Sheibani V, Arabzadeh S, Afarineshkhaki M, Shamsizadeh A, Aminizadeh H, Azizolahi S. Effect of Norepinephrine depletion on induction of experience dependent plasticity in male rat barrel cortex. Physiol Pharmacol 2008; 11 (4) :244-251
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http://ppj.phypha.ir/article-1-370-en.html
Abstract: (19637 Views)
Introduction: Barrel cortex of rats is a part of somatosensory cortex, which receives information from facial whiskers. Vibrisectomy by sensory deprivation leads to some changes in the barrel cortex, which have been known as experience dependent plasticity. On the other hand, Norepinephrine (NE) and locus coeruleus, which is the main source of NE, influenced response properties of cortical barrel neurons. In this study, the effect of NE depleted and sensory deprivation on induction of experience dependent plasticity was investigated.
Materials and methods: In this study sixty wistar rats (250±25gr) were used. Rats were divided into four groups: 1.Control group (Intact). 2. NE depleted group in which Norepinephrine was selectively depleted by IP injection of DSP4. 3. Sensory deprivation group that all whiskers (except the whisker D2) on the left side were trimmed every other day. 4. NE depleted + sensory deprivation group.
By using extracellular single unit recordings, the excitatory (magnitude and latency) and initiatory (Conditioning Test Ratio, CTR index) receptive fields of barrel cortical neurons were calculated.
Results: Sensory deprivation led to an increase both in the response magnitude to principle whisker deflection (spared whisker) and in the CTR. In NE depleted + sensory deprivation group, the response magnitude and CTR index were the same as control group.
Conclusion: The result showed that experience dependent plasticity has a facilitating effect on excitatory receptive field while decreasing the inhibitory circuits in the brain. When NE content of the brain was depleted before sensory deprivation, these changes were not seen. We conclude that NE depletion inhibits the plastic changes in the response properties of neurons following sensory deprivation.