Neuroscience
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We hypothesised that, since anomalous neck proprioceptive input can produce perturbing effects on posture, neck muscle fatigue could alter body balance control through a mechanism connected to fatigue-induced afferent inflow. Eighteen normal subjects underwent fatiguing contractions of head extensor muscles. Sway during quiet stance was recorded by a dynamometric platform, both prior to and after fatigue and recovery, with eyes open and eyes closed. ⋯ Contractions of the same duration, but not inducing EMG signs of fatigue, had much less influence on body sway or subjective scoring. We argue that neck muscle fatigue affects mechanisms of postural control by producing abnormal sensory input to the CNS and a lasting sense of instability. Vision is able to overcome the disturbing effects connected with neck muscle fatigue.
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Comparative Study
Localization of KCNQ5 in the normal and epileptic human temporal neocortex and hippocampal formation.
The KCNQ family of voltage-dependent non-inactivating K+ channels is composed of five members, four of which (KCNQ2-5) are expressed in the CNS and are responsible for the M-current. Mutations in either KCNQ2 or KCNQ3 lead to a hereditary form of dominant generalized epilepsy. Using specific antisera to the KCNQ2, KCNQ3 and KCNQ5 subunits, we found that KCNQ3 co-immunoprecipitated with KCNQ2 and KCNQ5 subunits, but no association was detected between KCNQ2 and KCNQ5. ⋯ In the sclerotic areas of the CA fields of epileptic patients, a marked loss of KCNQ5 immunoreactive pyramidal neurons was found in relation with the loss of neurons in these regions. However, in the regions adjacent to the sclerotic areas, the distribution and intensity of KCNQ5 immunostaining was apparently normal. The widespread distribution of KCNQ5 subunits, its persistence in pharmacoresistant epilepsy, along with the significant role of the M-current in the control of neuronal excitability, makes this protein a possible target for the development of anticonvulsant drugs.
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Hypocretin/orexin modulates sleep-wake state via actions across multiple terminal fields. Within waking, hypocretin may also participate in high-arousal processes, including those associated with stress. The current studies examined the extent to which alterations in neuronal activity, as measured by Fos immunoreactivity, occur within both hypocretin-synthesizing and hypocretin-1 receptor-expressing neurons across varying behavioral state/environmental conditions associated with varying levels of waking and arousal. ⋯ Additionally, these data suggest that waking per se may not be associated with increased hypocretin neurotransmission. In contrast, high-arousal states, including stress, appear to be associated with substantially higher rates of hypocretin neurotransmission. Finally, these studies provide further evidence indicating coordinated actions of hypocretin across a variety of arousal-related basal forebrain and brainstem regions in the behavioral state modulatory actions of this peptide system.
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Overexpression of dopamine D(2) receptors by adenoviral vector-mediated gene transfer in the rat striatum was evaluated by positron emission tomography in vivo and by ex vivo autoradiography in 5-, 13-, and 24-month-old Fischer 344 rats. Each rat had hemilateral gene transfer of D(2) receptors mediated by adenoviral vectors (AdCMV. DopD(2)R) in the striatum with contralateral striatal injection of control vectors (AdCMV. ⋯ A group of rats underwent follow-up assessment by positron emission tomography. The overexpression of D(2) receptors decreased with time in all three groups; however, the decrease rate of the D(2) receptors expression was significantly smaller in the 24-month-old group than in the 5-month-old group. We confirmed that the adenoviral vector-mediated gene transfer of D(2) receptors compensated the decreased density of striatal D(2) receptors in the 24-month-old rats up to the level in the control striatum of 5-month-old rats, and the decrease rate of the overexpression was significantly smaller in aged rats.
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Comparative Study
Temporal pattern of hippocampal high-frequency oscillations during sleep after stimulant-evoked waking.
Hippocampal ripple oscillations (140-200 Hz) are believed to be critically involved in the consolidation of memory traces during slow-wave sleep (SWS). We investigated the temporal pattern of ripple occurrence in relation to sleep phases following different types of waking. Amphetamine, the atypical wakening drug modafinil or non-pharmacological sleep deprivation lead to an increased ripple occurrence ("rebound") during the subsequent SWS episode. ⋯ At the end of the recovery period paradoxical sleep (PS) acted like waking, elevating ripple occurrence during subsequent SWS episodes. On the other hand, PS decreased ripple occurrence if recovery from the rebound was not yet complete. Thus occurrence and structure of ripple oscillations are regulated by the timing and duration of previous SWS, PS and waking episodes.