57 research outputs found
[The role of sensory nerves in the development of inflammation of oral tissues]
No full textExperimental stimulation and clinical procedures applied on the tooth crown cause vascular reactions in the dental pulp of cats and rats. These reactions depend on the activation of trigeminal afferent nerves and release of neuropeptides. A brief stimulation causes vasodilation, which is mainly mediated by calcitonin gene-related peptide (CGRP). A longer stimulation results in plasma extravasation which is mediated mainly by substance P (SP) and prostaglandins in the pulp. In adjacent oral tissues the mechanisms following stimulation or local irritation are more complex and other mediators are also involved. Nitric oxide (NO) which is instantly produced in the tissues is such a novel mediator. The chemosensitive nature of the nerves involved (capsaicin sensitive) may lead to their activation also by inflammatory mediators released in the tissues. Thus, sensory nerves may modulate the progress of inflammation. Since sensory nerves in oral tissues are often the first structures to be activated during clinical procedures, tissue reactions that occur can be assumed to be initiated and perpetuated by the sensory neuropeptides. Much work is now made to modulate the sensory nerveinduced cascade of events in oral tissues to find new treatment strategies
[Breakthrough in pain research. Charting of the synaptic network may lead to new analgesics]
No full textIncreased pain fibre activity in response to tissue injury results in changes in gene expression and prolonged changes in nerves and their environment. The resulting hyperalgesia and prolonged spontaneous pain are due both to increased sensitivity of peripheral nociceptors (primary hyperalgesia) and to faciliated spinal cord transmission (secondary hyperalgesia, receptive field expansion and allodynia). Hyperexcitability of dorsal horn neurones is first triggered by increased neuronal barrage into the central nervous system ("wind-up"), and later by retrograde chemical influences from the peripheral inflammation (central sensitisation). Central transmission and hyperexcitability are mediated by excitatory amino acids (aspartate and glutamate) and by tachykinins (substance P). Normally, the net effect of the activity in a complex network of inhibitory neurones in the spinal cord ("gate control"), driven by descending projections from brain stem sites, is to dampen and counteract the spinal cord hyperexcitability produced by tissue or nerve injury. Thus, peripherally evoked pain impulses pass through a filtering process involving gamma-aminobutyric acid, glycine and enkephalins. The activity of these substances in the spinal cord usually attenuates and limits the duration of pain. In the case of persistent pain, there is evidence of pathological reduction of the supraspinal net inhibitory actions in combination with ectopic afferent input in damaged nerves. Hence, the pathology of chronic pain (neuropathic pain) differs from that of nociceptive pain and conventional pharmacological treatment of chronic central pain is usually less successful than treatment of inflammation-related pain. The many newly discovered mechanisms for the transmission and modulation of pain impulses are characterised by complex activity-dependent plasticity, which means that therapeutic strategies for persistent pain must be adapted to changing targets--either at the site of injury or at other sites in the central nervous system
[A breakthrough in the research on pain. Survey of the synaptic network may result in new analgesics]
No full textIncreased pain fibre activity in response to tissue injury results in changes in gene expression, and prolonged changes in nerves and their environment. The resulting hyperalgesia and prolonged spontaneous pain are due both to increased sensitivity of peripheral nociceptors (primary hyperalgesia) and to facilitated spinal cord transmission (secondary hyperalgesia, receptive field expansion and allodynia). Hyperexcitability of dorsal horn neurones is first triggered by increased neuronal barrage into the central nervous system ('wind-up'), and later by retrograde chemical influences from the peripheral inflammation (central sensitisation). Central transmission and hyperexcitability are mediated by excitatory amino acids (aspartate and glutamate) and by tachykinins (substance P). Normally, the net effect of the activity in a complex network of inhibitory neurones in the spinal cord ('gate control'), driven by descending projections from brain stem sites, is to dampen and counteract the spinal cord hyperexcitability produced by tissue or nerve injury. Thus, peripherally evoked pain impulses pass through a filtering process involving gamma-aminobutyric acid, glycine and enkephalins. The activity of these substances in the spinal cord usually attenuates and limits the duration of pain. In the case of persistent pain, there is evidence of pathological reduction of the supraspinal net inhibitory actions in combination with ectopic afferent input in damaged nerves. Hence, the pathology of chronic pain (neuropathic pain) differs from that of nociceptive pain, and conventional pharmacological treatment of chronic central pain is usually less successful than treatment of inflammation-related pain. The many newly discovered mechanisms for the transmission and modulation of pain impulses are characterised by complex activity-dependent plasticity, which means that therapeutic strategies for persistent pain must be adapted to changing targets--either at the site of injury or at other sites in the central nervous system
The enhancement of carbachol-induced salivary secretion by VIP and CGRP in rat parotid gland is mimicked by forskolin
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The blocking effect of iontophoretic administration of lidocaine on neurogenic vascular reactions in rat dental pulp
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INVOLVEMENT OF SUBSTANCE-P BUT NOT NITRIC-OXIDE OR CALCITONIN-GENE-RELATED PEPTIDE IN NEUROGENIC PLASMA EXTRAVASATION IN RAT INCISOR PULP AND LIP
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