle depresses sea-surface temperature by enhancing ocean heat uptake in low latitudes. We estimate that a 10% increase in the hydrological cycle will contribute a basin-scale sea-surface temperature decrease of around 0.1°C away from high latitudes, with larger decreases locally. We conclude that an intensified hydrological cycle is likely to contribute a weak negative feedback to anthropogenic climate change.

How well do we understand and evaluate climate change feedback processes?

Processes in the climate system that can either amplify or dampen the climate response to an external perturbation are referred to as climate feedbacks. Climate sensitivity estimates depend critically on radiative feedbacks associated with water vapor, lapse rate, clouds, snow, and sea ice, and global estimates of these feedbacks differ among general circulation models. By reviewing recent observational, numerical, and theoretical studies, this paper shows that there has been progress since the Third Assessment Report of the Intergovernmental Panel on Climate Change in (i) the understanding of the physical mechanisms involved in these feedbacks, (ii) the interpretation of intermodel differences in global estimates of these feedbacks, and (iii) the development of methodologies of evaluation of these feedbacks (or of some components) using observations. This suggests that continuing developments in climate feedback research will progressively help make it possible to constrain the GCMs’ range of climate feedbacks and climate sensitivity through an ensemble of diagnostics based on physical understanding and observations.

Developmental changes in presynaptic muscarinic modulation of excitatory and inhibitory neurotransmission in rat piriform cortex in vitro: relevance to epileptiform bursting susceptibility

Suppression of depolarizing postsynaptic potentials and isolated GABA-A receptor-mediated fast inhibitory postsynaptic potentials by the muscarinic acetylcholine receptor agonist, oxotremorine-M (10 microM), was investigated in adult and immature (P14-P30) rat piriform cortical (PC) slices using intracellular recording. Depolarizing postsynaptic potentials evoked by layers II-III stimulation underwent concentration-dependent inhibition in oxotremorine-M that was most likely presynaptic and M2 muscarinic acetylcholine receptor-mediated in immature, but M1-mediated in adult (P40-P80) slices; percentage inhibition was smaller in immature than in adult piriform cortex. In contrast, compared with adults, layer Ia-evoked depolarizing postsynaptic potentials in immature piriform cortex slices in oxotremorine-M, showed a prolonged multiphasic depolarization with superimposed fast transients and spikes, and an increased 'all-or-nothing' character. Isolated N-methyl-d-aspartate receptor-mediated layer Ia depolarizing postsynaptic potentials (although significantly larger in immature slices) were however, unaffected by oxotremorine-M, but blocked by dl-2-amino-5-phosphonovaleric acid. Fast inhibitory postsynaptic potentials evoked by layer Ib or layers II-III-fiber stimulation in immature slices were significantly smaller than in adults, despite similar estimated mean reversal potentials ( approximately -69 and -70 mV respectively). In oxotremorine-M, only layer Ib-fast inhibitory postsynaptic potentials were suppressed; suppression was again most likely presynaptic M2-mediated in immature slices, but M1-mediated in adults. The degree of fast inhibitory postsynaptic potential suppression was however, greater in immature than in adult piriform cortex. Our results demonstrate some important physiological and pharmacological differences between excitatory and inhibitory synaptic systems in adult and immature piriform cortex that could contribute toward the increased susceptibility of this region to muscarinic agonist-induced epileptiform activity in immature brain slices.

Diagnostic analysis of atmospheric moisture and clear-sky radiative feedback in the Hadley Centre and Geophysical Fluid Dynamics Laboratory (GFDL) climate models

The interannual variability of the hydrological cycle is diagnosed from the Hadley Centre and Geophysical Fluid Dynamics Laboratory (GFDL) climate models, both of which are forced by observed sea surface temperatures. The models produce a similar sensitivity of clear-sky outgoing longwave radiation to surface temperature of ∼2 W m−2 K−1, indicating a consistent and positive clear-sky radiative feedback. However, differences between changes in the temperature lapse-rate and the height dependence of moisture fluctuations suggest that contrasting mechanisms bring about this result. The GFDL model appears to give a weaker water vapor feedback (i.e., changes in specific humidity). This is counteracted by a smaller upper tropospheric temperature response to surface warming, which implies a compensating positive lapse-rate feedback.

Tumour necrosis factor alpha induces rapid reduction in AMPA receptor-mediated calcium entry in motor neurones by increasing cell surface expression of the GluR2 subunit: relevance to neurodegeneration

The AMPA receptor (AMPAR) subunit GluR2, which regulates excitotoxicity and the inflammatory cytokine tumour necrosis factor alpha (TNF alpha) have both been implicated in motor neurone vulnerability in Amyotrophic Lateral Sclerosis/Motor Neurone Disease. TNF alpha has been reported to increase cell surface expression of AMPAR subunits to increase synaptic strength and enhance excitotoxicity, but whether this mechanism occurs in motor neurones is unknown. We used primary cultures of mouse motor neurones and cortical neurones to examine the interaction between TNF alpha receptor activation, GluR2 availability, AMPAR-mediated calcium entry and susceptibility to excitotoxicity. Short exposure to a physiologically relevant concentration of TNFalpha (10 ng/ml, 15 min) caused a marked redistribution of both GluR1 and GluR2 to the cell surface as determined by cell surface biotinylation and immunofluorescence. Using Fura-2 AM microfluorimetry we showed that exposure to TNFalpha caused a rapid reduction in the peak amplitude of AMPA-mediated calcium entry in a PI3-kinase and p38 kinase-dependent manner, consistent with increased insertion of GluR2-containing AMPAR into the plasma membrane. This resulted in a protection of motor neurones against kainate-induced cell death. Our data therefore, suggests that TNF alpha acts primarily as a physiological regulator of synaptic activity in motor neurones rather than a pathological drive in ALS

The role of eddies in driving the tropospheric response to stratospheric heating perturbations

A simplified general circulation model has been used to investigate the chain of causality whereby changes in tropospheric circulation and temperature are produced in response to stratospheric heating perturbations. Spinup ensemble experiments have been performed to examine the evolution of the tropospheric circulation in response to such perturbations. The primary aim of these experiments is to investigate the possible mechanisms whereby a tropospheric response to changing solar activity over the 11-yr solar cycle could be produced in response to heating of the equatorial lower stratosphere. This study therefore focuses on a stratospheric heating perturbation in which the heating is largest in the tropics. For comparison, experiments are also performed in which the stratosphere is heated uniformly at all latitudes and in which it is heated preferentially in the polar region. Thus, the mechanisms discussed have a wider relevance for the impact of stratospheric perturbations on the troposphere. The results demonstrate the importance of changing eddy momentum fluxes in driving the tropospheric response. This is confirmed by the lack of a similar response in a zonally symmetric model with fixed eddy forcing. Furthermore, it is apparent that feedback between the tropospheric eddy fluxes and tropospheric circulation changes is required to produce the full model response. The quasigeostrophic index of refraction is used to diagnose the cause of the changes in eddy behavior. It is demonstrated that the latitudinal extent of stratospheric heating is important in determining the direction of displacement of the tropospheric jet and storm track.