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PLASTICITY: IMPLICATIONS FOR OPIOID AND OTHER PHARMACOLOGICAL INTERVENTIONS IN SPECIFIC PAIN STATES

Dickenson, Anthony H (1997) PLASTICITY: IMPLICATIONS FOR OPIOID AND OTHER PHARMACOLOGICAL INTERVENTIONS IN SPECIFIC PAIN STATES.

Short Abstract:

The spinal mechanisms of action of opioids under normal conditions are reasonably well understood. Of importance to the control of different pain states is the realization that the spinal effects of opioids can be enhanced or reduced depending on pathology and activity in other segmental and non-segmental pathways. This account will consider this plasticity in relation to the control of different pain states using opioids as a theme. The complex and contradictory findings on the supraspinal actions of opioids are explicable in terms of heterogeneous descending pathways to different spinal targets using multiple transmitters and receptors - opioids can therefore both increase and decrease activity in descending pathways. One could envisage that these pathways exhibit considerable plasticity. There is increasing evidence that delta opioid receptor agonists have the potential to replace morphine as major analgesics with reduced side-effect profiles. The concept of pre-emptive analgesia, based on preventing the induction of some of the negative plastic influences on opioid controls and the detrimental effects of pain, is correct but experimental verification of the hypothesis in the clincial setting is difficult. One of the reasons is a delayed compensatory upregulation of inhibitory systems, particularly in inflammation, which may counter persistent painful inputs. Combination therapy with opioids may be beneficial in many pain states where either negative influences are blocked or inhibitory controls enhanced. Finally, the developmental aspects of these systems is discussed with regard to the treatment of pain in young children, where inhibitory systems in the spinal cord are immature..

Long Abstract:

The spinal mechanisms of action of opioids under normal conditions are reasonably well understood. Of importance to the control of different pain states is the realization that the spinal effects of opioids can be enhanced or reduced depending on pathology and activity in other segmental and non-segmental pathways. This account will consider this plasticity in relation to the control of different pain states using opioids as a theme. The complex and contradictory findings on the supraspinal actions of opioids are explicable in terms of heterogeneous descending pathways to different spinal targets using multiple transmitters and receptors - opioids can therefore both increase and decrease activity in descending pathways. One could envisage that these pathways exhibit considerable plasticity. There is increasing evidence that delta opioid receptor agonists have the potential to replace morphine as major analgesics with reduced side-effect profiles. The concept of pre-emptive analgesia, based on preventing the induction of some of the negative plastic influences on opioid controls and the detrimental effects of pain, is correct but experimental verification of the hypothesis in the clincial setting is difficult. One of the reasons is a delayed compensatory upregulation of inhibitory systems, particularly in inflammation, which may counter persistent painful inputs. Combination therapy with opioids may be beneficial in many pain states where either negative influences are blocked or inhibitory controls enhanced. Finally, the developmental aspects of these systems is discussed with regard to the treatment of pain in young children, where inhibitory systems in the spinal cord are immature..

Keywords:	Opioids; analgesia; nociception; spinal cord; peptides; excitatory amino acids; hypersensitivity; cholecystokinin; development of pain
Subjects:	BBS Special Issues: Controversies in Neuroscience: V - Persistent Pain Psychology: Clinical Psychology Neuroscience: Neurochemistry Neuroscience: Neuroendocrinology Neuroscience: Neuropharmacology
ID code:	bbs00000452
Deposited by:	Anthony H Dickenson on 01 May 2001