Subject(s)
Androstadienes/therapeutic use , Anti-Inflammatory Agents/therapeutic use , Dermatitis, Atopic/drug therapy , Dermatologic Agents/therapeutic use , Psoriasis/drug therapy , Administration, Topical , Adult , Androstadienes/adverse effects , Anti-Inflammatory Agents/adverse effects , Child , Chronic Disease , Dermatologic Agents/adverse effects , Fluticasone , Glucocorticoids , HumansABSTRACT
In the human thalamic ventralis lateralis nucleus the spontaneous activity of 235 single units during 38 stereotactic operations in locally anaesthetized parkinsonian patients was analysed. Two basic cell types (A and B) were shown to exist in this nucleus: (i) with unitary irregular (2-40/s) discharges characterized by a tendency to spike grouping in the range of 4-6 Hz and 10-30 Hz (A-type, 74%), (ii) with bursting discharges firing in short trains (5-30 ms) characterized by an unstable rhythmic 3-6 Hz pattern similar to a low-threshold Ca2+ intrinsic burst structure of discharges (B-type, 26%). The functional brain changes after a motor tests performance were accompanied by the appearance of two different transient modifications of activity of A-cells pattern into rhythmic burst discharges: (i) in the range of 3-6 Hz, similar to the bursts found for B-cells and recorded mainly in the anterior ventrolateral region in rigid patients, (ii) in the range of 5 +/- 1 Hz, characterized by other interspike interval and recorded in the posterior ventrolateral region in patients with tremor. Modifications during short-term anaesthesia resulted in 10-15 Hz burst discharges that were associated with gradual disappearance of A-cells activity. In contrast to what happens for A-cells, the activity of bursting B-units was characterized by an invariant intrinsic structure of discharges irrespective of the functional brain changes or the forms of parkinsonian pathology. The nature of A- and B-units as well as the mechanisms of transient modifications of their spontaneous activity patterns due to the functional brain changes are discussed.
Subject(s)
Motor Neurons/physiology , Parkinson Disease/physiopathology , Thalamic Nuclei/cytology , Thalamic Nuclei/physiology , Action Potentials/drug effects , Action Potentials/physiology , Anesthetics, Intravenous/administration & dosage , Electromyography , Evoked Potentials/drug effects , Evoked Potentials/physiology , Humans , Parkinson Disease/complications , Propanidid/administration & dosage , Psychomotor Performance , Sleep/physiology , Tremor/etiology , Tremor/physiopathology , Wakefulness/physiologyABSTRACT
The study examined the potentiation of the antinociceptive action of opioid analgesics produced by gaseous superoxide (GS) in the rat hind paw withdrawal test (PWT) and by GS or hydrogen peroxide (HP) in the formalin test. In the PWT, inhalation of GS for 50 minutes before i.p. injection of threshold doses of morphine (0.5 mg/kg) and trimeperidine (1.0 mg/kg) increased the threshold of nociception (TN) by a maximum of 43.0% (p < 0.05) and 113.4% (p < 0.01) respectively. The GS/trimeperidine-dependent increase in TN showed two peaks, the second of which could be suppressed by nialamide. Naloxone abolished the GS/ morphine-dependent increased in the TN. In the formalin test, a significant antinociceptive effect developed after GS inhalation or HP administration (intranasally, 2 x 5 microliters of 2 x 10(-5) mol/l solution in saline) in combination with low doses of Omnopon (0.06-0.75 mg/kg). These results suggest that both GS and HP potentiate the antinociceptive effects of opioid analgesics.
Subject(s)
Analgesics, Opioid/pharmacology , Superoxides/pharmacology , Animals , Drug Synergism , Free Radicals , Male , Morphine/pharmacology , Naloxone/pharmacology , Nialamide/pharmacology , Promedol/pharmacology , Rats , Superoxide Dismutase/pharmacologyABSTRACT
The tripeptide glutamyl-arginyl-proline (ERP) mimicking some structural features of the N-terminal fragment of adrenocorticotropic hormone, ACTH(5-7), has been synthesized. In contrast with ACTH fragments, ERP (0.015-0.15 mg/kg; intraperitoneal injection) hindered the formation of food-reinforced task in adult albino male rats. Besides, ERP caused a rapid inhibition of the previously formed conditioned task. Similar doses of ERP changed orientative-trying reaction and emotional behavior in rats in the 'open field' test. ERP at a dose of 0.15 mg/kg administered prior to the injection of 0.5 mg/kg ACTH(1-39) prevented increases in locomotor activity normally induced by this hormone. Thus, ERP disrupts learning, impairs performance of acquired task and blocks behavioral effects of ACTH and its fragments.
