Pilocarpine for anticholinergic adverse effects associated with desipramine treatment.
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Antidepressive Agents, Tricyclic↗
Biomedical subjects
R S Salah
Publications and source records attributed to R S Salah.
Tinnitus and ECT.
We report the case of a 69-year-old man with major depressive disorder and occupational tinnitus; both problems were refractory to several different treatment modalities, but were successfully treated with electroconvulsive therapy (ECT). The tinnitus was present for 15-20 years, but had worsened during the 3 years before treatment, causing him significant distress. Extensive organic workup did not identify a treatable etiology for his symptoms. To date, he has been hospitalized four times due to depressive symptoms associated with tinnitus. He has received ECT each time, and has responded well on each occasion.
Aged↗
Differential agonist profile of the enantiomers of 3-PPP at striatal dopamine autoreceptors: dependence on extracellular dopamine.
The effects of the enantiomers of 3-hydroxyphenyl-N-n-propylpiperidine (3-PPP) at dopamine (DA) synthesis modulating autoreceptors, measured as DOPA accumulation after decarboxylase inhibition, were assessed in vivo and in rat striatal slices. In vivo, (+)-3-PPP inhibited DOPA accumulation in the striatum, nucleus accumbens, and medial prefrontal cortex, whereas (-)-3-PPP either increased (striatal) or had no effect (accumbens, prefrontal cortex), on DOPA accumulation. In vitro, both (+)- and (-)-3-PPP reduced basal DOPA accumulation with a similar order of potency (apparent EC50 = 2.1 and 1.0 microns, respectively) and maximal effect, although they were less potent than the D2 DA receptor agonist quinpirole (EC50 = 0.15 microM). The inhibition of tyrosine hydroxylation was also observed in slices obtained from reserpine-pretreated rats and was blocked by the selective D2 DA antagonist (-)-sulpiride. This suggests that 3-PPP inhibition of DOPA accumulation was mediated directly by stimulation of DA D2 receptors. Increasing the amount of extracellular DA by depolarizing slices with 30 mM K+ did not alter the qualitative effects of either quinpirole or (+)-3-PPP. However, the stimulation of DA autoreceptors by (-)-3-PPP was no longer apparent under conditions of elevated extracellular DA. Under these depolarizing conditions, (-)-3-PPP actually antagonized the inhibitory effect afforded by either quinpirole or pergolide. A similar switch in profile was observed with transdihydrolisuride (TDHL). The data support the notion that (-)-3-PPP and TDHL are partial agonists at synthesis modulating DA autoreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Dopamine autoreceptors modulate the phosphorylation of tyrosine hydroxylase in rat striatal slices.
The hypothesis that dopamine (DA) autoreceptors modulate the phosphorylation of tyrosine hydroxylase (TH; EC 1.14.16.2) was investigated in rat striatal slices. Tissue was prelabeled with 32P inorganic phosphate, and TH recovered by immunoprecipitation with anti-TH rabbit serum. The TH monomer was resolved on sodium dodecyl sulfate polyacrylamide gels, and the extent of phosphorylation was determined by scanning densitometry of autoradiographs. Depolarization of striatal slices with 55 mM K+ markedly increased the incorporation of 32P into several proteins, including the TH monomer (Mr = 60,000). A similar increase in TH phosphorylation occurred in response to the adenylate cyclase activator forskolin and the cyclic AMP analog dibutyryl cyclic AMP. An increase in TH phosphorylation was not observed in response to the D1-selective agonist SKF 38393. The D2-selective DA autoreceptor agonist pergolide decreased the phosphorylation of TH below basal levels and blocked the increase in phosphorylation elicited by 55 mM K+. The inhibitory effect of pergolide was antagonized by the D2-selective antagonist eticlopride. Changes observed in the phosphorylation of TH were mirrored by changes in tyrosine hydroxylation in situ. These observations support the hypothesis that a reduction in TH phosphorylation is the mechanism by which DA autoreceptors modulate tyrosine hydroxylation in nigrostriatal nerve terminals.
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
The effects of central injections of adenosine analogs on blood pressure and heart rate in the rat.
Rats were implanted with chronic indwelling cannulae into the lateral cerebral ventricle. After recovery from surgery, acute experiments on blood pressure were conducted under methoxyflurane/nitrous oxide anesthesia. Rats were injected intracerebroventricularly with two adenosine analogs, 5'-N-ethylcarboxaminidoadenosine (NECA) and (-)-N-(1-methyl-2-phenylethyl)adenosine(L-phenylisopropyladenosine) (L-PIA), and the effects on blood pressure and heart rate recorded. Both analogs produced dose-related reductions in blood pressure and heart rate with L-PIA producing a more potent depression of heart rate than NECA. These effects on blood pressure and heart rate were antagonized by parenteral injections of caffeine. In separate experiments, the responses of blood pressure and heart rate to microinjection of NECA into the brainstem of rats anaesthetized with methoxyflurane/nitrous oxide were also examined. Microinjection of 2.7 nmol/kg into the fourth ventricle in the region of the area postrema produced a profound and long-lasting depression of blood pressure and heart rate. These results show that central injections of analogs of adenosine can influence the areas of the central nervous system involved in the control of cardiovascular function.
2-Chloroadenosine↗