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Activation of several protein kinases causes both forms of sensitization via posttranslational, translational, and transcriptional regulation.
Thus, a stimulus could sometimes induce both forms of sensitization simultaneously rather than one or the other exclusively.
These inefficiencies had implications for program cost-effectiveness by limiting beneficiary time spent in vegetable production, training sessions and other forms of sensitization.
Different forms of sensitization include limbic kindling of seizures (compare temporal lobe epilepsy and simple partial seizures) and time-dependent sensitization of behavioral, neurochemical, immunological, and endocrinological variables.
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Thus, dishabituation may represent a form of sensitization that is gated by habituation (see Sect. 4.3.2).
However, this form of sensitization is clearly distinguishable from the first, which was elicited by the primary stimulus itself.
This form of sensitization is related to changes in the properties of primary nociceptive afferents (peripheral sensitization), whereas central sensitization requires functional changes in the CNS (neuroplasticity).
This form of sensitization has been variously referred to as "conventional" or "nociceptive" sensitization [ 39] or "extrinsic" sensitization [ 10, 27, 37, 42, 48, 49].
Kindling is a form of sensitization in which repeated application of electrical stimuli applied to the brain at low levels culminates in the induction of full-blown seizures when the same stimulus is applied at a later time.
Both peripheral sensitization and the classical or modern forms of central sensitization contribute to hyperalgesia (increased responsiveness to noxious stimuli) although their mechanisms and loci in the pain pathway may vary.
These modern forms of central sensitization have been likened to synaptic plasticity-related learning and memory [ 59- 63].
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