Neuroscience letters
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Neuroscience letters · May 2009
Comparative StudyElectrical and magnetic repetitive transcranial stimulation of the primary motor cortex in healthy subjects.
Repetitive transcranial magnetic stimulation (rTMS) delivered in short trains at 5Hz frequency and suprathreshold intensity over the primary motor cortex (M1) in healthy subjects facilitates the motor-evoked potential (MEP) amplitude by increasing cortical excitability through mechanisms resembling short-term synaptic plasticity. In this study, to investigate whether rTES acts through similar mechanisms we compared the effects of rTMS and repetitive transcranial electrical stimulation (rTES) (10 stimuli-trains, 5Hz frequency, suprathreshold intensity) delivered over the M1 on the MEP amplitude. Four healthy subjects were studied in two separate sessions in a relaxed condition. rTMS and anodal rTES were delivered in trains to the left M1 over the motor area for evoking a MEP in the right first dorsal interosseous muscle. ⋯ The MEP elicited by single-pulse TES delivered during muscle contraction had a smaller amplitude than the last MEP in the rTES trains. Repetitive supraorbital nerve stimulation left the conditioned MEP unchanged. Our results suggest that 5 Hz-rTES delivered in short trains increases cortical excitability and does so by acting on the excitatory interneurones probably through mechanisms similar to those underlying the rTMS-induced MEP facilitation.
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Neuroscience letters · May 2009
Intrathecal oxybuprocaine and proxymetacaine produced potent and long-lasting spinal anesthesia in rats.
Proxymetacaine and oxybuprocaine were clinically used for topical ocular anesthesia but never for spinal anesthesia, and therefore spinal anesthetic effects of proxymetacaine and oxybuprocaine were performed and compared with bupivacaine and lidocaine. After rats were injected intrathecally with proxymetacaine, oxybuprocaine, bupivacaine, and lidocane, dose-response curves were constructed. We evaluated the potencies (ED(50)) and durations (time to full recovery) of proxymetacaine and oxybuprocaine on spinal blockades of motor function, proprioception, and nociception and compared with bupivacaine and lidocaine in rats. ⋯ Intrathecal proxymetacaine, oxybuprocaine, and bupivacaine also produced longer sensory blockade than motor blockade. These data demonstrated that oxybuprocaine and proxymetacaine produced more potent spinal blockades, when compared with bupivacaine or lidocaine. Oxybuprocaine and bupivacaine with a more sensory-selective action over motor blockade produced longer spinal blockade than did proxymetacaine or lidocaine.
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Neuroscience letters · May 2009
Inhibitory effect of selective serotonin reuptake inhibitors on the vesicular monoamine transporter 2.
The neuronal vesicular monoamine transporter (VMAT2) is the target molecule of action of some psychostimulants, such as methamphetamine and 3,4-methylenedioxymethamphetamine (MDMA). The present study examined the effect of antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), on VMAT2 activity by measuring adenosine triphosphate-dependent [(3)H]dopamine uptake into synaptic vesicles prepared from rat striatum. SSRIs, fluoxetine, paroxetine, and fluvoxamine, inhibited vesicular [(3)H]dopamine uptake in vitro. ⋯ Moreover, kinetic analysis revealed that inhibition by reserpine, a typical VMAT2 inhibitor, was uncompetitive, decreasing maximum velocity and affinity for dopamine. Inhibition by fluoxetine was noncompetitive, only decreasing maximum velocity for dopamine. These results suggest that fluoxetine inhibited the activity of VMAT2 by a mechanism different from that of reserpine and did not directly interact with the active site of VMAT2.
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Neuroscience letters · Apr 2009
Anatibant, a selective non-peptide bradykinin B2 receptor antagonist, reduces intracranial hypertension and histopathological damage after experimental traumatic brain injury.
Bradykinin, the main metabolite of the kallikrein-kinin system and one of the first mediators released during inflammation, is well known to increase the permeability of the blood brain barrier (BBB) by activation of kinin B2 receptors and hence promote brain edema formation following traumatic brain injury (TBI). Anatibant (LF 16-0687), a selective non-peptide bradykinin B2 receptor antagonist, reduces brain edema after experimental TBI, however, so far no data are available if Anatibant reduces also the sequels of brain edema formation, i.e. morphological brain damage. Therefore, we investigated the effect of Anatibant (3.0 mg/kg b.w.) on intracranial pressure (ICP) and contusion volume after experimental TBI. ⋯ ICP was measured 3, 6, and 10 h after injury and contusion volume was quantified 24 h after trauma. Our data demonstrate a significant reduction of ICP (16.6+/-1.67 mmHg vs. 24.40+/-3.58 mmHg; n=6; p=0.002) and of contusion volume 24 h after trauma (28.28+/-5.18 mm3 vs. 35.0+/-3.32 mm3 n=7; p=0.003) in treated mice. Therefore we conclude, that inhibition of bradykinin B2 receptors seems to be a promising treatment option, and might therefore be investigated in clinical trails for the treatment of TBI.
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Neuroscience letters · Apr 2009
Electrophysiology reveals semantic priming at a short SOA irrespective of depth of prime processing.
The otherwise robust behavioral semantic priming effect is reduced to the point of being absent when a letter search has to be performed on the prime word. As a result the automaticity of semantic activation has been called into question. It is unclear, however, in how far automatic processes are even measurable in the letter search priming paradigm as the prime task necessitates a long prime-probe stimulus-onset asynchrony (SOA). ⋯ Stimuli were presented at two different SOAs (240 ms vs. 840 ms) and participants performed either a grammatical discrimination (Experiment 1) or a letter search (Experiment 2) on the prime. Irrespective of prime task, the modulation of the N400, the ERP correlate of semantic activation, provided clear-cut evidence of semantic processing at the short SOA. Implications for theories of semantic activation as well as the constraints of the delayed prime task procedure are discussed.