Sensitization
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- This article is about neurobiologic sensitization. For metallurgic sensitization, see weld decay.
Sensitization is an example of non-associative learning in which the progressive amplification of a response follows repeated administrations of a stimulus (Bell et al., 1995).
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[edit] Types of sensitization
For example, electrical or chemical stimulation of the rat hippocampus causes strengthening of synaptic signals, a process known as long-term potentiation or LTP (Collingridge, Isaac & Wang, 2005). LTP is thought to underlie memory and learning in the human brain.
A different type of sensitization is that of kindling, where repeated stimulation of hippocampal or amygdaloid neurons eventually leads to seizures. Thus, kindling has been suggested as a model for temporal lobe epilepsy (Morimoto, Fahnestock & Racine, 2004).
A third type is central sensitization, where nociceptive neurons in the dorsal horns of the spinal cord become sensitized by peripheral tissue damage or inflammation (Ji et al., 2003). These various types indicate that sensitization may underlie both pathological and adaptive functions in the organism, but whether they also share the same physiological and molecular properties is not yet established (McEarchern & Shaw, 1999).
Sensitization is a term referred to in psychology as how your body reacts to a drug.
[edit] Aetiology
Sensitization has been implied as a causal or maintaining mechanism in a wide range of apparently unrelated pathologies including substance abuse and dependence, allergies, asthma, and some medically unexplained syndromes such as fibromyalgia and multiple chemical sensitivity. Sensitization has also been suggested in relation to psychological disorders such as post-traumatic stress disorder, panic anxiety and mood disorders (Rosen & Schulkin, 1998; Antelman, 1988; Post, 1992).
[edit] Experimental basis
Eric Kandel was one of the first to describe sensitization based on his experiments with the seasnail Aplysia in the 1960's and 1970's. Kandel and his colleagues gave Aplysia electric shocks to the head, which caused it to retract its siphon and gills (Kandel, 2004). Eventually, very little stimulation was needed to provoke the response, indicating that Aplysia had been sensitized. When tested several days after the initial trials, this response was still manifest. In 2000, Eric Kandel was awarded the Nobel Prize in Physiology or Medicine for his research in neuronal learning processes.
[edit] References
- Antelman, S. M.: Time-dependent sensitization as the cornerstone for a new approach to pharmacotherapy: drugs as foreign/stressful stimuli. Drug Development Research. 1988: 14; 1-30.
- Bell, I.R., Hardin, E.E., Baldwin, C.M. & Schwartz, G.E.: Increased limbic system symptomatology and sensitizability of young adults with chemical and noise sensitivities. Environmental Research. 1995; 70: 84-97.
- Collingridge, G.L., Isaac, J.T.R. & Wang, Y.T.: Receptor trafficking and synaptic plasticity. Nature Reviews. 2004; 5: 952-962.
- Ji, R., Kohno, T., Moore, K.A. & Woolf, C.J.: Central sensitization and LTP: do pain and memory share similar mechanisms? Trends in Neurosciences. 2003; 26(12): 696-705.
- Kandel, E.R.: The molecular biology of memory storage: a dialog between genes and synapses. Bioscience Reports. 2004; 24(4-5): 477-522.
- McEachern, J.C. & Shaw, C.A.: The plasticity-pathology continuum: defining a role for the LTP-phenomenon. Journal of Neuroscience Research. 1999; 58: 42-61.
- Morimoto, K., Fahnestock, M. & Racine, R.J.: Kindling and status epilepticus models of epilepsy: rewiring the brain. Progress in Neurobiology. 2004; 73: 1-60.
- Post, R.M.: Transduction of psychosocial stress into the neurobiology of recurrent affective disorder. American Journal of Psychiatry. 1992; 149(8): 999-1010.
- Rosen, J.B. & Schulkin, J.: From normal fear to pathological anxiety. Psychological Review. 1998: 105(2); 325-350.
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