Browsing by Subject "LTP"

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  • Halonen, Risto; Kuula, Liisa; Lahti, Jari; Makkonen, Tommi; Räikkönen, Katri; Pesonen, Anu-Katriina (2019)
    A common single nucleotide polymorphism (SNP) of the brain-derived neurotrophic factor (BDNF) gene, Val66Met, has been reported to impair BDNF secretion and memory function. However, few studies have investigated the interaction of BDNF genotype and sleep characteristics, such as sleep spindles, that promote long-term potentiation during sleep. In this study we compared overnight visual memory between the carriers of BDNF Met and non-carriers (Val homozygotes), and examined how sleep spindle density associated with memory performance. The sample constituted of 151 adolescents (mean age 16.9 years; 69% Val homozygotes, 31% Met carriers). The learning task contained high and low arousal pictures from Interactive Affective Picture System. The learning task and all-night polysomnography were conducted at the homes of the adolescents. Slow (10–13 Hz) and fast (13–16 Hz) spindles were detected with automated algorithm. Neither post-sleep recognition accuracy nor spindle density differed between Val homozygotes and Met carriers. While frontal slow and fast spindle densities associated with better recognition accuracy in the entire sample, examining the allelic groups separately indicated paralleling associations in Val homozygotes only. Interaction analyses revealed a significant genotype-moderated difference in the associations between frontal fast sleep spindles and high arousal pictures. In sum, sleep spindles promote or indicate visual learning in Val homozygote adolescents but not in Met carriers. The result suggests that the role of sleep spindles in visual recognition memory is not equal across individuals but moderated by a common gene variant.
  • Popova, Dina; Castren, Eero; Taira, Tomi (2017)
    Recent studies demonstrate that chronic administration of the widely used antidepressant fluoxetine (FLX) promotes neurogenesis, synaptogenesis and synaptic plasticity in the adult hippocampus, cortex and amygdala. However, the mechanisms underlying these effects and how are they related to the clinical antidepressant efficacy are still poorly understood. We show here that chronic FLX administration decreases hippocampus-associated neophobia in naive mice. In parallel, electrophysiological recordings in hippocampal CA3-CA1 circuitry revealed that the FLX treatment resulted in increased short and long-term plasticity likely attributed to changes in presynaptic function. These changes were accompanied by enhancement in the expression of proteins related to vesicular trafficking and release, namely synaptophysin, synaptotagmin 1, MUNC 18 and syntaxin 1. Thus, chronic FLX administration is associated with enhanced synaptic dynamics atypical of mature CA1 synapses, elevated hippocampal plasticity, improved hippocampus-dependent behavior as well as altered expression of synaptic proteins regulating neurotransmitter trafficking and release. The results support the idea that antidepressants can promote neuronal plasticity and show that they can increase the functional dynamic range and information processing in synaptic circuitries. (C) 2017 Elsevier Ltd. All rights reserved.
  • Luchkina, Natalia V.; Huupponen, Johanna; Clarke, Vernon R. J.; Coleman, Sarah K.; Keinanen, Kari; Taira, Tomi; Lauri, Sari E. (2014)
  • Atanasova, Tsvetomira; Kharybina, Zoya; Kaarela, Tiina Anna Marjatta; Huupponen, Johanna Tuulia; Luchkina, Natalia; Taira, Tomi Petteri; Lauri, Sari Elina (2019)
    During the course of development, molecular mechanisms underlying activity-dependent synaptic plasticity change considerably. At immature CA3-CA1 synapses in the hippocampus, PKA-driven synaptic insertion of GluA4 AMPA receptors is the predominant mechanism for synaptic strengthening. However, the physiological significance of the developmentally restricted GluA4-dependent plasticity mechanisms is poorly understood. Here we have used microelectrode array (MEA) recordings in GluA4 deficient slice cultures to study the role of GluA4 in early development of the hippocampal circuit function. We find that during the first week in culture (DIV2-6) when GluA4 expression is restricted to pyramidal neurons, loss of GluA4 has no effect on the overall excitability of the immature network, but significantly impairs synchronization of the CA3 and CA1 neuronal populations. In the absence of GluA4, the temporal correlation of the population spiking activity between CA3-CA1 neurons was significantly lower as compared to wild-types at DIV6. Our data show that synapse-level defects in transmission and plasticity mechanisms are efficiently compensated for to normalize population firing rate at the immature hippocampal network. However, lack of the plasticity mechanisms typical for the immature synapses may perturb functional coupling between neuronal sub-populations, a defect frequently implicated in the context of developmentally originating neuropsychiatric disorders.
  • Tolmacheva, Aleksandra; Savolainen, Sarianna; Kirveskari, Erika; Lioumis, Pantelis; Kuusela, Linda; Brandstack, Nina; Ylinen, Aarne; Mäkelä, Jyrki P.; Shulga, Anastasia (2017)
    A large proportion of spinal cord injuries (SCI) are incomplete. Even in clinically complete injuries, silent non-functional connections can be present. Therapeutic approaches that can strengthen transmission in weak neural connections to improve motor performance are needed. Our aim was to determine whether long-term delivery of paired associative stimulation (PAS, a combination of transcranial magnetic stimulation [TMS] with peripheral nerve stimulation [PNS]) can enhance motor output in the hands of patients with chronic traumatic tetraplegia, and to compare this technique with long-term PNS. Five patients (4 males; age 38-68, mean 48) with no contraindications to TMS received 4 weeks (16 sessions) of stimulation. PAS was given to one hand and PNS combined with sham TMS to the other hand. Patients were blinded to the treatment. Hands were selected randomly. The patients were evaluated by a physiotherapist blinded to the treatment. The follow-up period was 1 month. Patients were evaluated with Daniels and Worthingham's Muscle Testing (0-5 scale) before the first stimulation session, after the last stimulation session, and 1 month after the last stimulation session. One month after the last stimulation session, the improvement in the PAS-treated hand was 1.02 +/- 0.17 points (p <0.0001, n = 100 muscles from 5 patients). The improvement was significantly higher in PAS-treated than in PNS-treated hands (176 +/- 29%, p = 0.046, n = 5 patients). Longterm PAS might be an effective tool for improving motor performance in incomplete chronic SCI patients. Further studies on PAS in larger patient cohorts, with longer stimulation duration and at earlier stages after the injury, are warranted.
  • Kaukinen, Sami (University of Helsinki, 1997)