Neurokinin-1 receptor antagonism by SR140333: enhanced in vivo ACh in the hippocampus and promnestic post-trial effects

Kart, Emriye; Jocham, Gerhard; Müller, Christian P.; Schlömer, Cerstin; Brandão, Marcus Lira; Huston, Joseph P.; Silva, M. Angelica De Souza

doi:10.1016/j.peptides.2004.07.003

Cited by 23 publications

(7 citation statements)

References 66 publications

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“…The effects of mitragynine on passive avoidance learning were tested in a two‐compartment shuttle box (Columbus Instruments, Columbus, OH, USA; Kart et al . ).…”

Section: Methodsmentioning

confidence: 97%

Abuse potential and adverse cognitive effects of mitragynine (kratom)

et al. 2014

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Mitragynine is the major psychoactive alkaloid of the plant kratom/ketum. Kratom is widely used in Southeast Asia as a recreational drug, and increasingly appears as a pure compound or a component of 'herbal high' preparations in the Western world. While mitragynine/kratom may have analgesic, muscle relaxant and anti-inflammatory effects, its addictive properties and effects on cognitive performance are unknown. We isolated mitragynine from the plant and performed a thorough investigation of its behavioural effects in rats and mice. Here we describe an addictive profile and cognitive impairments of acute and chronic mitragynine administration, which closely resembles that of morphine. Acute mitragynine has complex effects on locomotor activity. Repeated administration induces locomotor sensitization, anxiolysis and conditioned place preference, enhances expression of dopamine transporter- and dopamine receptor-regulating factor mRNA in the mesencephalon. While there was no increase in spontaneous locomotor activity during withdrawal, animals showed hypersensitivity towards small challenging doses for up to 14 days. Severe somatic withdrawal signs developed after 12 hours, and increased level of anxiety became evident after 24 hours of withdrawal. Acute mitragynine independently impaired passive avoidance learning, memory consolidation and retrieval, possibly mediated by a disruption of cortical oscillatory activity, including the suppression of low-frequency rhythms (delta and theta) in the electrocorticogram. Chronic mitragynine administration led to impaired passive avoidance and object recognition learning. Altogether, these findings provide evidence for an addiction potential with cognitive impairments for mitragynine, which suggest its classification as a harmful drug.

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“…The effects of mitragynine on passive avoidance learning were tested in a two‐compartment shuttle box (Columbus Instruments, Columbus, OH, USA; Kart et al . ).…”

Section: Methodsmentioning

confidence: 97%

Abuse potential and adverse cognitive effects of mitragynine (kratom)

et al. 2014

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“…The NK1 receptor antagonist WIN51,708 (10 and 20 mg/kg ip) did not produce a place conditioning effect (Nikolaus, Huston & Hasenöhrl 1999; De Araújo, Huston & Brandao 2001). Likewise, the NK1 receptor antagonist SR140333 (1, 3, 9 mg/kg ip) did not produce an effect (Kart et al . 2004), and the NK3 receptor antagonist SR142801 (0.02, 0.2, 2, 20 mg/kg ip) also did not produce an effect (Jocham et al .…”

Section: Studies Using Systemic Drug Treatmentsmentioning

confidence: 99%

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

2007

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Conditioned place preference (CPP) continues to be one of the most popular models to study the motivational effects of drugs and non-drug treatments in experimental animals. This is obvious from a steady year-to-year increase in the number of publications reporting the use this model. Since the compilation of the preceding review in 1998, more than 1000 new studies using place conditioning have been published, and the aim of the present review is to provide an overview of these recent publications. There are a number of trends and developments that are obvious in the literature of the last decade. First, as more and more knockout and transgenic animals become available, place conditioning is increasingly used to assess the motivational effects of drugs or non-drug rewards in genetically modified animals. Second, there is a still small but growing literature on the use of place conditioning to study the motivational aspects of pain, a field of pre-clinical research that has so far received little attention, because of the lack of appropriate animal models. Third, place conditioning continues to be widely used to study tolerance and sensitization to the rewarding effects of drugs induced by pre-treatment regimens. Fourth, extinction/reinstatement procedures in place conditioning are becoming increasingly popular. This interesting approach is thought to model certain aspects of relapse to addictive behavior and has previously almost exclusively been studied in drug self-administration paradigms. It has now also become established in the place conditioning literature and provides an additional and technically easy approach to this important phenomenon. The enormous number of studies to be covered in this review prevented in-depth discussion of many methodological, pharmacological or neurobiological aspects; to a large extent, the presentation of data had to be limited to a short and condensed summary of the most relevant findings.

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“…ACh levels in the dHipp are enhanced during IA and drug treatments that enhance IA also enhance ACh levels in the dHipp (Kart, Jocham, Muller, Schlomer, Brandao, Huston, and de Souza Silva, 2004; Nail-Boucherie, Dourmap, Jaffard, and Costentin, 1998; Qi and Gold, 2009). Disrupting IA by inhibiting MS neural activity is reversed by enhancing ACh release in the dHipp (Degroot and Parent, 2001).…”

Section: Bf Cholinergic Neurons In Fear and Extinction Memorymentioning

confidence: 99%

The role of basal forebrain cholinergic neurons in fear and extinction memory

Knox

2016

Neurobiology of Learning and Memory

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Cholinergic input to the neocortex, dorsal hippocampus (dHipp), and basolateral amygdala (BLA) is critical for neural function and synaptic plasticity in these brain regions. Synaptic plasticity in the neocortex, dHipp, ventral Hipp (vHipp), and BLA has also been implicated in fear and extinction memory. This finding raises the possibility that basal forebrain (BF) cholinergic neurons, the predominant source of acetylcholine in these brain regions, have an important role in mediating fear and extinction memory. While empirical studies support this hypothesis, there are interesting inconsistencies among these studies that raise questions about how best to define the role of BF cholinergic neurons in fear and extinction memory. Nucleus basalis magnocellularis (NBM) cholinergic neurons that project to the BLA are critical for fear memory and contextual fear extinction memory. NBM cholinergic neurons that project to the neocortex are critical for cued and contextual fear conditioned suppression, but are not critical for fear memory in other behavioral paradigms and in the inhibitory avoidance paradigm may even inhibit contextual fear memory formation. Medial septum and diagonal band of Broca cholinergic neurons are critical for contextual fear memory and acquisition of cued fear extinction. Thus, even though the results of previous studies suggest BF cholinergic neurons modulate fear and extinction memory, inconsistent findings among these studies necessitates more research to better define the neural circuits and molecular processes through which BF cholinergic neurons modulate fear and extinction memory. Furthermore, studies determining if BF cholinergic neurons can be manipulated in such a manner so as to treat excessive fear in anxiety disorders are needed.

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Neurokinin-1 receptor antagonism by SR140333: enhanced in vivo ACh in the hippocampus and promnestic post-trial effects

Cited by 23 publications

References 66 publications

Abuse potential and adverse cognitive effects of mitragynine (kratom)

Abuse potential and adverse cognitive effects of mitragynine (kratom)

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

The role of basal forebrain cholinergic neurons in fear and extinction memory

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