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S F Ali

Neurochemistry Laboratory, Division of Neurotoxicology, HFT-132, National Center Toxicological Research, FDA, 3900 NCTR Road, Jefferson, AR 72079-9502, USA. sali@nctr.fda.gov

9 papers in the library · 174 citations · publishing 1996-2011

Papers

Noribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine.

Annals of the New York Academy of Sciences September 1, 2000 M H Baumann, J P Pablo, S F Ali et al. 37 citations

Ibogaine, a plant-derived alkaloid being studied for substance use disorders, is rapidly converted in the body to its metabolite noribogaine. In rats, noribogaine reaches higher blood levels than ibogaine and persists for at least 24 hours. Noribogaine did not cause tremors or forepaw treading, unlike ibogaine, but both drugs elevated stress hormones corticosterone and prolactin, with ibogaine more potent for corticosterone. Neither drug affected dopamine levels in the nucleus accumbens, but both increased serotonin levels, with noribogaine more potent. Noribogaine is biologically active and likely contributes to ibogaine's effects but may be safer, producing fewer adverse effects like tremors and stress-axis activation.

A dose-response study of ibogaine-induced neuropathology in the rat cerebellum.

Toxicological sciences : an official journal of the Society of Toxicology September 1, 2000 Z Xu, L W Chang, W Slikker et al. 37 citations

Ibogaine, a psychoactive compound from a West African shrub, can damage brain cells in rats even after a single dose. In rats given 100 mg/kg, the cerebellum showed clear signs of neurodegeneration, specifically in Purkinje neurons. Similar damage occurred in all rats given 75 mg/kg, though the affected areas were narrower. At 50 mg/kg, only 2 of 6 rats showed damage, but those affected had patches of astrocyte activation. No damage was seen in rats given 25 mg/kg, suggesting this dose may be a safe threshold with no observable adverse effects. The findings highlight ibogaine's potential neurotoxicity, which is relevant given its use in addiction treatment.

Neuroendocrine and neurochemical effects of acute ibogaine administration: a time course evaluation.

Brain research October 21, 1996 S F Ali, G D Newport, W Slikker et al. 29 citations

A single injection of ibogaine (IBO) rapidly increases the hormones prolactin and corticosterone in adult male rats, with prolactin returning to normal within 60 minutes and corticosterone within 24 hours. IBO also reduces dopamine in the striatum and frontal cortex for up to two hours while raising dopamine metabolites, indicating altered dopamine processing. Some dopamine metabolite levels remain below normal 24 hours later. Serotonin and its metabolite decrease only in the striatum at 60 minutes. These effects may relate to ibogaine's reported ability to help reduce drug craving, but further research is needed.

Ibogaine blocked methamphetamine-induced hyperthermia and induction of heat shock protein in mice.

Brain research March 27, 1999 X Yu, S Z Imam, G D Newport et al. 17 citations

In female C57BL/6N mice, methamphetamine caused a rise in body temperature and increased levels of a stress protein (HSP-72) in the caudate nucleus. Ibogaine alone lowered body temperature. When ibogaine was given before methamphetamine, it completely prevented the hyperthermia and reduced HSP-72 expression. These results suggest ibogaine can block methamphetamine-induced brain stress and temperature changes.

Comparative neurobiological effects of ibogaine and MK-801 in rats.

Drug and alcohol dependence May 1, 2000 M H Baumann, R B Rothman, S F Ali 15 citations

Ibogaine, a plant alkaloid, reduces dopamine levels across several brain regions in rats while increasing dopamine metabolites, indicating enhanced dopamine turnover. This effect differs from MK-801, an NMDA antagonist, which does not lower dopamine but modestly raises metabolites in some areas. Both drugs elevate corticosterone, but only ibogaine increases prolactin. The findings suggest ibogaine's in vivo actions on dopamine and neuroendocrine secretion are not solely due to NMDA receptor antagonism.

Acute ibogaine injection induces expression of the immediate early genes, egr-1 and c-fos, in mouse brain.

Brain research. Molecular brain research December 10, 1999 S F Ali, N Thiriet, J Zwiller 13 citations

A single injection of ibogaine in adult male mice significantly increased the activity of two immediate early genes, egr-1 and c-fos, in several brain regions within 30 minutes. Egr-1 messenger RNA rose in the nucleus accumbens, caudate-putamen, frontal cortex, septum, dentate gyrus, and CA3 region of the hippocampus. C-fos gene expression increased in the caudate-putamen, frontal cortex, dentate gyrus, septum, and CA1 region of the hippocampus. The authors suggest this gene activation may partly stem from ibogaine's stimulant properties, similar to other psychostimulants.

Effects of ibogaine, and cocaine and morphine after ibogaine, on ventral tegmental dopamine neurons.

Life sciences January 1, 1996 E D French, K Dillon, S F Ali 12 citations

Ibogaine, a plant-derived alkaloid, acutely excites dopamine neurons in the ventral tegmental area (VTA) of anesthetized rats, but this effect is not long-lasting. Pretreatment with ibogaine 6-8 hours or 19 hours before testing did not alter the spontaneous firing of VTA dopamine neurons or their response to morphine or cocaine. Because ibogaine's excitatory effect on these neurons is transient and does not persistently change how dopamine neurons respond to these drugs, other mechanisms must explain its proposed antiaddictive properties.

Analysis of electrical brain waves in neurotoxicology: γ-hydroxybutyrate.

Current neuropharmacology March 1, 2011 Z K Binienda, M A Beaudoin, B T Thorn et al. 10 citations

Fast Fourier Transform (FFT) analysis of electrocorticogram (ECoG) recordings in conscious rats reveals that different drugs alter brainwave frequencies in distinct ways. Domoic acid administration links slow-wave delta and theta activity with behavioral seizure type. Ibogaine pretreatment before cocaine increases power in the alpha(1) band, suggesting serotonergic involvement, and lowers the threshold for cocaine-induced electrographic seizures by increasing delta and theta power. Two weeks of daily cocaine reduces slow-wave ECoG activity 24 hours after the last injection, mirroring reduced frontal cortex metabolism in chronic human users. Gamma-hydroxybutyrate (GHB) at 400 and 800 mg/kg increases energy across all except beta(2) bands, producing EEG patterns resembling absence seizures in human petit mal epilepsy.

Application of electrophysiological method to study interactions between ibogaine and cocaine.

Annals of the New York Academy of Sciences September 1, 2000 Z Binienda, M A Beaudoin, B T Thorn et al. 4 citations

Pretreatment with ibogaine dampens the brain's reaction to cocaine in rats. In awake adult male rats, cocaine alone caused a brief increase in alpha1 brain wave power and desynchronization in alpha2 and beta bands, along with a surge in dopamine levels in the caudate nucleus. After ibogaine pretreatment, cocaine instead produced a prolonged increase in delta, theta, and alpha1 power lasting up to an hour, and dopamine levels decreased further rather than rising. Dopamine turnover increased with ibogaine alone but not when cocaine followed. These changes in electrical brain activity and neurotransmitter levels indicate a reduced response to cocaine after ibogaine pretreatment.