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  • 1990-1994  (3)
  • Dorsal noradrenergic bundle  (1)
  • Fat pads  (1)
  • Tail flick latency  (1)
Materialart
Erscheinungszeitraum
  • 1990-1994  (3)
Jahr
Schlagwörter
  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Neuroradiology 33 (1991), S. 38-42 
    ISSN: 1432-1920
    Schlagwort(e): Facet joints ; Lumbar spine ; Joint inclusions ; Fat pads
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The polar recesses, superior and inferior to lumbar facet joints, are filled by fat pads from which fatfilled synovial folds project between the articular surfaces for a distance of two to four millimetres. The intracapsular superior recess lies between the ligamentum flavum and the lamina above. The extracapsular inferior recess lies on the back of the lamina below and communicates with the joint through a hole in the inferior capsule. The intracapsular folds move freely in and out of the joint during movements. These features are demonstrated in anatomic studies using transverse sections and radiologic studies using computed tomography. In about 4% of lumbar spines examined, the intraarticular fat pads are enlarged and extend from the joint recess(es) into the middle third of one or more facet joints. The fat pads can be identified in CT scans by their radiolucency and distinguished from vacuum phenomenon by measuring their attenuation values. The cause of the intra-articular enlargement of the fat pads is unknown, but it is suggested that their extension into the middle third of the joint may be secondary to degenerative change in the motion segment with capsular laxity in the affected joint.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-2072
    Schlagwort(e): Yohimbine ; Morphine ; Naloxone ; Withdrawal ; Tail flick latency ; Rat
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Noradrenergic neuronal hyperactivity following chronic morphine administration has been postulated to cause withdrawal signs and symptoms. Suppression of this hyperactivity, for example, by clonidine attenuates withdrawal. It might follow, therefore, that the prevention of suppression of noradrenergic systems during chronic morphine administration might diminish hyperactivity and prevent withdrawal. If the normalization of noradrenergic activity during opioid administration did not also suppress analgesia, it might be of medical and theoretical interest. To test this hypothesis, we gave the alpha-2-antagonist yohimbine to rats in order to increase noradrenergic activity during morphine treatment and then subsequently precipitated morphine withdrawal with naloxone. Six groups were examined: saline controls (N=11), morphine (N=11), morphine + 2.0 mg/kg/day yohimbine (N=15), morphine + 3.0 mg/kg/day yohimbine (N=5), 2.0 mg/kg/day yohimbine (N=11) and 3.0 mg/kg/day yohimbine (N=5). Subjects received 75 mg morphine pellets implanted on day 1,4 and 6 of the treatment or sham implantation. Yohimbine was delivered throughout the morphine treatment by subcutaneously implanted osmotic pumps. On day 7, all subjects were given 1.0 mg/kg naloxone and rated for behavioral signs of withdrawal. Analgesia was measured by observing tail flick latencies (TFL) before and after chronic drug treatments. Naloxone-precipitated withdrawal was characterized by irritability, ptosis, penile erection, diarrhea, rhinorrhea, abnormal posture, wetdog shakes, jumping, and teeth chattering, none of which were observed in groups receiving only saline or yohimbine. Withdrawal behavior was attenuated in a dose-dependent manner when yohimbine was administered during morphine treatment but analgesia was not attenuated. It appears that yohimbine-induced antagonism of alpha-2-adrenergic receptors diminishes the development of the potential for adrenergic hyperactivity and morphine withdrawal without reducing opioid analgesia.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Psychopharmacology 104 (1991), S. 377-385 
    ISSN: 1432-2072
    Schlagwort(e): Conditioned reinforcement ; Dopamine ; Noradrenaline ; d-Amphetamine ; Dorsal noradrenergic bundle ; Nucleus accumbens
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Three experiments examined the behavioural, pharmacological and neural specificity of the previously reported potentiation of responding with conditioned reinforcement following intra-accumbensd-amphetamine, by studying the effects of intraaccumbens dopamine (DA) and noradrenaline, using an acquisition of a new response procedure. In experiment 1, the effects of intra-cerebral DA infusions (5, 20, 50 µg/2 µl) were compared in four conditions: (i) intra-accumbens DA following positive pairing of the conditioned stimulus (CS) and water during training; (ii) as (i) but also following a systemic dose of the DA receptor antagonist alpha-flupenthixol; (iii) intra-accumbens DA following random pairing of the CS and water during training; and (iv) as (i) but with intra-caudate rather than intra-accumbens DA. The results showed that only with intra-accumbens DA in the positive pairing condition was there a significant dose-dependent increase in responding. In experiment 2, the effects of a higher range of doses (20, 100, 200 µg) and smaller infusion volume (5, 25, 50 µg/l µl) of intra-accumbens DA were studied, in comparison with a similar range of doses (5, 25, 50 µg/l µl) of intra-accumbens noradrenaline (NA). Only DA produced a selective, dose-dependent increase in responding with conditioned reinforcement. In experiment 3 neurotoxic lesions of the dorsal noradrenergic bundle (DNAB) using 6-hydroxydopamine producing profound (about 90%) depletion of cortical and nucleus accumbens NA levels had no effect on the increased responding with conditioned reinforcement produced by intra-accumbensd-amphetamine (3, 10, 30 µg/l µl). The results are discussed in terms of the neurochemical mediation of the potentiation of the effects of conditioned reinforcers byd-amphetamine and the role of DA-dependent mechanisms of the nucleus accumbens in reward-related processes.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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