Disease relevance of p-Chloramphetamine

• Injection of 2.5,5, 10, or 20 milligrams of p-chloroamphetamine per kilogram of body weight into rats produced evidence of cytopathological changes in sections of brain stained by a Nissl or silver method [1].
• A single dose of p-chloroamphetamine, 10 mg per kilogram, produced postural abnormalities, tremor, myoclonus, and autonomic signs in rats 5 minutes after intraperitoneal injection [2].
• Midalcipran enhanced the behavioral changes induced by 1-tryptophan in the rat and antagonized p-chloramphetamine-induced hyperthermia in mice [3].
• The lesions produced a significant hyperalgesia and strongly attenuated the analgesic effect of PCA in the hot-plate test [4].
• The influence of D- and L-amphetamine, fenfluramine, and p-chloroamphetamine on female copulatory behavior (lordosis response) and the induction of stereotype activity was compared [5].

Psychiatry related information on p-Chloramphetamine

• PCA- but not SCOP-induced amnesia was attenuated by the post-training administration of two benzomorphans, (+)N-allylnormetazocine ((+)SKF-10,047) and (+/- )pentazocine ((+/- )PTZ) [6].
• The behavioural results showed that the pCA lesion caused a transient increase in impulsivity whereas the 5,7-DHT lesion temporarily reduced the motor activity and slightly impaired choice accuracy [7].
• RESULTS: Of the test compounds, PCA, DOI and 8-OH-DPAT increased reaction times, whereas ritanserin reduced them [8].
• p-Chlorophenylalanine and p-chloroamphetamine pretreatment of apomorphine-challenged rats: effects on solitary and social behavior [9].
• The acute effects of p-chloroamphetamine (PCA) on one-way active avoidance learning and on central monoamine concentrations were examined in the male rat [10].

High impact information on p-Chloramphetamine

• Third, knockout mice for alpha1b-adrenergic (alpha1b-AR KO) or 5-HT(2A) (5-HT(2A)-R KO) receptor, respectively, exhibit a behavioral and biochemical hyperreactivity to the acute injection of p-chloroamphetamine (alpha1b-AR KO; 5-HT levels) and d-amphetamine (5-HT(2A)-R KO; NE levels) [11].
• Plasma from p-chloroamphetamine-treated, nephrectomized rats was used to obtain the renin-releasing factor, which was fractionated by ultrafiltration into fractions of molecular weight ranges of 1000 to 5000, 5000 to 10,000, and 10,000 to 20,000 [12].
• The third comes from experiments in which rats were treated with p-chloroamphetamine and 5,7-dihydroxytryptamine (serotonin neurotoxins), 6-hydroxydopamine (catecholamine neurotoxin), or p-chlorophenylalanine (inhibitor of tryptophan hydroxylase) [13].
• Fos expression was blocked by p-chloroamphetamine, a serotoninergic neurotoxin [14].
• Because increases in 5-HT transmission result in concomitant multiple 5-HT receptor activation, the effects of the 5-HT releasing compound p-chloroamphetamine (PCA) were compared with those of the selective 5-HT1A receptor agonist 8-OH-DPAT in the rat [15].

Chemical compound and disease context of p-Chloramphetamine

• The effects of p-chloroamphetamine administration on locomotor activity and serotonin in neonatal and adult rats [16].
• However, the AChE inhibitors, tetrahydroaminoacridine (THA) and physostigmine (PHY) attenuated both PCA- and SCOP-induced amnesia when administered immediately after the training session [6].
• p-Chloroamphetamine antagonism of cobaltous chloride-induced hypothermia in mice [17].
• The dopamine depleter alpha-methyl-p-tyrosine significantly reduced p-chloroamphetamine-induced hyperthermia [18].
• The effects of the amphetamine derivatives (+/-)-amphetamine (A), 2-, 3- and 4-chloroamphetamine (CA), 4-methylamphetamine (MA) and chlorphentermine (CP) in producing central stimulation (increase in motor activity), antagonism of the reserpine syndrome, potentiation of 1-dopa and 5-hydroxytryptophan (5HTP) responses in mice were investigated [19].

Biological context of p-Chloramphetamine

• This effect was mimicked by another substituted amphetamine, p-chloroamphetamine (pCA), but with a temporal-response curve that was to the left of MDMA's. However, pure uptake inhibitors like fluoxetine, cocaine, and the selective 5-HT2A/2C agonist, DOB, were unable to produce a long-lasting translocation of PKC binding sites in rat cortex [20].
• Significant increases in urinary excretion of sodium (UNa V) and the Na/K ratio were observed after the administration of p-chloroamphetamine (200-600 micrograms i.v.t.). p-Chloroamphetamine in large doses also increased blood pressure and antidiuresis [21].
• The reduced effect of PCA may have been caused by down-regulation of 5-HT2 receptors [22].
• Metabolic activation of the serotonergic neurotoxin para-chloroamphetamine to chemically reactive intermediates by hepatic and brain microsomal preparations [23].
• Neither PCPA nor PCA treatment altered the maximal level of 5-HT2A receptor-mediated PI hydrolysis [24].

Anatomical context of p-Chloramphetamine

• Since previous studies have shown that lesions in the hypothalamus prevent the effect of p-chloroamphetamine on renin secretion, we tested whether a hypothalamic extract can release renin from kidney slices [12].
• [3H]paroxetine binding and serotonin content of rat cortical areas, hippocampus, neostriatum, ventral mesencephalic tegmentum, and midbrain raphe nuclei region following p-chlorophenylalanine and p-chloroamphetamine treatment [25].
• A single injection of pCA reduces 5HT levels in the above mentioned brain regions as well as in the brain stem [26].
• PCA is injected subcutaneously; this route of administration avoids mechanical disruption of the blood brain barrier [27].
• Release of 5-HT by PCA produced a rapid and severe reduction of phrenic nerve activity [28].

Associations of p-Chloramphetamine with other chemical compounds

• The effects of p-chloroamphetamine and d-fenfluramine on 5-HIAA in brain, CSF, and plasma were nonsignificant [29].
• In vivo comparisons of the stereoisomers of methylenedioxymethamphetamine indicated two phases of serotonin depletion similar to those reported for p-chloroamphetamine [30].
• Furthermore, selective denervation of 5-HT projections by p-chloroamphetamine treatment attenuated the increase in zif268 and c-fos expression induced by cocaine in the striatum [31].
• In particular, our data suggest that the neurotoxic action of p-chloroamphetamine may not be targeted solely on serotonergic axons and terminals of the dorsal raphe nucleus but includes those of the median raphe nucleus [32].
• Exposure to footshock (1 mA) for 30 sec induced a marked analgesia that was enhanced by pretreatment with the 5HT synthesis inhibitor, p-chlorophenylalanine, and attenuated by the 5HT releasing drugs p-chloroamphetamine and fenfluramine, by the 5HT re-uptake inhibitor, fluoxetine and by the 5HT agonists, 5-methoxy-N,N-dimethyltryptamine and MK212 [33].

Gene context of p-Chloramphetamine

• However, it has not been determined whether BDNF promotes the survival of 5-HT axons during PCA-insult or facilitates their regenerative sprouting after injury [34].
• After a single subcutaneous injection of para-chloroamphetamine (PCA; 9 mg/ml) that lesions the majority of serotonergic axons in the rat cortex, we injected adenoviral vectors containing cDNAs for brain-derived neurotrophic factor (Adv.BDNF), neurotrophin-3 (Adv.NT-3), or nerve growth factor (Adv.NGF) into the rat frontal cortex [35].
• Moreover, our results indicate that p-chloroamphetamine-induced hyperglycemia is mediated by 5-HT1A and 5-HT2B/2C receptors [36].
• 5-HT1A agonist and dexamethasone reversal of para-chloroamphetamine induced loss of MAP-2 and synaptophysin immunoreactivity in adult rat brain [37].
• The 5-HT3 receptor antagonists ICS 205-930 (50 nM) and MDL 72222 (100 nM) prevented this facilitation caused by 100 nM p-chloroamphetamine [38].

Analytical, diagnostic and therapeutic context of p-Chloramphetamine

• The microglial response was maximal 3 weeks after PCA treatment, became less evident 6 weeks after treatment, and by 9 weeks no difference was observed between treated and control rats [27].
• Thus, the avoidance deficit caused by PCA is independent of the descending serotonergic pathways and of the analgesia induced by PCA [4].
• 5-HT was depleted by either multiple p-chlorophenylalanine (pCPA) or PCA injections.The extent of 5-HT depletion following pCPA or PCA was monitored using 5-HT immunocytochemistry [39].
• In the flinch-jump test 5,6-DHT lesioned rats receiving PCA did not differ from the saline control group [4].
• Furthermore, the amount of 5-hydroxytryptamine released by electrical stimulation of either the dorsal raphe nucleus or median raphe nucleus was markedly reduced in rats pretreated with p-chloroamphetamine [32].

References