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Prominent models of fear focus on the role of cognition in the development and maintenance of maladaptive responses.
Rodent models of fear learning and memory have taken great strides towards elucidating the specific neuronal circuitries underlying the learning of fear responses.
Thus NPY act as a resilience factor by impairing associative implicit memory after stressful and aversive events, as evident in models of fear conditioning, presumably via Y1 receptors in the amygdala and prefrontal cortex.
First proposed by Witte in the early 1990s [18], the EPPM represents an integration and expansion of previous psychosocial models of "fear appeal".
Studies of rodents have assessed anxiety using animal models of fear, e.g. the light/dark test and the elevated plus-maze paradigm to measure state anxiety, and the free exploratory test to measure trait anxiety [3] [10].
The theorized mechanisms underlying PE are based on emotional processing theory and broader extinction models of fear reduction.
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As can be seen in Table 5, in a main effects model of fear, effortful control only showed a trend toward relating to fearful temperament (b = −.77, t = −2.03, p = .059).059
The results offer the first convincing experimental support for the stimulus estimation model of fear overprediction.
The amygdala plays a key role in this neural model of fear as it evaluates incoming sensory stimuli with regard to potential threat [4], [6].
Although the notion of US input as weak runs counter to prevailing views of the nature of associative learning (as well as the associative or Hebbian LTP model of fear conditioning [36], [37]), we postulate that the 'weakness' of US input may be limited to this particular subset of neurons.
The model of fear underlying this investigation holds that vulnerability-related perceptions forming a cognitively active schema comprise the core constructs of dental fear.
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