bluuebunny/crossref_metadata_2025_split huggingface dataset:
O programa de pesquisa da ecologia histórica
Authors: Balée William 
Published: April 2018

Resumo:
Ecologia histórica é um novo programa de pesquisa interdisciplinar relacionado à compreensão das dimensões temporal e espacial nas relações das sociedades humanas com o seu ambiente local e os efeitos globais cumulativos dessas relações. Ecologia histórica contém postulados centrais que se referem a tipos qualitativos de alterações humano-mediadas dos ambientes naturais e seus efeitos na diversidade das espécies, entre outros parâmetros. Um termo central usado em ecologia histórica para situar comportamento humano e agência no ambiente é a paisagem, como derivado da geografia histórica, e não ao contrário de ecossistema, o qual provém de sistemas ecológicos. Ecologia histórica é similar à teoria dinâmica de não-equilíbrio, no entanto difere, no seu postulado, de alteração humano-mediada como um princípio de transformação da paisagem. Tais alterações, contra intuitivamente, podem envolver sucessão antropogênica primária e secundária que resultam em incremento líquido de diversidade alfa e beta. Ecologia histórica aplicada pode suprir as condições referenciais de profundidade temporal e conhecimento tradicional para restaurar paisagens pretéritas.

Abstract:
Historical ecology is a new interdisciplinary research program concerned with comprehending temporal and spatial dimensions in the relationships of human societies to local environments and the cumulative global effects of these relationships. Historical ecology contains core postulates that concern qualitative types of humanmediateddisturbanceofnaturalenvironmentsandtheeffectofthese on species diversity, among other parameters. A central term used in historical ecology to situate human behavior and agency in the environment is the landscape, as derived from historical geography, instead of the ecosystem, which is from systems ecology. Historical ecology is similar to nonequilibrium dynamic theory, but differs in its postulate of human-mediated disturbance as a principle of landscape transformation. Such disturbances counterintuitively may involve anthropogenic primary and secondary succession that result in net increases of alpha and even beta diversity. Applied historical ecology can supply the reference conditions of time depth and traditional knowledge to restore past landscapes.
Alpha Oscillations Are Causally Linked to Inhibitory Abilities in Ageing
Authors: Borghini Giulia , Candini Michela , Filannino Cristina , Hussain Masud , Walsh Vincent , Romei Vincenzo , Zokaei Nahid , Cappelletti Marinella 
Published: April 2018

Aging adults typically show reduced ability to ignore task-irrelevant information, an essential skill for optimal performance in many cognitive operations, including those requiring working memory (WM) resources. In a first experiment, young and elderly human participants of both genders performed an established WM paradigm probing inhibitory abilities by means of valid, invalid, and neutral retro-cues. Elderly participants showed an overall cost, especially in performing invalid trials, whereas younger participants' general performance was comparatively higher, as expected.Inhibitory abilities have been linked to alpha brain oscillations but it is yet unknown whether in aging these oscillations (also typically impoverished) and inhibitory abilities are causally linked. To probe this possible causal link in aging, we compared in a second experiment parietal alpha-transcranial alternating current stimulation (tACS) with either no stimulation (Sham) or with two control stimulation frequencies (theta- and gamma-tACS) in the elderly group while performing the same WM paradigm. Alpha- (but not theta- or gamma-) tACS selectively and significantly improved performance (now comparable to younger adults' performance in the first experiment), particularly for invalid cues where initially elderly showed the highest costs. Alpha oscillations are therefore causally linked to inhibitory abilities and frequency-tuned alpha-tACS interventions can selectively change these abilities in the elderly.SIGNIFICANCE STATEMENTIgnoring task-irrelevant information, an ability associated to rhythmic brain activity in the alpha frequency band, is fundamental for optimal performance. Indeed, impoverished inhibitory abilities contribute to age-related decline in cognitive functions like working memory (WM), the capacity to briefly hold information in mind. Whether in aging adults alpha oscillations and inhibitory abilities arecausallylinked is yet unknown. We experimentally manipulated frequency-tuned brain activity using transcranial alternating current stimulation (tACS), combined with a retro-cue paradigm assessing WM and inhibition. We found that alpha-tACS induced a significant improvement in target responses and misbinding errors, two indexes of inhibition. We concluded that in aging alpha oscillations are causally linked to inhibitory abilities, and that despite being impoverished, these abilities are still malleable.
Contingent Vulnerability of Entorhinal Parvalbumin-Containing Neurons in Alzheimer’s Disease
Authors: Solodkin Ana , Veldhuizen Stacy D. , Van Hoesen Gary W. 
Published: April 2018

Calcium-binding proteins containing local circuit neurons are distributed ubiquitously in the human cerebral cortex where they colocalize with a subpopulation of cells that contain GABA. Several reports using a variety of pathological models, including Alzheimer’s disease (AD), have suggested that cells containing calcium-binding proteins are resistant to pathological insults. In this report, we test the hypothesis that AD pathology can differentially affect parvalbumin-containing cells depending on their location in the entorhinal cortex and the state of projection neurons with which they are associated. Using cases with different quantities of AD pathology, we determined the density of immunostaining for parvalbumin in the entorhinal cortex, and we correlated this with the concomitant pathological lesions in the various layers of this cortex.Our results show a clear decrease in parvalbumin immunostaining in some parts of the entorhinal cortex when AD neuropathological markers are present. As the density of pathological markers in the entorhinal cortex becomes greater and more widespread, there is a decrease of parvalbumin immunostaining in additional layers, although in all cases, some cells persist.Parvalbumin-containing neurons are clearly vulnerable in AD, but not because of neurofibrillary tangle formation. Instead, they are rendered vulnerable only after substantial loss of projection neurons; only then do they, too, become part of the lesion.
Blue-Cone Horizontal Cells in the Retinae of Horses and OtherEquidae
Authors: Sandmann Daniele , Boycott Brian B. , Peichl Leo 
Published: April 2018

The morphology of horizontal cells chiefly of the horse, but also of asses, mules, and a zebra, has been examined by Lucifer yellow injections into lightly fixed retinae and by immunocytochemistry. In common with other mammals, equids have a B-type horizontal cell, i.e., a cell with dendrites synapsing with cones and possessing a single axon synapsing with rods. Most mammalian retinae have a further type of horizontal cell, the A-type, also synapsing with cones but without an axon. The second type of horizontal cell in equids also has no axon; otherwise, it is most unusual. Compared with other mammalian A-type cells, it has a very large dendritic field, both absolutely and relative to the dendritic fields of B-type cells. The dendrites are fine and sparsely branching. Their most striking feature is that they bear a low density of irregularly spaced synaptic terminal aggregates, suggesting their cone contacts are selective. Immunolabeling of S (blue)-cones in horse retina showed that they comprise, depending on retinal location, 10–25% of the cone population. For a single horse A-type cell, it is shown that 44 of its 45 terminal aggregates are congruent with the pedicles of S-cones. Immunostaining with a calbindin antibody demonstrated that each type of horizontal cell forms an independent regular mosaic. The density ratio of B- to A-type cells varied between 5 and 10. This is the first demonstration in a mammalian retina of a horizontal cell type with a direct input exclusively from S-cones.
Phasic Firing of Single Neurons in the Rat Nucleus Accumbens Correlated with the Timing of Intravenous Cocaine Self-Administration
Authors: Peoples Laura L. , West Mark O. 
Published: April 2018

To examine potential neural mechanisms involved in cocaine self-administration, the activity of single neurons in the nucleus accumbens of rats was recorded during intravenous cocaine self-administration. Lever pressing was reinforced according to a fixed-ratio 1 schedule. On a time base comparable to the interinfusion interval, half the neurons exhibited phasic firing patterns time locked to the cocaine reinforced lever press. For almost all neurons, this pattern consisted of a change in firing rate postpress, typically a decrease, followed by a reversal of that change. The postpress change was closely related to the lever press. Typically, it began within the first 0.2 min postpress and culminated within the first 1.0 min postpress. For a small portion of responsive neurons, the reversal of the postpress change was punctate and occurred within 1–3 min of either the last lever press or the next lever press so that firing was stable during much of the interinfusion interval. For the majority of neurons, the reversal was progressive; it began within 2 min after the previous lever press, and it was not complete until the last 0.1–2.0 min before the next lever press. The duration of this progressive reversal, but not of the postpress change, was positively correlated with the interinfusion interval. Thus, in addition to exhibiting changes in firing related to the occurrence of self-infusion, the majority of neurons also exhibited progressive changes in firing related to thespacingof infusions. In a structure that has been shown to be necessary for cocaine self-administration, such a firing pattern is a likely neurophysiological component of the mechanism that transduces declining drug levels into increased drug-related appetitive behavior. It is, thus, a neural mechanism that may contribute to compulsive drug-maintained drug taking.
Chronic Psychosocial Stress Causes Apical Dendritic Atrophy of Hippocampal CA3 Pyramidal Neurons in Subordinate Tree Shrews
Authors: Magariños Ana Marı́a , McEwen Bruce S. , Flügge Gabriele , Fuchs Eberhard 
Published: April 2018

We have shown previously that repeated laboratory restraint stress or daily corticosterone administration affects the structure of CA3 hippocampal neurons in rats. In the present study, we investigated the effect of repeated daily psychosocial stress on the structure of hippocampal CA3 pyramidal neurons in male tree shrews (Tupaia belangeri). Male tree shrews develop social hierarchies in which subordinates show characteristic changes in physiological and behavioral parameters when confronted with a dominant. In the present experiments,subordinateanimals lost body weight soon after starting the daily social conflict, and urinary excretion of cortisol was elevated throughout the experiment as compared with the control period. Golgi-impregnated brain tissue from subordinates exposed to 28 d (1 hr/d) of social confrontations was compared with that fromcontrol nonstressedanimals. The apical dendrites of the CA3 pyramidal cells from subordinates had a decreased number of branch points and total dendritic length as compared with controls. No differences were observed in apical dendritic spine density or in the basal dendritic tree morphology. The stress-induced CA3 apical dendritic atrophy in subordinates was prevented by administering daily oral doses of the antiepileptic drug phenytoin (Dilantin, Sigma, St. Louis, MO) (200 mg/kg), which interferes with excitatory amino acid (EAA) action. These results suggest that the naturalistic stressorpsychosocial stressinduces specific structural changes in hippocampal neurons of subordinate male tree shrews. These changes, like those in the rat after glucocorticoid treatment or restraint stress, probably are mediated by activation of the hypothalamo–pituitary–adrenal-axis acting in concert with endogenous EAAs from mossy fiber input.
17β-Estradiol Potentiates Kainate-Induced Currents via Activation of the cAMP Cascade
Authors: Gu Qin , Moss Robert L. 
Published: April 2018

Evidence for nongenomic actions of steroids is now coming from a variety of fields of steroid research. Mechanisms of steroid action are being studied with regard to the membrane receptors and the activation of second messengers. The present study investigated the mechanism for the rapid effect of estrogen on acutely dissociated hippocampal CA1 neurons by using the whole-cell, voltage-clamp recording. Under the perforated patch configuration, 17β-estradiol potentiated kainate-induced currents in 38% of tested neurons. The potentiation was stereospecific, rapid in onset, and reversible after the removal of the steroid. Dose–response curves show that the potentiation by 17β-estradiol was evident at a concentration as low as 10 nmand saturated at 10 μm. 17β-Estradiol did not affect the kinetics (i.e., affinity and cooperativity) and reversal potential of kainate-induced currents. This suggests that the potentiation did not result from direct interaction with kainate receptors nor the activation of ion channels other than kainate receptor-channels. The potentiation by 17β-estradiol was similar to the enhancement of kainate-induced currents evoked by 8-bromo-cAMP, and was modulated by an inhibitor of phosphodiesterase (IBMX). The estrogen potentiation was blocked by a specific blocker of PKA (Rp-cAMPS). Under standard recording configuration, the effect was significantly affected by intracellular perfusing with GDP-β-S or GTP-γ-S. The data suggest that the potentiation of kainate-induced currents by 17β-estradiol was likely a G-protein(s) coupled, cAMP-dependent phosphorylation event. By involvement of this nongenomic mechanism, estrogen may play a role in the modulation of excitatory synaptic transmission in the hippocampus.
Developmental Changes of Inhibitory Synaptic Currents in Cerebellar Granule Neurons: Role of GABAAReceptor α6 Subunit
Authors: Tia Sutthichai , Wang Jin Feng , Kotchabhakdi Naiphinich , Vicini Stefano 
Published: April 2018

Eye opening and increased motor activity after the second postnatal week in rats imply an extensive development of motor control and coordination. We show a parallel developmental change in spontaneous IPSC (sIPSC) kinetics in cerebellar granule neurons. sIPSCs were studied by whole-cell recordings in cerebellar slices, prepared from 7–30 postnatal day old rats. Early in development, sIPSCs had slow decay kinetics whereas in older rats faster decaying sIPSCs were found in larger proportion. Currents elicited by 1 mmGABA pulses (GABACs) in nucleated patches excised from cerebellar granule neurons revealed that GABACs kinetics better approximate sIPSC decay in young but not in more developed rats. The expression of α6 subunit of GABAAreceptors, unique in cerebellar granule neurons, has been shown to increase during development. Therefore, we took advantage of the recently reported selective inhibition of GABAAreceptors by furosemide to characterize the relative contribution of α6 subunits to native receptors in inhibitory synapses of cerebellar granule neurons. Although furosemide inhibition of sIPSCs amplitude was highly variable among distinct granule cells, it increased during development. At the same time, furosemide failed to inhibit sIPSCs recorded from Purkinje neurons. From the comparison of furosemide inhibition and kinetics of sIPSCs with GABACs recorded from mammalian HEK293 cells transfected with combinations of α1 and α6 GABAAreceptor subunits together with β2γ2 subunits, we propose that an increased α6 subunit contribution in the molecular assembly of postsynaptic receptors in cerebellar glomeruli is responsible for the developmental changes observed.
Endogenous Substance P Mediates Cold Water Stress-Induced Increase in Interleukin-6 Secretion from Peritoneal Macrophages
Authors: Zhu Goafa F. , Chancellor-Freeland Cheryl , Berman Ari S. , Kage Reinhard , Leeman Susan E. , Beller David I. , Black Paul H. 
Published: April 2018

Previous studies from this laboratory had shown that exposure of mice to cold water stress leads to an increase in the secretion of interleukin-1 (IL-1) and tumor necrosis factor-α (TNFα) from their peritoneal macrophages. We now report that the secretion of IL-6 from peritoneal macrophages is also increased after cold water stress and that the peptide substance P (SP) participates in this stress-induced response. The stress paradigm involved subjecting male C57BL/6J mice to 5 min swim tests in 10 ± 2°C water twice daily for 4 d. Cold water stress augments the lipopolysaccharide-induced IL-6 secretion from peritoneal macrophages, elevates immunoreactive SP (iSP) in the peritoneal wash fluid, and reduces iSP in certain peritoneum-containing tissues or organs (i.e., diaphragm, abdominal wall, ileum, and rectum). The 10 d stress time course studies indicate that increased IL-6 secretion is positively related to elevated iSP in the peritoneal wash fluid and inversely related to reduced iSP in certain peritoneum-containing tissues. Pretreatment with capsaicin, which depletes SP in the sensory nerve endings, eliminates stress-control differences in the peritoneal wash fluid and in certain peritoneal tissues. Moreover, RP67,580, a specific SP antagonist, eliminates the cold water stress-induced augmentation of IL-6 secretion from peritoneal macrophages. These results suggest that cold water stress promotes the release of SP from peritoneal tissues into the peritoneal cavity, where it participates in the cold water stress-induced macrophage functional alterations.
Muscarinic Activation of a Voltage-Dependent Cation Nonselective Current in Rat Association Cortex
Authors: Haj-Dahmane Samir , Andrade Rodrigo 
Published: April 2018

The ionic mechanism underlying the acetylcholine-induced depolarization of layer V pyramidal neurons of rat prefrontal cortex was examined using whole-cell recording inin vitrorat brain slices. Consistent with previous results, pressure application of acetylcholine to layer V pyramidal neurons elicited a strong depolarization. Pharmacological analysis of this response indicated that it was mediated by the stimulation of muscarinic receptors as it was mimicked by muscarinic agonists, but not by nicotine, and was blocked by atropine.The inward current responsible for the depolarization resulted from the activation of a voltage-dependent, cation nonselective current. Thus, the amplitude of the current was critically dependent on extracellular sodium concentration but not on extracellular potassium or chloride concentration. Examination of theI–Vrelationship for the muscarinic current using voltage clamp revealed that the current reversed near −15 mV and exhibited a strong voltage dependence, turning off rapidly in the subthreshold range. The voltage dependence of the current led to the appearance of a current associated with a conductance decrease when examined using steady-state voltage- or current-clamp measurements. This might have led to earlier misidentification of this response as mediated by a decrease in potassium conductance.These results question the traditional interpretation that muscarinic depolarization in cortex is mediated by a decrease in potassium conductance. They indicate that the fundamental mechanism responsible for muscarinic depolarization in prefrontal cortex involves the activation of a voltage-dependent, cation nonselective current. This current might represent a previously unsuspected mechanism capable of mediating slow depolarization in the central nervous system.
Layer-Specific Properties of the Transient K Current (IA) in Piriform Cortex
Authors: Banks Matthew I. , Haberly Lewis B. , Jackson Meyer B. 
Published: April 2018

Piriform cortex in the rat is highly susceptible to induction of epileptiform activity. Experimentsin vivoandin vitroindicate that this activity originates in endopiriform nucleus (EN). In slices, EN neurons are more excitable than layer II (LII) pyramidal cells, with more positive resting potentials and lower spike thresholds. We investigated potassium currents in EN and LII to evaluate their contribution to these differences in excitability. Whole-cell currents were recorded from identified cells in brain slices. A rapidly inactivating outward current (IA) had distinct properties in LII (IA,LII) versus EN (IA,EN). The peak amplitude ofIA,ENwas 45% smaller thanIA,LII, and the kinetics of activation and inactivation was significantly slower forIA,EN. The midpoint of steady-state inactivation was hyperpolarized by 10 mV forIA,ENversusIA,LII, whereas activation was similar in the two cell groups. Other voltage-dependent potassium currents were indistinguishable between EN and LII. Simulations using a compartmental model of LII cells argue that different cellular distributions ofIAchannels in EN versus LII cells cannot account for these differences. Thus, at least some of the differences are intrinsic to the channels themselves. Current-clamp simulations suggest that the differences betweenIA,LIIandIA,ENcan account for the observed difference in resting potentials between the two cell groups. Simulations show that this difference in resting potential leads to longer first spike latencies in response to depolarizing stimuli. Thus, these differences in the properties ofIAcould make EN more susceptible to induction and expression of epileptiform activity.
Schwann Cell Apoptosis during Normal Development and after Axonal Degeneration Induced by Neurotoxins in the Chick Embryo
Authors: Ciutat Dolors , Calderó Jordi , Oppenheim Ronald W. , Esquerda Josep E. 
Published: April 2018

In the present work, we show that chick embryo Schwann cells die by apoptosis both during normal development and after axonal degeneration induced by neurotoxin treatment. Schwann cell apoptosis during development takes place during a period roughly coincidental with normally occurring motoneuron death. Administration of NMDA to chick embryos on embryonic day 7 induces extensive excitotoxic motoneuronal damage in the spinal cord without any apparent effects on neurons in the dorsal root ganglia (DRG). The death of Schwann cells inventralnerve roots after NMDA treatment causes degenerative changes that display ultrastructural features of apoptosis and exhibitin situdetectable DNA fragmentation. By contrast, NMDA treatment does not increase the death of Schwann cells indorsalnerve roots.In situdetection of DNA fragmentation in combination with the avian Schwann cell marker 1E8 antibody demonstrates that dying cells in ventral nerve roots are in the Schwann cell lineage. Administration of cycloheximide does not prevent the toxic effects of NMDA on motoneurons, but dramatically reduces the number of pyknotic Schwann cells and DNA fragmentation profiles in the ventral nerve roots.In ovoadministration of various tissue extracts (muscle, brain, and spinal cord) from the chick embryo or of the motoneuron conditioned medium fails to prevent Schwann cell apoptosis in NMDA-treated embryos. Intramuscular administration of the snake toxin β-bungarotoxin produces a massive death of both lateral motor column motoneurons and DRG neurons, resulting in a substantial increase in the number of pyknotic Schwann cells in both ventral and dorsal nerve roots. It is concluded that during development, axonal-derived trophic signals are involved in the regulation of Schwann cell survival in peripheral nerves.