The Neurotoxic Effects of Continuous Cocaine and Amphetamine in Habenula: Implications for the Substrates of Psychosis

Ellison, Gaylord; Irwin, Scott A.; Keys, Alan; Noguchi, Kevin K.; Sulur, G

doi:10.1037/e495672006-007

Cited by 14 publications

(8 citation statements)

References 67 publications

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“…On withdrawal day 8, we did not find DA depletion in either the CPu or in the NAC. Our results are in contrast to neurochemical studies that have shown that continuous release, albeit of higher AMPH doses, as compared with repeated intermittent or ESC AMPH administration, has a selective neurotoxic effect on DA terminals in the CPu (Ellison et al 1996;Gately et al 1987;Ricaurte et al 1984;Ryan et al 1990). However, the current results are in line with our previous findings that withdrawal from intermittent and ESC AMPH schedules did not lead to any significant neurochemical changes as compared with SAL treatment (Murphy et al 2003).…”

Section: Discussioncontrasting

confidence: 79%

Withdrawal from continuous amphetamine administration abolishes latent inhibition but leaves prepulse inhibition intact

et al. 2006

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Section: Discussioncontrasting

confidence: 79%

Withdrawal from continuous amphetamine administration abolishes latent inhibition but leaves prepulse inhibition intact

et al. 2006

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“…First, electrical stimulation of the MHb and the fasciculus retroflexus produces rewarding effects (Sutherland & Nakajima 1981). Second, most stimulant drugs of abuse cause axonal degeneration in the LHb and the fasciculus retroflexus, and nicotine causes degeneration of neurons in the portion of the fasciculus retroflexus that connects the MHb to the IPN (Ellison 2002, Ellison et al 1996). Third, a derivative of the alkaloid ibogaine, 18-methoxycoronaridine (18-MC) (Vastag 2005), is a potent antagonist of β4* nAChRs (Glick et al 2002) with significant antiaddictive properties (Maisonneuve & Glick 2003).…”

Section: Distinct Nicotinic Receptor Subtypes Mediate Withdrawalmentioning

confidence: 99%

Reward, Addiction, Withdrawal to Nicotine

Biasi

Dani

2011

Annu. Rev. Neurosci.

321

311

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Nicotine is the principle addictive component that drives continued tobacco use despite users’ knowledge of the harmful consequences. The initiation of addiction involves the mesocorticolimbic dopamine system, which contributes to the processing of rewarding sensory stimuli during the overall shaping of successful behaviors. Acting mainly through nicotinic receptors containing the α4 and β2 subunits, often in combination with the α6 subunit, nicotine increases the firing rate and the phasic bursts by midbrain dopamine neurons. Neuroadaptations arise during chronic exposure to nicotine, producing an altered brain condition that requires the continued presence of nicotine to be maintained. When nicotine is removed, a withdrawal syndrome develops. The expression of somatic withdrawal symptoms depends mainly on the α5, α2, and β4 nicotinic subunits involving the epithalamic habenular complex and its targets. Thus, nicotine taps into diverse neural systems and an array of nicotinic acetylcholine receptor (nAChR) subtypes to influence reward, addiction, and withdrawal.

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“…Both self-administration and DA release are correlated with the highest LHb firing rate ( 20 , 23 , 67 , 91 ). Importantly, chronic intake of cocaine, which leads to FR degeneration, is able to disrupt circadian rhythms probably due to the lack of LHb control on monoamine nuclei [( 20 , 96 ); Figure 2 ].…”

Section: The Habenulamentioning

confidence: 99%

“…The LHb has been proposed as a target for DBS to treat addiction because of its close functional relationship with the reward system ( 98 ). However, chronic exposure to cocaine, amphetamine, methamphetamine, MDMA, or nicotine results in the degeneration of the FR, which blocks the effect of DBS on drug intake ( 96 , 99 , 100 ). As long as FR is able to transmit information, the LHb can be considered as a main target for DBS in the treatment of addiction.…”

Section: The Habenulamentioning

confidence: 99%

Insights into the Role of the Habenular Circadian Clock in Addiction

Salaberry

Mendoza

2016

Front. Psychiatry

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Drug addiction is a brain disease involving alterations in anatomy and functional neural communication. Drug intake and toxicity show daily rhythms in both humans and rodents. Evidence concerning the role of clock genes in drug intake has been previously reported. However, the implication of a timekeeping brain locus is much less known. The epithalamic lateral habenula (LHb) is now emerging as a key nucleus in drug intake and addiction. This brain structure modulates the activity of dopaminergic neurons from the ventral tegmental area, a central part of the reward system. Moreover, the LHb has circadian properties: LHb cellular activity (i.e., firing rate and clock genes expression) oscillates in a 24-h range, and the nucleus is affected by photic stimulation and has anatomical connections with the main circadian pacemaker, the suprachiasmatic nucleus. Here, we describe the current insights on the role of the LHb as a circadian oscillator and its possible implications on the rhythmic regulation of the dopaminergic activity and drug intake. These data could inspire new strategies to treat drug addiction, considering circadian timing as a principal factor.

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The Neurotoxic Effects of Continuous Cocaine and Amphetamine in Habenula: Implications for the Substrates of Psychosis

Cited by 14 publications

References 67 publications

Withdrawal from continuous amphetamine administration abolishes latent inhibition but leaves prepulse inhibition intact

Withdrawal from continuous amphetamine administration abolishes latent inhibition but leaves prepulse inhibition intact

Reward, Addiction, Withdrawal to Nicotine

Insights into the Role of the Habenular Circadian Clock in Addiction

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