Different precipitation response over land and ocean to orbital and greenhouse gas forcing.

Various proxies suggest a nearly in-phase variation of monsoons with local summer insolation. Oceanic proxies of monsoons document a more complex response. Climate model simulations also indicate that the response is different over land and ocean. Here using a transient simulation by a climate model over the last 22,000 years we have unraveled the factors that lead to these differences within the Indian subcontinent. We show that during the deglacial (22-12 ka) precipitation over India and the Bay of Bengal (BoB) are in phase, whereas they are out of phase across the Holocene ([Formula: see text] 12 ka to 0 ka). During the deglacial, water vapor amplifies the effect of solar forcing on precipitation over both the regions, whereas contributions from surface latent heat fluxes over the BoB drive an opposite response across the Holocene. We find that greenhouse gas forcing drives similar precipitation response over land and ocean, whereas orbital forcing produces a different response over land and ocean. We have further demonstrated that during periods of abrupt climate change [such as the Bølling-Allerød ([Formula: see text] 14 ka)], water vapor affects precipitation mainly through its influence on the vertical stability of the atmosphere. These results highlight the complex nature of precipitation over the BoB and thus has implications for the interpretation of monsoon proxies.

Modulation of Indian monsoon by water vapor and cloud feedback over the past 22,000 years.

To predict how monsoons will evolve in the 21st century, we need to understand how they have changed in the past. In paleoclimate literature, the major focus has been on the role of solar forcing on monsoons but not on the amplification by feedbacks internal to the climate system. Here we have used the results from a transient climate simulation to show that feedbacks amplify the effect of change in insolation on the Indian summer monsoon. We show that during the deglacial (22 ka to 10 ka) monsoons were predominantly influenced by rising water vapor due to increasing sea surface temperature, whereas in the Holocene (10 ka to 0 ka) cloud feedback was more important. These results are consistent with another transient simulation, thus increasing confidence despite potential model biases. We have demonstrated that insolation drives monsoon through different pathways during cold and warm periods, thereby highlighting the changing role of internal factors.

Heart rate calculation from ensemble brain wave using wavelet and Teager-Kaiser energy operator.

Electroencephalogram (EEG) signal artifacts are caused by various factors, such as, Electro-oculogram (EOG), Electromyogram (EMG), Electrocardiogram (ECG), movement artifact and line interference. The relatively high electrical energy cardiac activity causes EEG artifacts. In EEG signal processing the general approach is to remove the ECG signal. In this paper, we introduce an automated method to extract the ECG signal from EEG using wavelet and Teager-Kaiser energy operator for R-peak enhancement and detection. From the detected R-peaks the heart rate (HR) is calculated for clinical diagnosis. To check the efficiency of our method, we compare the HR calculated from ECG signal recorded in synchronous with EEG. The proposed method yields a mean error of 1.4% for the heart rate and 1.7% for mean R-R interval. The result illustrates that, proposed method can be used for ECG extraction from single channel EEG and used in clinical diagnosis like estimation for stress analysis, fatigue, and sleep stages classification studies as a multi-model system. In addition, this method eliminates the dependence of additional synchronous ECG in extraction of ECG from EEG signal process.

Glutamate-dopamine crosstalk in the rat prefrontal cortex is modulated by Alpha7 nicotinic receptors and potentiated by PNU-120596.

The aim of this study was to explore the modulation by alpha7 nicotinic receptors (nAChRs) of dopamine and glutamate release in the rat prefrontal cortex where these receptors are implicated in attentional processes and are therapeutic targets for cognitive deficits. The presence of presynaptic alpha7 nAChRs on glutamate terminals is supported by the ability of the subtype-selective agonist Compound A to evoke [(3)H]D-aspartate release from synaptosomes: This response was potentiated by the selective allosteric potentiator PNU-120596 and blocked by alphabungarotoxin. Compound A also evoked dopamine overflow in the prefrontal cortex in vivo, and this was potentiated by PNU-120596. alpha7 nAChR-evoked [(3)H]dopamine release from tissue prisms in vitro was blocked by antagonists of NMDA and AMPA receptors. These data are consistent with a model in which alpha7 nAChRs present on glutamate terminals increase glutamate release that (1) contributes to presynaptic facilitation and synaptic plasticity and (2) co-ordinately enhances dopamine release from neighbouring boutons.

alpha7 and non-alpha7 nicotinic acetylcholine receptors modulate dopamine release in vitro and in vivo in the rat prefrontal cortex.

Nicotine enhances attentional and working memory aspects of executive function in the prefrontal cortex (PFC) where dopamine plays a major role. Here, we have determined the nicotinic acetylcholine receptor (nAChR) subtypes that can modulate dopamine release in rat PFC using subtype-selective drugs. Nicotine and 5-Iodo-A-85380 (beta2* selective) elicited [(3)H]dopamine release from both PFC and striatal prisms in vitro and dopamine overflow from medial PFC in vivo. Blockade by dihydro-beta-erythroidine supports the participation of beta2* nAChRs. However, insensitivity of nicotine-evoked [(3)H]dopamine release to alpha-conotoxin-MII in PFC prisms suggests no involvement of alpha6beta2* nAChRs, in contrast to the striatum, and this distinction is supported by immunoprecipitation of nAChR subunits from these tissues. The alpha7 nAChR-selective agonists choline and Compound A also promoted dopamine release from PFC in vitro and in vivo, and their effects were enhanced by the alpha7 nAChR-selective allosteric potentiator PNU-120596 and blocked by specific antagonists. DNQX and MK801 inhibited [(3)H]dopamine release evoked by choline and PNU-120596, suggesting crosstalk between alpha7 nAChRs, glutamate and dopamine in the PFC. In vivo, systemic (but not local) administration of PNU-120596, in the absence of agonist, facilitated dopamine overflow in the medial PFC, consistent with the activation of extracortical alpha7 nAChRs by endogenous acetylcholine or choline. These data establish that both beta2* and alpha7 nAChRs can modulate dopamine release in the PFC in vitro and in vivo. Through their distinct actions on dopamine release, these nAChR subtypes could contribute to executive function, making them specific therapeutic targets for conditions such as schizophrenia and attention deficit hyperactivity disorder.