Does High Frequency Transcutaneous Electrical Nerve Stimulation (TENS) Affect EEG Gamma Band Activity?

BACKGROUND: Transcutaneous electrical nerve stimulation (TENS) is a noninvasive, inexpensive and safe analgesic technique used for relieving acute and chronic pain. However, despite all these advantages, there has been very little research into the therapeutic effects of TENS on brain activity. To the best of our knowledge, there is no evidence on the effect of high frequency TENS on the gamma band activity. OBJECTIVE: Investigation of the effect of high frequency TENS on the electroencephalographic (EEG) gamma band activity after inducing ischemic pain in healthy volunteers is considered. MATERIAL AND METHODS: The modified version of Submaximal effort tourniquet test was carried out to induce tonic pain in 15 right-handed healthy volunteers. The high frequency TENS (150µs in duration, frequency of 100 Hz) was applied for 20 minutes. Pain intensity was assessed at using Visual Analog Scale (VAS) in two conditions (after-pain, after-TENS). EEG gamma band activity was recorded by a 19-channel EEG in three conditions (baseline, after-pain and after- TENS). The repeated measure ANOVA and paired-sample T- tests were used for data analysis. RESULTS: EEG analysis showed an increase in gamma total power after inducing pain as compared to baseline and a decrease after the application of TENS (mean±SD: .043±.029 to .088±.042 to .038±.022 µV2 ).The analysis of VAS values demonstrated that the intensity of induced pain (mean±SD: 51.53±9.86) decreased after the application of TENS (mean±SD: 18.66±10.28). All these differences were statistically significant (p<.001). CONCLUSION: The results of this study revealed that the high frequency TENS can reduce the enhanced gamma band activity after the induction of tonic pain in healthy volunteers. This finding might help as a functional brain biomarker which could be useful for pain treatment, specifically for EEG-based neurofeedback approaches.

Neuroprotective effects of NMDA and group I metabotropic glutamate receptor antagonists against neurodegeneration induced by homocysteine in rat hippocampus: in vivo study.

Homocysteine (Hcy), a neurotoxic amino acid, is a risk factor for neurodegenerative diseases. Previous in vitro studies have demonstrated that group I metabotropic glutamate receptors along with N-methyl-D-aspartic acid (NMDA) receptors participate in acute and chronic aspects of Hcy-induced neuronal damage. In the present study, we examined whether the same mechanism may be involved in homocysteine neurotoxicity in vivo. Memantine, MPEP, and LY367385 were used as NMDA, mGlu5, and mGlu1 antagonists, respectively. Repeated i.c.v injection of Hcy was performed for three consecutive days. Neuronal loss in different zones of the hippocampus was assessed by Nissl, Fluoro-Jade B, and TUNEL staining. Neuronal degeneration was observed in both types of apoptosis and necrosis. All glutamate receptor antagonists, even when given alone, provided some degree of neuroprotection. The degree of protection was dependent on the area of the hippocampus. While memantine was more potent against Hcy-induced apoptosis, the potency of mGluR antagonists in neuronal protection against apoptosis and necrosis was almost equal. No more protection was observed when all three antagonists were used simultaneously. It seems that Fluoro-Jade could be a useful marker of apoptotic cell death. Taken together, results demonstrate that, in vivo, Hcy neurotoxicity is mediated mainly by the NMDA receptors and group I mGluRs.

The Effect of Intra-CA1 Agmatine Microinjection on Water Maze Learning and Memory in Rat.

BACKGROUND: Reports on agmatine are controversial showing that it may improve memory, it can deteriorate memory and some did not notice any interference with learning and memory. In the present study, the effect of directly intra-CA1 agmatine microinjection on water maze learning and memory has been assessed. METHODS: The cannuls were implanted in hippocampal CA1 regions of rats in a sterotaxic frame after general anesthesia. After one week recovery period, the animals were assessed in the reference memory version of water maze. Agmatine (1, 10, 100 or 200 µg/0.5 µl) or saline were infused 20 minutes before or immediately after training. RESULTS: Agmatine-treated rats did not show any significant difference neither in water maze acquisition nor in consolidation task in comparison with control and sham groups. CONCLUSION: Agmatine does not affect water maze learning and memory.