Neuroscience
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Cardiorespiratory control neurons in the brainstem nucleus tractus solitarius (NTS) undergo dramatic expansion of dendritic arbors during the early postnatal period, when functional remodeling takes place within the NTS circuitry. However, the underlying molecular mechanisms of morphological maturation of NTS neurons are largely unknown. Our previous studies point to the neurotrophin brain-derived neurotrophic factor (BDNF), which is abundantly expressed by NTS-projecting primary sensory neurons, as a candidate mediator of NTS dendritogenesis. ⋯ Moreover, previously documented dramatic increases in NTS glial proliferation in victims of sudden infant death syndrome (SIDS) underscore the importance of our findings and the need to better understand the role of glia and their interactions with BDNF during NTS circuit maturation. Furthermore, while it has previously been demonstrated that the specific effects of BDNF on dendritic growth are context-dependent, the role of glia in this process is unknown. Thus, our data carry important implications for mechanisms of dendritogenesis likely beyond the NTS.
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Comparative Study
Differential maturation of the molecular clockwork in the olfactory bulb and suprachiasmatic nucleus of the rabbit.
Recent studies suggest that the main olfactory bulb (OB) represents a functional circadian pacemaker. In many altricial mammals, during pre-visual stages of development the olfactory system plays a vital role in their survival. One remarkable example is the European rabbit; the newborns are normally raised in a dark nursery burrow, and the lactating female briefly visits her young approximately once every 24 h. ⋯ We report for the first time that Per1, Cry1, and Bmal1 are expressed in the OB of newborn and juvenile rabbits. In addition, the diurnal pattern of clock gene expression develops earlier in the OB than in the SCN of newborn rabbits. Given the early maturation of the molecular clockwork and the biological relevance of this structure during development, it is possible that the OB plays an important role in temporal regulation during pre-visual life in rabbits.
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Human movements are quickly adjusted to variations of inertial load. However, this adjustment does not always imply a full compensation, so that kinematic movement characteristics vary. The present experiment served to explore the consequences of a complex dynamic transformation, implemented by a sliding first-order lever, on the endpoint distributions of goal-directed movements. ⋯ However, when the lever was used, the effect of the inertial anisotropy of the arm on movement amplitudes was reduced, accompanied by a longer movement time overall, in particular for movements with higher inertial load of the arm. These observations suggest an interaction of the use of internal models and impedance control in the presence of variable inertial loads. Most likely the influence of the dynamic transformation of the sliding lever is absorbed by increased joint impedance, which also reduces the influence of the inertial anisotropy of the arm which otherwise is (incompletely) compensated based on an internal model of the dynamic transformation of the arm.
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Metabotropic glutamate receptors (mGluR) can control neuronal excitability by modulating several ionic channels. In hippocampal pyramidal cells, groups I/II mGluR are located extrasynaptically, suggesting that their endogenous activation is dependent on the glutamate clearance rate and therefore on excitatory amino-acid transporters (EAAT) efficiency. Deficiency of glutamate uptake can generate seizures in rodents and has been suggested as a mechanism of seizure generation in some human epileptic syndromes. ⋯ Moreover, this endogenous activation of groups I/II mGluR leads to (i) the reduction of the slow afterhyperpolarization current (I(sAHP)), increasing the firing pattern of pyramidal cells, and (ii) the potentiation of extrasynaptic NMDAR-mediated responses, enabling glutamate spillover to generate a suprathreshold depolarization for several seconds. Our data show that an insufficient buffering of extracellular glutamate enables a cross talk between groups I/II mGluR and NMDAR, which, combined with a decrease of I(sAHP), leads to the hyperexcitability of the hippocampal network, facilitating the genesis of epileptical-like activity in response to glutamate release. These findings highlight the importance of the control exerted by EAAT on mGluR.
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We investigated the role of inositol 1, 4, 5-trisphosphate receptors (IP3Rs) that were activated during preconditioning low-frequency afferent stimulation (LFS) in the subsequent induction of synaptic plasticity in CA1 neurons in hippocampal slices from mature guinea pigs. In standard perfusate, long-term potentiation (LTP) was induced in the field excitatory postsynaptic potential (EPSP) by the delivery of LFS (80 pulses at 1 Hz), and was reversed by an identical LFS applied 20 min later. ⋯ The excitatory postsynaptic current (EPSC) through NMDARs recorded from CA1 pyramidal neurons increased significantly 20 min after a single LFS and this increase was inhibited when the LFS was delivered in the presence of an IP3R antagonist or a Ca(2+)/calmodulin-dependent protein kinase II inhibitor. These results suggest that activation of IP3Rs by a preconditioning LFS results in postsynaptic protein phosphorylation and/or enhancement of NMDAR activation during a subsequent LFS, leading to reversal of LTP in the field EPSP in hippocampal CA1 neurons.