Brain research
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Chronic tinnitus, also known as ringing in the ears, affects up to 15% of the adults and causes a serious socio-economic burden. At present, there is no treatment available which substantially reduces the perception of this phantom sound. In the past few years, preclinical and clinical studies have unraveled central mechanisms involved in the pathophysiology of tinnitus, replacing the classical periphery-based hypothesis. ⋯ A therapy with a potential to counteract deeply located pathological activity is deep brain stimulation, which has already been demonstrated to be effective in neurological diseases such as Parkinson's disease. In this review, several brain targets are discussed as possible targets for deep brain stimulation in tinnitus. The potential applicability of this treatment in tinnitus is discussed with examples from the preclinical field and clinical case studies.
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The nociceptive flexion reflex (NFR) is a widely used tool to investigate spinal nociception for scientific and diagnostic purposes, but its clinical use is currently limited due to the painful measurement procedure, especially restricting its applicability for patients suffering from chronic pain disorders. Here we introduce a less painful algorithm to assess the NFR threshold. Application of this new algorithm leads to a reduction of subjective pain ratings by over 30% compared to the standard algorithm. ⋯ Furthermore, we show that the new algorithm can be applied at shorter interstimulus intervals than are commonly used with the standard algorithm, since reflex threshold values remain unchanged and no habituation effects occur when reducing the interstimulus interval for the new algorithm down to 3s. Finally we demonstrate the utility of the new algorithm to investigate the modulation of nociception through different states of attention. Taken together, the here presented new algorithm could increase the utility of the NFR for investigation of nociception in subjects who were previously not able to endure the measurement procedure, such as chronic pain patients.
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We studied the processes of inhibition and facilitation in the dentate gyrus (DG) and the CA3 field by examining the effects of paired-pulse stimulation on the evoked population spike (PS) in dorsal (DH) and ventral (VH) hippocampal slices from the adult rat. The antidromic-orthodromic (A-O) and the orthodromic-orthodromic (O-O) paired-pulse stimulation protocols were used at varying inter-pulse intervals (IPI). In the DG, the A-O stimulation produced an early depression of PS lasting 30-40ms which was significantly stronger in the VH compared with DH. ⋯ The facilitation observed with the O-O stimulation was much stronger in DH than VH and in DH only it was significantly reduced by the antagonist of GABAB receptors CGP52432. Furthermore, the facilitation was insensitive to changes in [Ca(2+)]o in both hippocampal poles. These findings suggest that the dorsal compared with ventral DG is more amenable to fast-frequency input but filters out slow-frequency inputs more reliably while the gating and amplification of the excitatory input in the CA3 circuitry is more prominent in DH than in VH.
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Post-traumatic stress disorder (PTSD) is characterized in part by impaired extinction of conditioned fear. Traumatic brain injury (TBI) is thought to be a risk factor for development of PTSD. We tested the hypothesis that controlled cortical impact (CCI) would impair extinction of fear learned by Pavlovian conditioning, in mice. ⋯ In pre- or post-injury paradigms, CCI did not influence fear learning and extinction. Furthermore, CCI did not affect locomotor activity or elevated plus maze testing. Our results demonstrate that, within the time frame studied, CCI does not impair the acquisition and expression of conditioned fear or extinction memory.
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The immunoreactive responses are a two-edged sword after spinal cord injury (SCI). Macrophages are the predominant inflammatory cells responsible for this response. However, the mechanism underlying the effects of HBOT on the immunomodulation following SCI is unclear now. ⋯ This was associated simultaneously with the levels of alternatively activated macrophages (M2 phenotype: arginase-1- or CD206-positive), and decreased levels of classically activated macrophages (M1 phenotype: iNOS- or CD16/32-positive). These changes were associated with functional recovery in the HBOT-transplanted group, which correlated with preserved axons and increased myelin sparing. Our results suggested that HBOT after SCI modified the inflammatory environment by shifting the macrophage phenotype from M1 to M2, which may further promote the axonal extension and functional recovery.