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1.
Land use policy ; 71: 183-203, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33867619

RESUMO

This paper presents an evaluation of local efforts to manage Great Lakes coastal shorelands through master plans, focusing on Michigan localities. We framed the analysis around the concepts of capacity, knowledge, and commitment. We conducted plan content evaluations, structured surveys of local officials, and multiple unstructured interviews of local officials and citizens through a participatory action research (PAR) program. We analyzed those data, along with census data, using descriptive statistics, correlations, regression analyses, and triangulation of observations. We found that Michigan's coastal localities are largely failing to consider their coastal areas in their planning, or to adopt meaningful plan policies to manage them, for at least four reasons: damaging erosion and storm events have been relatively infrequent; localities rely on the state to address coastal issues; insurance programs effectively indemnify them when a storm does happen; and-to some extent-shoreland owners push back against proactive local management. To the extent localities are planning, higher overall plan quality is associated with having in-house planning staff (a measure of both capacity and knowledge) and development pressure (knowledge and commitment). To the extent plans address their coastal areas specifically, the adoption of plan policies advancing coastal area management is associated directly with having higher median house values (capacity), in-house planning staff (capacity and knowledge), and development pressure (knowledge and commitment). Focus on coastal management is inversely associated, however, with the use of planning consultants. Higher plan quality is correlated significantly with the adoption of more robust plan policies overall. In sum, having knowledge about coastal dynamics appears important in explaining local planning efforts, but having the capacity to act on that knowledge and the commitment to do so are equally or more important.

2.
Learn Mem ; 23(12): 689-698, 2016 12.
Artigo em Inglês | MEDLINE | ID: mdl-27918273

RESUMO

Single prolonged stress (SPS) has been used to examine mechanisms via which stress exposure leads to post-traumatic stress disorder symptoms. SPS induces fear extinction retention deficits, but neural circuits critical for mediating these deficits are unknown. To address this gap, we examined the effect of SPS on neural activity in brain regions critical for extinction retention (i.e., fear extinction circuit). These were the ventral hippocampus (vHipp), dorsal hippocampus (dHipp), basolateral amygdala (BLA), prelimbic cortex (PL), and infralimbic cortex (IL). SPS or control rats were fear conditioned then subjected to extinction training and testing. Subsets of rats were euthanized after extinction training, extinction testing, or immediate removal from the housing colony (baseline condition) to assay c-Fos levels (measure of neural activity) in respective brain region. SPS induced extinction retention deficits. During extinction training SPS disrupted enhanced IL neural activity and inhibited BLA neural activity. SPS also disrupted inhibited BLA and vHipp neural activity during extinction testing. Statistical analyses suggested that SPS disrupted functional connectivity within the dHipp during extinction training and increased functional connectivity between the BLA and vHipp during extinction testing. Our findings suggest that SPS induces extinction retention deficits by disrupting both excitatory and inhibitory changes in neural activity within the fear extinction circuit and inducing changes in functional connectivity within the Hipp and BLA.


Assuntos
Tonsila do Cerebelo/metabolismo , Córtex Cerebral/metabolismo , Extinção Psicológica/fisiologia , Medo/fisiologia , Hipocampo/metabolismo , Estresse Psicológico/metabolismo , Tonsila do Cerebelo/patologia , Animais , Córtex Cerebral/patologia , Eletrochoque , Análise Fatorial , Reação de Congelamento Cataléptica , Hipocampo/patologia , Imuno-Histoquímica , Masculino , Transtornos da Memória/metabolismo , Transtornos da Memória/patologia , Vias Neurais/metabolismo , Vias Neurais/patologia , Neurônios/metabolismo , Neurônios/patologia , Proteínas Proto-Oncogênicas c-fos/metabolismo , Ratos Sprague-Dawley , Estresse Psicológico/patologia
3.
Behav Brain Res ; 341: 189-197, 2018 04 02.
Artigo em Inglês | MEDLINE | ID: mdl-29292158

RESUMO

Neural circuits via which stress leads to disruptions in fear extinction is often explored in animal stress models. Using the single prolonged stress (SPS) model of post traumatic stress disorder and the immediate early gene (IEG) c-Fos as a measure of neural activity, we previously identified patterns of neural activity through which SPS disrupts extinction retention. However, none of these stress effects were specific to fear or extinction learning and memory. C-Jun is another IEG that is sometimes regulated in a different manner to c-Fos and could be used to identify emotional learning/memory specific patterns of neural activity that are sensitive to SPS. Animals were either fear conditioned (CS-fear) or presented with CSs only (CS-only) then subjected to extinction training and testing. C-Jun was then assayed within neural substrates critical for extinction memory. Inhibited c-Jun levels in the hippocampus (Hipp) and enhanced functional connectivity between the ventromedial prefrontal cortex (vmPFC) and basolateral amygdala (BLA) during extinction training was disrupted by SPS in the CS-fear group only. As a result, these effects were specific to emotional learning/memory. SPS also disrupted inhibited Hipp c-Jun levels, enhanced BLA c-Jun levels, and altered functional connectivity among the vmPFC, BLA, and Hipp during extinction testing in SPS rats in the CS-fear and CS-only groups. As a result, these effects were not specific to emotional learning/memory. Our findings suggest that SPS disrupts neural activity specific to extinction memory, but may also disrupt the retention of fear extinction by mechanisms that do not involve emotional learning/memory.


Assuntos
Condicionamento Psicológico/fisiologia , Extinção Psicológica/fisiologia , Medo/fisiologia , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Neurônios/enzimologia , Estresse Psicológico/enzimologia , Animais , Complexo Nuclear Basolateral da Amígdala/enzimologia , Complexo Nuclear Basolateral da Amígdala/patologia , Hipocampo/enzimologia , Hipocampo/patologia , Imuno-Histoquímica , Masculino , Neurônios/patologia , Córtex Pré-Frontal/enzimologia , Córtex Pré-Frontal/patologia , Ratos Sprague-Dawley , Estresse Psicológico/patologia
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