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1.
Ecol Evol ; 4(18): 3555-70, 2014 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-25478148

RESUMO

The two major aims of this study are (1) To test the performance of the Landscape Reconstruction Algorithm (LRA) to quantify past landscape changes using historical maps and related written sources, and (2) to use the LRA and map reconstructions for a better understanding of the origin of landscape diversity and the recent loss of species diversity. Southern Sweden, hemiboreal vegetation zone. The LRA was applied on pollen records from three small bogs for four time windows between AD 1700 and 2010. The LRA estimates of % cover for woodland/forest, grassland, wetland, and cultivated land were compared with those extracted from historical maps within 3-km radius around each bog. Map-extracted land-use categories and pollen-based LRA estimates (in % cover) of the same land-use categories show a reasonable agreement in several cases; when they do not agree, the assumptions used in the data (maps)-model (LRA) comparison are a better explanation of the discrepancies between the two than possible biases of the LRA modeling approach. Both the LRA reconstructions and the historical maps reveal between-site differences in landscape characteristics through time, but they demonstrate comparable, profound transformations of the regional and local landscapes over time and space due to the agrarian reforms in southern Sweden during the 18th and 19th centuries. The LRA was found to be the most reasonable approach so far to reconstruct quantitatively past landscape changes from fossil pollen data. The existing landscape diversity in the region at the beginning of the 18th century had its origin in the long-term regional and local vegetation and land-use history over millennia. Agrarian reforms since the 18th century resulted in a dramatic loss of landscape diversity and evenness in both time and space over the last two centuries leading to a similarly dramatic loss of species (e.g., beetles).

2.
Neurochem Int ; 43(1): 73-7, 2003 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-12605884

RESUMO

Muscarinic facilitation of 14C-ACh release from post-ganglionic parasympathetic nerve terminals was studied in bladder strips prepared from spinal intact (SI) and spinal cord transected (SCT) rats. The spinal cord was transected at the lower thoracic spinal segments 3 weeks prior to the experiments. Using non-facilitatory stimulation (2 Hz) the release of ACh in spinal intact rats did not change in the presence of a non-specific muscarinic antagonist, atropine (100 nM), an M(1) specific antagonist (pirenzepine, 50 nM) or an M(1)-M(3) specific antagonist (4-DAMP, 5 nM). However, during a facilitatory stimulation paradigm (10 Hz or 40 Hz, 100 shocks) atropine and pirenzepine, but not 4-DAMP inhibited the release of ACh in bladders from spinal intact rats, indicating an M(1) receptor-mediated facilitation. In spinal cord transected rats, 2 Hz stimulation-induced release was significantly inhibited by atropine or 4-DAMP but not by pirenzepine indicating that a pre-junctional facilitatory mechanism mediated via M(3) muscarinic receptors could be induced by a non-facilitatory stimulation paradigm after spinal injury. In bladders of spinal cord transected rats, 10 Hz stimulation-evoked release of ACh was also inhibited by atropine and 4-DAMP (5 nM) but not by pirenzepine (50 nM). These results indicate that pre-junctional muscarinic receptors at cholinergic nerve endings in the bladder change after chronic spinal cord injury. It appears that low affinity M(1) muscarinic receptors are replaced by high affinity M(3) receptors. This change in modulation of ACh release may partly explain the bladder hyperactivity after chronic spinal cord injury.


Assuntos
Neurotransmissores/metabolismo , Receptores Muscarínicos/metabolismo , Traumatismos da Medula Espinal/metabolismo , Bexiga Urinária/metabolismo , Animais , Atropina/farmacologia , Estimulação Elétrica , Feminino , Antagonistas Muscarínicos/farmacologia , Piperidinas/farmacologia , Pirenzepina/farmacologia , Ratos , Ratos Sprague-Dawley , Receptor Muscarínico M3 , Receptores Muscarínicos/efeitos dos fármacos , Bexiga Urinaria Neurogênica/metabolismo
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