Additive effect of rimonabant and citalopram on extracellular serotonin levels monitored with in vivo microdialysis in rat brain

Ortega, Jorge E.; Gonzalez-Lira, Victor; Horrillo, I.; Herrera‐Marschitz, Mario; Callado, Luís F.; Meana, J. Javier

doi:10.1016/j.ejphar.2013.03.043

Cited by 22 publications

(7 citation statements)

References 46 publications

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“…The apparent discrepancy between cortical and subcortical cannabinoid modulations also exists for monoamines: systemic SR141716A administration facilitates the release of serotonin, dopamine and noradrenaline in the prefrontal cortex [744,745] whereas in the nucleus accumbens, only serotonin is stimulated by CB 1 R blockade [744,746]. This assumes that functional cannabinoid receptors are present in cortical and hippocampal monoaminergic nerve terminals.…”

Section: Cannabinoid Interaction With Serotonin and Noradrenalinementioning

confidence: 99%

Cannabis: A Treasure Trove or Pandora's Box?

Solymosi

Köfalvi

2017

MRMC

122

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We summarize our current knowledge on the recreational use of cannabis with respect to the modes of consumption, short-term effects, chronic health consequences and cannabis use disorder. Next, we overview the molecular targets of a dozen major and minor bioactive cannabinoids in the body. This helps us introduce the endocannabinoid system in an unprecedented detail: its up-todate molecular biology, pharmacology, physiology and medical significance, and beyond. In conclusion, we offer an unbiased survey about cannabis to help better weigh its medical value versus the associated risks.

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Section: Cannabinoid Interaction With Serotonin and Noradrenalinementioning

confidence: 99%

Cannabis: A Treasure Trove or Pandora's Box?

Solymosi

Köfalvi

2017

MRMC

122

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“…; Ortega et al . ). Clearly, enhancing forebrain monoamine function alone by SSRIs appears to be insufficient to broadly improve cognitive dysfunction in major depression.…”

Section: Discussionmentioning

confidence: 97%

“…The lack of effect of SSRIs on acetylcholine efflux is of interest as these agents show limited effects in treating cognitive symptoms in major depression (Jeon et al 2014;Keefe et al 2014) despite their pronounced effects on enhancing forebrain monoamine availability (Owen and Whitton 2006;Fernandez-Pastor et al 2013;Kaminska et al 2013;Ortega et al 2013). Clearly, enhancing forebrain monoamine function alone by SSRIs appears to be insufficient to broadly improve cognitive dysfunction in major depression.…”

Section: Discussionmentioning

confidence: 99%

Effects of lisdexamfetamine alone and in combination with s‐citalopram on acetylcholine and histamine efflux in the rat pre‐frontal cortex and ventral hippocampus

Hutson

Heins

Folgering

2015

Journal of Neurochemistry

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Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by poor attention, impulse control and hyperactivity. A significant proportion of ADHD patients are also co-morbid for other psychiatric problems including mood disorders and these patients may be managed with a combination of psychostimulants and anti-depressants. While it is generally accepted that enhanced catecholamine signalling via the action of psychostimulants is likely responsible for the cognitive improvement in ADHD, other neurotransmitters including acetylcholine and histamine may be involved. In the present study, we have examined the effect of lisdexamfetamine dimesylate (LDX), an amphetamine pro-drug that is approved for the treatment of ADHD on acetylcholine and histamine efflux in pre-frontal cortex and hippocampus alone and in combination with the anti-depressant s-citalopram. LDX increased cortical acetylcholine efflux, an effect that was not significantly altered by co-administration of s-citalopram. Cortical and hippocampal histamine were markedly increased by LDX, an effect that was attenuated in the hippocampus but not in pre-frontal cortex when co-administered with s-citalopram. Taken together, these results suggest that efflux of acetylcholine and histamine may be involved in the therapeutic effects of LDX and are differentially influenced by the co-administration of s-citalopram. Attention deficit hyperactivity disorder (ADHD) is characterized by poor attention, impulse control and hyperactivity. Some ADHD patients are also co-morbid for mood disorders and may be managed with psychostimulants (e.g. lisdexamfetamine, LDX) and anti-depressants (e.g. s-citalopram). LDX increased the efflux of acetylcholine and histamine, neurotransmitters involved in cognitive function, which were differentially influenced when co-administered with s-citalopram. Acetylcholine and histamine may be involved in the therapeutic effects of LDX and are differentially affected by the co-administration of s-citalopram.

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“…For example, serotonin levels in the brain are increased during the night and its receptors during the day [52,53], supporting that the circadian administration of either SSRIs, melatonin or a combination of them, has an important role to elicit effective antidepressant actions. It is important to mention that SSRIs cause an increase of serotonin levels in the synaptic cleft [54]. In this regard, melatonin increases total serotonin levels in the brain [55].…”

Section: Discussionmentioning

confidence: 99%

The Timing of Melatonin Administration Is Crucial for Its Antidepressant-Like Effect in Mice

Estrada-Reyes

Valdés-Tovar

Arrieta-Báez

et al. 2018

IJMS

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Melatonin is synthesized by the pineal gland with a circadian rhythm in synchrony with the environmental light/dark cycle. A gradual increase in circulating levels of melatonin occur after lights off, reaching its maximum around the middle of the dark phase. Agonists of melatonin receptors have proved effectiveness as antidepressants in clinical trials. However, there is contradictory evidence about the potential antidepressant effect of melatonin itself. Herein we studied melatonin administration in mice at two zeitgeber times (ZT; ZT = 0 lights on; 12:12 L/D), one hour before the beginning (ZT11) and at the middle (ZT18) of the dark phase after either a single or a three-dose protocol. Behavioral despair was assessed through a forced-swimming test (FST) or a tail suspension test (TST), at ZT18.5. A single dose of 4 mg/kg melatonin at ZT11 was effective to reduce the immobility time in both tests. However, acute administration of melatonin at ZT18 was not effective in mice subjected to FST, and a higher dose (16 mg/kg) was required to reduce immobility time in the TST. A three-dose administration protocol of 16 mg/kg melatonin (ZT18, ZT11, and ZT18) significantly reduced immobility time in FST. Data indicate that the timely administration of melatonin could improve its antidepressant-like effect.

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Additive effect of rimonabant and citalopram on extracellular serotonin levels monitored with in vivo microdialysis in rat brain

Cited by 22 publications

References 46 publications

Cannabis: A Treasure Trove or Pandora's Box?

Cannabis: A Treasure Trove or Pandora's Box?

Effects of lisdexamfetamine alone and in combination with s‐citalopram on acetylcholine and histamine efflux in the rat pre‐frontal cortex and ventral hippocampus

The Timing of Melatonin Administration Is Crucial for Its Antidepressant-Like Effect in Mice

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