Central Inhibition


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Central Inhibition

 

an active nervous process arising in the central nervous system and leading to the suppression or prevention of excitation. A distinction is made between postsynaptic inhibition, which involves the action of a specific mediator on the postsynaptic membrane of a neuron, and presynaptic inhibition, which is based on the depolarization of a presynaptic nerve ending at the point of contact with another axonal nerve ending. All types of inhibition occurring in conditioned reflex activity are regarded as forms of central inhibition.

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The current study demonstrates that adult rats with a thoracic 25.0 mm NYU contusion exhibit behavioral hypersensitivity relevant to human SCI, determined by cutaneous allodynia and thermal hyperalgesia development, combined with a loss of central inhibition and enhanced excitability due to molecular changes in GluR3, [GAD.sub.65/67] and GLRA3.
The role of central inhibition in ambiguity resolution
Without the specification of a goal state (or reason for selecting), this kind of central inhibition would not come into play.
To make the connection between central inhibition and lexical ambiguity resolution stronger it is first crucial to see whether it is possible to observe semantic negative priming from the non-selected meaning of the homograph.
The impact of individual strategies on central inhibition
One way to test the role of central inhibition in homograph resolution is to check for strategic effects on priming.
Inhibitory mechanisms can be divided into two kinds: central inhibition and lateral inhibition.
If central inhibition works to resolve ambiguity, then some kind of negative priming should occasionally be observed.
Instead, when the selection of the meaning is generated internally, depending on the goal of the task, then central inhibition should act with higher intensity, allowing us to observe negative priming.
While no single set of data or hypothesis explains all involuntary contractions or occurrences of urgency/frequency, four concepts seem to be valid: 1) patients with OAB have faulty central inhibition, which leads to enhancement of excitatory neurotransmission in the micturition reflex pathway (neurogenic); 2) there is partial denervation of smooth muscle, which leads to co-ordinated myogenic contractions and increased bladder pressure (myogenic); 3) there is a "leaking" of acetylcholine from parasympathetic nerves during filling/storage, which leads to afferent activation (neurogenic-myogenic); and 4) abnormal signals originating in the urothelium are influenced by generation and release of local mediators (e.g., acetylcholine, nitric oxide, urothelial-derived inhibitory factor).

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