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Current Research
Higher level processing of sensory messages in different pain states
In chronic pain states, pain can persist even after local recovery of damaged tissue and does not always reflect the degree of tissue damage. On the other hand, while nociceptive pain is elicited by stimulation of the sensory endings in the tissue, neuropathic pain (NP) results from injury or disease of neurons in the peripheral or central nervous system (Schaible and Richter, 2004). Despite the loss of input, peripheral nerve injury results in positive symptoms in a number of patients where central sensitization, related to channel and receptor changes within the spinal cord that increase the output of neurons within the nociceptive pathway and changes in top-down processing through descending pathways appear to be maladaptive compensations for the sensory loss. This type of pain usually occurs within days, weeks, or months after the injury and tends to occur in waves of frequency and intensity indicative of multiple processes of pain and modulation. The main signs of neuropathic pain (NP) are spontaneous pain, hyperalgesia and allodynia but other signs or symptoms that are usually present are mood disorders like depression and anxiety It is also known that pain is enhanced by unpleasant emotional states such as fear, anxiety, depression and insomnia and reduced by pleasant emotions The amygdala (AMY), as part of the limbic system, plays a key role in the affective and autonomic aspects of pain, the evaluation of the emotional significance of sensory stimuli, emotional learning and memory, fear, anxiety and depression.
Contrary to acute pain cases, analgesics can be inefficient in chronic pain conditions, and the use of drugs like antidepressants and anticonvulsants in pain control as become widespread Anticonvulsants have shown to be useful for chronic NP, and gabapentin and pregabalin are the two anticonvulsants that have the strongest evidence for the treatment of pain. They selectively bind to the alpha/2delta-subunit protein of calcium channels in various regions of the brain and the superficial dorsal horn of the spinal cord, inhibiting the release of excitatory neurotransmitters that are important in the first stages of pain processing. Their efficacy however is controlled by descending pathways from the brain.
Our first goal is to characterize the neurons of the AMY through extracellular in vivo electrophysiology, in the spinal nerve ligation (SNL) model, We also propose to analyze the effects of the systemic and spinal injection of pregabalin in the activity of AMY neurones. We then intend to link in with concurrent interests in the group and probe, using site °V specific neuronal ablation, the roles of defined spinal and brain stem populations of neurons, such as within the RVM to probe the input and modulating pathways to the AMY. Further studies would investigate other pain models to compare across different patterns of afferent and central activity.