Modulation of spinal excitability: co-operation between neurokinin and excitatory amino acid neurotransmitters.
Activation of C fibres with strong 'potentially tissue damaging' chemical, mechanical or thermal stimuli produces painful sensations that are significantly enhanced during pathological conditions, such as neuropathy and inflammation. The pronounced painful symptoms of hyperalgesia and allodynia are induced, in part, by the development of spinal hyperexcitability. This involves plastic changes in synaptic transmission between primary afferents and dorsal horn neurones induced by sustained activity of peripheral nociceptors. L. Urban, S. W. N. Thompson and A. Dray describe some of the central mechanisms that account for central hyperexcitability occurring in hyperalgesia and allodynia based on evidence from experiments both in vivo and in vitro with neurokinin and N-methyl-D-aspartate receptor antagonists.
Urban
L
L
Dept of Pharmacology, Sandoz Institute for Medical Research, London, UK.
Thompson
S W
SW
Dray
A
A
D000818:Animals; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018846:Excitatory Amino Acids / Q000502:physiology*; D006801:Humans; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology*; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D015320:Tachykinins / Q000502:physiology*
D018691:Excitatory Amino Acid Antagonists; D018846:Excitatory Amino Acids; D018377:Neurotransmitter Agents; D017470:Receptors, Glutamate; D015320:Tachykinins