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  • 1
    ISSN: 1432-1106
    Keywords: Cutaneous reflexes ; Long-Latency reflexes ; Precision grip ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hand muscle reflexes following muscle stretch and electrical nerve stimulation show a typical pattern consisting of short- and long-latency reflexes. The present investigation was designed to test reflexes following pure cutaneous stimulation. Air puffs were delivered to the palmar tip and the nail bed of the first, second and fifth fingers during isotonic contraction of hand muscles. The EMGs from the thenar muscles, the first dorsal interosseous muscle and the hypothenar muscles were recorded. Reflexes were obtained in all muscles, with a typical configuration consisting of a short-latency excitatory component (cutaneous longlatency reflex I, cLLR I) and a second excitatory component (cutaneous long-latency reflex II, cLLR II), with an inhibitory component between them. The size of cLLR II differed depending on the area stimulated and the muscle recorded. We found the largest responses always in the muscle acting on the stimulated finger. The reflex size depended on the strength of air puff stimulation. Allowing small displacements of the fingers led to an additional increase in the size of the reflex. The pattern of reflexes was identical independent of whether the finger tip or the nail bed was stimulated, but the size of the reflexes was smaller following nail bed stimulation. Following blockade of the cutaneous nerve branches of the thumb with local anaesthetics, air puff stimulation of the thumb no longer elicited this reflex pattern. Hence, under our experimental conditions, cutaneous receptors were the only source of afferent input for these reflexes. The results suggest that these cutaneous reflexes are mainly dedicated to controlling the stimulated finger independent of whether the palmar tip or the nail bed is stimulated. A possible physiological function is the adapting of grip force during handling of delicate objects if a perturbation is applied either to the object or the hand.
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  • 2
    ISSN: 1432-2072
    Keywords: Caudate nucleus ; Hippocampus ; Serotonin ; Dopamine ; Chlorimipramine ; Fluvoxamine ; 6-Nitroquipazine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Slices of rabbit hippocampus or caudate nucleus were incubated with [3H]-5-HT (0.1 µM, 60 min) or with [3H]-DA. In hippocampal tissue, the 5-HT uptake blockers chlorimipramine, fluvoxamine, and 6-nitroquipazine (0.1, 1, 10 µM) reduced the percentage content of [3H]-5-HT in a concentration dependent manner. The degree of inhibition of [3H]-5-HT content produced by the 5-HT uptake inhibitors was not affected by the MAO inhibitors pargyline or amezinium (which by themselves enhanced [3H] loading) or the catecholamine uptake inhibitor nomifensine (which by itself did not affect [3H] loading). In caudate nucleus tissue, however, the [3H]-5-HT accumulation was reduced only at the highest concentration of the 5-HT uptake blockers (10 µM). In the additional presence of the MAO inhibitors or nomifensine (which by themselves increased or diminished, respectively, the [3H] labelling) the 5-HT uptake inhibitors became more potent in reducing the percentage [3H]-5-HT accumulation of caudate nucleus slices. These results indicate (1) that a false labelling of [3H]-5-HT into dopaminergic terminals in the caudate nucleus can be prevented by nomifensine, (2) that the 5-HT uptake blockers seem to accumulate within the dopaminergic terminals, where they may display a MAO inhibitory property. The 5-HT uptake blockers were ineffective on the percentage tritium accumulation of caudate nucleus slices incubated with [3H]-DA, regardless of the presence of pargyline or nomifensine. Tritiated DA and deaminated [3H]-metabolites were separated in the superfusate of [3H]-DA-release experiments in caudate nucleus tissue. In the presence of 6-nitroquipazine the percentage efflux of unmetabolized [3H]-DA was significantly enhanced in a concentration and time dependent manner. In comparison to 6-nitroquipazine, fluvoxamine was less potent in that respect. 6-Nitroquipazine inhibited the electrically evoked [3H]-DA and [3H]-ACh release from caudate nucleus slices in a concentration dependent manner. The effects on [3H]-DA release were abolished in the presence of pargyline. The inhibition of [3H]-ACh release was significantly diminished by the D2-receptor antagonist domperidone. In conclusion, some 5-HT-related drugs may diminish the release of ACh from caudate nucleus slices via an enhanced dopaminergic transmission due to inhibition of MAO within the dopaminergic terminals.
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  • 3
    ISSN: 1432-1912
    Keywords: A1 adenosine receptors ; Serotonin release ; Hippocampus ; Caudate nucleus ; Rabbit ; Endogenous adenosine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of A1 adenosine receptor ligands on the evoked release of serotonin (5-HT) were studied in slices of the hippocampus and the caudate nucleus of the rabbit, preincubated with 3H-5-HT. In hippocampal tissue electrical stimulation elicited a release which was inhibited by the adenosine receptor agonist N6-cyclohexyladenosine (CHA) and enhanced by the selective A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). The concentration-response curve of CHA was shifted to the right by DPCPX. The shift corresponded to a pA2 value of 9.4 for DPCPX. CHA, R-N6-phenylisopropyladenosine (R-PIA) and DPCPX were ineffective in caudate nucleus tissue. When instead of electrical pulses high K+ was used to induce 5-HT release in the presence of the Na+ channel blocker tetrodotoxin (TTX), which was present in order to exclude effects mediated by interneurones, CHA was equally effective in the hippocampus but again failed to modify 5-HT release in the caudate nucleus. The disinhibition by DPCPX of the evoked 5-HT release was used to calculate the extracellular concentration of endogenous adenosine at the A1 receptor. The calculation greatly depended on the dissociation constant of adenosine at the A1 receptor. It is concluded that A1 adenosine receptors, activated by the endogenous agonist at a concentration of about 0.7 μmol/l, are located on serotonergic nerve endings in the hippocampus, but not in the caudate nucleus. The estimated extracellular concentration of endogenous adenosine is in reasonable agreement with actually measured concentrations reported in the literature.
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