Brain research
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In standing humans, it is not certain whether anticipatory postural adjustments associated with rapid, voluntary elbow flexion movements (focal movements) originate as a selection from preset synergies or as the result of specific planning of motor commands. We studied these muscle recruitment patterns when the same focal movement was made under behavioral conditions of a self-paced task (SPT) and a reaction-time task (RTT). While standing still, eight normal subjects performed focal movements under the SPT and RTT behavioral conditions and under three different biomechanical conditions: (1) unloaded-upright, (2) loaded-upright (holding a 3800-g metal bar), and (3) unloaded-forward leaning. ⋯ The amplitude, timing, and net movements of lower extremity joints were influenced by the behavioral conditions. However, the behavioral conditions significantly affected the phasing (including order of activation) and duration of anticipatory postural EMG activity and the phasing of COP displacements under certain biomechanical conditions. These findings support the theory that anticipatory postural adjustments are planned in detail.
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Subcutaneously (s.c.) administered [Arg8]vasopressin (AVP) potentiated seizures induced by intracerebroventricular (i.c.v.) injection of 1.95 mg pilocarpine (a muscarinic cholinergic agonist). A bell-shaped relation between dose and effect was found. I.c.v. pretreatment with a V1, V2 or oxytocin receptor antagonist was performed to determine whether and what type of receptor is involved in this proconvulsive effect of vasopressin. ⋯ Several selective antidiuretic agonists (V2), such as d[Val4]AVP, d[Phe2,Val4,D-Arg8]vasopressin (3 microg), [Val4,D-Arg8]vasopressin (3 microg) and d[Val4,D-Arg8]vasopressin (3 microg) were active. Other selective antidiuretic compounds, such as [Val4]AVP, dAVP, d[Tyr(Me)2]AVP and HO[D-Arg8]vasopressin (3 microg) did not influence seizures. These results demonstrate that a combination of substitution of aminoacid 4 (Gln) by Val and to a lesser extent deamination and the D-arginine form yield an active molecule, which can potentiate pilocarpine induced seizures and suggest the existence of a V2 receptor subtype in the brain.
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Nerve injury leads to central neuroimmunologic responses that may be integral to the development and maintenance of chronic neuropathic pain in humans. Recent data have demonstrated that cytokines and growth factors may be strongly implicated in the generation of pain states at both peripheral and central nervous system sites. We utilized immunohistochemical methods to investigate this phenomenon in rat models of neuropathic pain. ⋯ This study demonstrated increased specific cytokine and growth factor-like expression in the spinal cord following peripheral nerve injuries. It also showed a differential expression of bFGF in two distinct mononeuropathy models. These results provide further evidence that central cytokine production via a neuroimmune cascade may be involved in the development and maintenance of behaviors that mimic neuropathic pain following nerve injury.