IMMEDIATE AND LONG‐TERM EFFECTS OF p‐CHLOROAMPHETAMINE ON BRAIN AMINES*

Sanders‐Bush, Elaine; Steranka, Larry R.

doi:10.1111/j.1749-6632.1978.tb31525.x

Cited by 107 publications

(35 citation statements)

References 45 publications

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“…The finding that pCA pretreatment af fected brain 5-HT levels selectively is consis tent with the view that the persistent, long term biochemical effects of this drug are spe cific to the 5-HT neuronal system [5,16,21], In addition to the present replication of a decrease in 5-HT levels, pCA has been dem onstrated to decrease 5-HIAA levels, trypto phan hydroxylase activity, 5-HT uptake and turnover [21]. All these effects have been attributed to a single mechanism: B-9 cell group degeneration [7,17], The finding that 21-day lithium administration did not affect NE or DA brain levels is also consistent with other reports [1,9,23].…”

Section: Discussionmentioning

confidence: 57%

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Effect of Serotonin Depletion Induced by <i>p</i>-Chloroamphetamine on Changes in Rats’ Activity Levels Produced by Lithium

Cappeliez¹,

White²,

Duhamel³

1982

Neuropsychobiology

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The role of serotonin (5-HT) transmission in the production of changes in rats’ activity levels induced by 0.15 and 1.50 mEq/kg LiCl was assessed by selectively depleting 5-HT brain levels with p-chloroamphetamine prior to chronic administration of LiCl for 21 days. While p-chloroamphetamine pretreatment decreased 5-HT levels by 56%, irrespective of the fact that the animals had been administered either saline, 0.15, or 1.50 mEq/kg LiCl for 21 days, it did not alter the effects that each LiCl dose alone had on activity levels. Both LiCl administrations produced an 18% increase in 5-HT levels in rats pretreated with saline, yet diametrically opposed effects on activity levels. A parallel is drawn between these biochemical findings and previously reported data indicating that both LiCl doses produce an improvement in selective attention, yet opposed effects on rats’ activity levels. The hypothesis that 5-HT transmission might be crucially involved in mediating the dose-independent effect of lithium on selective attention is proposed for future research.

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Section: Discussionmentioning

confidence: 57%

“…The persistent, long-term biochemical effect of p-chloroamphetamine seems to be a specific depletion of 5-HT from neurones that contain this substance [5,21].…”

mentioning

confidence: 99%

Effect of Serotonin Depletion Induced by <i>p</i>-Chloroamphetamine on Changes in Rats’ Activity Levels Produced by Lithium

Cappeliez¹,

White²,

Duhamel³

1982

Neuropsychobiology

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“…In particular, after certain dosing conditions, MDMA (Green et al, 2003), PCA (Sanders-Bush and Steranka, 1978;Fuller, 1992), and FEN (Schuster et al, 1986;Appel et al, 1989Appel et al, , 1990McCann et al, 1997) produce long-term reductions in the concentrations of 5-HT and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA), the activity of 5-HT's rate limiting synthetic enzyme, tryptophan hydroxylase (TPH), and the abundance of membrane and vesicular 5-HT transporters, as measured by [ 3 H]paroxetine and [ 3 H]DTBZ binding, respectively. In addition, tract-tracing studies after MDMA show reduced anterograde [ 3 H]proline transport along ascending 5-HT axonal projections (Callahan et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Loss of Serotonin Transporter Protein after MDMA and Other Ring-Substituted Amphetamines

Xie

Tong

McLane

et al. 2006

Neuropsychopharmacol

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We studied in vivo expression of the serotonin transporter (SERT) protein after 3,4-methylenedioxymethamphetamine (MDMA), p-chloroamphetamine (PCA), or fenfluramine (FEN) treatments, and compared the effects of substituted amphetamines to those of 5,7-dihydroxytryptamine (5,7-DHT), an established serotonin (5-HT) neurotoxin. All drug treatments produced lasting reductions in 5-HT, 5-HIAA, and [ 3 H]paroxetine binding, but no significant change in the density of a 70 kDa band initially thought to correspond to the SERT protein. Additional Western blot studies, however, showed that the 70 kDa band did not correspond to the SERT protein, and that a diffuse band at 63-68 kDa, one that had the anticipated regional brain distribution of SERT protein (midbrain4 striatum4neocortex4cerebellum), was reduced after 5,7-DHT and was absent in SERT-null animals, was decreased after MDMA, PCA, or FEN treatments. In situ immunocytochemical (ICC) studies with the same two SERT antisera used in Western blot studies showed loss of SERT-immunoreactive (IR) axons after 5,7-DHT and MDMA treatments. In the same animals, tryptophan hydroxylase (TPH)-IR axon density was comparably reduced, indicating that serotonergic deficits after substituted amphetamines differ from those in SERT-null animals, which have normal TPH levels but, in the absence of SERT, develop apparent neuroadaptive changes in 5-HT metabolism. Together, these results suggest that lasting serotonergic deficits after MDMA and related drugs are unlikely to represent neuroadaptive metabolic responses to changes in SERT trafficking, and favor the view that substituted amphetamines have the potential to produce a distal axotomy of brain 5-HT neurons.

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“…Some of the available data indicate that the serotoninergic system may have a facilitative role in regulating the phasic release of luteinizing hormone (LH) and ovulation. For instance, in ovariectomized rats the daily proestrus-like increase in LH induced by estradiol implants was blocked by the adminis tration of /»-chlorophenylalanine, a serotonin synthesis in hibitor [7], or />-chloroamphetamine (PCA), a serotonin neurotoxin [17], and overcome by the treatment with 5-hy droxytryptophan (5-HTP), a serotonin precursor [7]. In ad dition to the facilitatory effects of 5-HTP, an inhibitory ac tion has also been described.…”

mentioning

confidence: 99%

Effect of the Serotoninergic System on Luteinizing Hormone Secretion in Prepubertal Female Rats

Moguilevsky¹,

Faigón

Scacchi

et al. 1985

Neuroendocrinology

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The effect of 5-hydroxytryptophan (5-HTP), a serotonin precursor, and p-chloroamphetamine (PCA), a serotonin neurotoxin, selective for serotoninergic neurons, that depletes serotonin (5-HT) levels in brain, on the luteinizing hormone (LH) release response to estrogen-progesterone (E-P) was studied in prepubertal female rats of different ages. E-P decreased LH levels on days 16, 18 and 20, increasing the levels of the pituitary hormone at day 26 of age. Destruction of the serotoninergic system advanced the onset of the positive feed-back mechanism, since the rats pretreated with PCA showed at day 20 an LH release by E-P administration while in the controls of the same age the ovarian hormones decreased the LH concentration. On the other hand, PCA potentiated the positive feed-back mechanism of E-P on LH in 26-day-old rats, while at this age the LH release response to E-P was significantly reduced by the administration of 5-HTP. These results suggest that the serotoninergic system has an inhibitory effect on the development of the positive feed-back of ovarian steroids on LH secretion, that could be representative of a regulatory participation of serotonin in the onset of puberty. 5-HTP stimulated LH release on days 16, 18 and 20, but did not modify the LH concentration of day 26. Since between 20 and 26 days of age the positive feed-back mechanism matures, the possibility arise that the modification in the effect of serotonin on LH release on day 26 is connected with the physiological changes in the gonadotropin control that occur after day 20 in the female rat.

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IMMEDIATE AND LONG‐TERM EFFECTS OF p‐CHLOROAMPHETAMINE ON BRAIN AMINES*

Cited by 107 publications

References 45 publications

Effect of Serotonin Depletion Induced by <i>p</i>-Chloroamphetamine on Changes in Rats’ Activity Levels Produced by Lithium

Effect of Serotonin Depletion Induced by <i>p</i>-Chloroamphetamine on Changes in Rats’ Activity Levels Produced by Lithium

Loss of Serotonin Transporter Protein after MDMA and Other Ring-Substituted Amphetamines

Effect of the Serotoninergic System on Luteinizing Hormone Secretion in Prepubertal Female Rats

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