Tree taxa shifted latitude or elevation range in response to changes in Quaternary climate. Because many modern trees display adaptive differentiation in relation to latitude or elevation, it is likely that ancient trees were also so differentiated, with environmental sensitivities of populations throughout the range evolving in conjunction with migrations. Rapid climate changes challenge this process by imposing stronger selection and by distancing populations from environments to which they are adapted. The unprecedented rates of climate changes anticipated to occur in the future, coupled with land use changes that impede gene flow, can be expected to disrupt the interplay of adaptation and migration, likely affecting productivity and threatening the persistence of many species.

Until now, Quaternary paleoecologists have regarded evolution as a slow process relative to climate change, predicting that the primary biotic response to changing climate is not adaptation, but instead (1) persistence in situ if changing climate remains within the species' tolerance limits, (2) range shifts (migration) to regions where climate is currently within the species' tolerance limits, or (3) extinction. We argue here that all three of these outcomes involve evolutionary processes. Genetic differentiation within species is ubiquitous, commonly via adaptation of populations to differing environmental conditions. Detectable adaptive divergence evolves on a time scale comparable to change in climate, within decades for herbaceous plant species, and within centuries or millennia for longer-lived trees, implying that biologically significant evolutionary response can accompany temporal change in climate. Models and empirical studies suggest that the speed with which a population adapts to a changing environment affects invasion rate of new habitat and thus migration rate, population growth rate and thus probability of extinction, and growth and mortality of individual plants and thus productivity of regional vegetation. Recent models and experiments investigate the stability of species tolerance limits, the influence of environmental gradients on marginal populations, and the interplay of demography, gene flow, mutation rate, and other genetic processes on the rate of adaptation to changed environments. New techniques enable ecologists to document adaptation to changing conditions directly by resurrecting ancient populations from propagules buried in decades-old sediment. Improved taxonomic resolution from morphological studies of macrofossils and DNA recovered from pollen grains and macroremains provides additional information on range shifts, changes in population sizes, and extinctions. Collaboration between paleoecologists and evolutionary biologists can refine interpretations of paleorecords, and improve predictions of biotic response to anticipated climate change.

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Background A central problem in posttraumatic stress disorder (PTSD) is a reduced capacity to suppress fear under safe conditions. Previously, we have shown that combat-related PTSD patients have impaired inhibition of fear-potentiated startle. Given the high comorbidity between PTSD and depression, our goal was to see whether this impairment is specific to PTSD, or a nonspecific symptom associated with both disorders. Methods Fear-potentiated startle (FPS) was assessed in 106 trauma-exposed individuals divided into four groups: a) No diagnosis control, b) PTSD only, c) major depression (MDD) only, and d) comorbid PTSD and MDD. We used a novel conditional discrimination procedure, in which one set of shapes (the danger signal) was paired with aversive airblasts to the throat, and different shapes (the safety signal) were presented without airblasts. The paradigm also included fear inhibition transfer test. Results Subjects with comorbid MDD and PTSD had higher FPS to the safety signal and to the transfer test compared to controls and MDD only subjects. In contrast to the control and MDD groups, the PTSD and comorbid PTSD and MDD groups did not show fear inhibition to safety cues. Conclusions These results suggest that impaired fear inhibition may be a specific biomarker of PTSD symptoms.

Objective To determine the effectiveness of Virtual Reality Exposure (VRE) augmented with D-cycloserine (50mg) or alprazolam (0.25mg), compared to placebo, in reducing PTSD due to military trauma in Iraq and Afghanistan. Method A double-blind, placebo-controlled randomized clinical trial comparing augmentation methods for VRE for subjects (n= 156) with PTSD was conducted. Results PTSD symptoms significantly improved from pre- to post-treatment over the 6-session VRE treatment (p<.001) across all conditions and were maintained at 3, 6, and 12 months follow-up. There were no overall differences between the D-cycloserine group on symptoms at any time-point. The alprazolam and placebo conditions significantly differed on the post-treatment Clinician Administered PTSD scale (p = .006) and the 3-month post-treatment PTSD diagnosis, such that the alprazolam group showed greater rates of PTSD (79.2% alprazolam vs. 47.8% placebo). Between-session extinction learning was a treatment-specific enhancer of outcome for the D-cycloserine group only (p<.005). At post-treatment, the D-cycloserine group was the lowest on cortisol reactivity (p<.05) and startle response during VR scenes (p<.05). Conclusions A small number of VRE sessions were associated with reduced PTSD diagnosis and symptoms in Iraq/Afghanistan veterans, although there was no control condition for the VRE. Overall, there was no advantage of D-cycloserine on PTSD symptoms in primary analyses. In secondary analyses, benzodiazepine use during treatment may impair recovery, and D-cycloserine may enhance VRE in patients who demonstrate within-session learning. D-cycloserine augmentation treatment in PTSD patients may reduce cortisol and startle reactivity compared to the alprazolam and placebo treatment, consistent with the animal literature.

The interlick interval distribution of rats while ingesting maltose under real and sham feeding conditions and while ingesting seven concentrations of sucrose under real feeding conditions was analyzed. The analysis revealed that the licking behavior of rats is organized into bursts of licking at a high rate. These bursts occurred in clusters that were separated by brief (250-500 ms) interruptions. The clusters were separated by intervals that ranged from 500 ms to many hundreds of seconds. Sham feeding increased the length of the meal by increasing the number but not the size of the clusters. Increasing the concentration of sucrose increased monotonically the size of the clusters but varied the number of clusters as an inverted-V-shaped function. This analysis revealed the details of the central nervous system's control over ingestive behavior.

The endogenous cannabinoid (eCB) system represents a major therapeutic target for the treatment of a variety of anxiety-related disorders. A recent study has demonstrated that pharmacologic or genetic disruption of CB1-receptor-mediated neurotransmission decreases the extinction of conditioned fear in mice. Here, we examined whether CB1 blockade would similarly disrupt extinction in rats, using fear-potentiated startle as a measure of conditioned fear. We also examined whether pharmacologic enhancement of CB1 activation would lead to enhancements in extinction. Our results indicate that systemic administration of the CB1 antagonist rimonabant (SR141716A) prior to extinction training led to significant, dose-dependent decreases in extinction. While the administration of the CB1 agonist WIN 55,212-2 did not appear to affect extinction, administration of AM404, an inhibitor of eCB breakdown and reuptake, led to dose-dependent enhancements in extinction. In addition to showing decreased fear 1 and 24 h after extinction training, AM404-treated animals showed decreased shock-induced reinstatement of fear. Control experiments demonstrated that the effects of AM404 could not be attributed to alterations in the expression of conditioned fear, locomotion, shock reactivity, or baseline startle, as these parameters seemed unchanged by AM404. Furthermore, coadministration of rimonabant with AM404 blocked this enhancement of extinction, suggesting that AM404 was acting to increase CB1 receptor activation during extinction training. These results demonstrate that the eCB system can be modulated to enhance emotional learning, and suggest that eCB modulators may be therapeutically useful as adjuncts for exposure-based psychotherapies such as those used to treat Post-Traumatic Stress Disorder and other anxiety disorders.