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H. Valerie Curran - One of the best experts on this subject based on the ideXlab platform.
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acute memory and Psychotomimetic effects of cannabis and tobacco both joint and individually a placebo controlled trial
Psychological Medicine, 2017Co-Authors: Chandni Hindocha, Tom P Freeman, Natacha D C Shaban, H. Valerie CurranAbstract:Background Cannabis and tobacco have contrasting cognitive effects. Smoking cannabis with tobacco is prevalent in many countries and although this may well influence cognitive and mental health outcomes, the possibility has rarely been investigated in human experimental psychopharmacological research. Method The individual and interactive effects of cannabis and tobacco were evaluated in 24 non-dependent cannabis and tobacco smokers in a randomized, placebo-controlled, double-blind, 2 (cannabis, placebo) × 2 (tobacco, placebo) crossover design. Verbal memory (prose recall), working memory (WM) performance including maintenance, manipulation and attention (N-back), Psychotomimetic, subjective and cardiovascular measures were recorded on each of four sessions. Results Cannabis alone impaired verbal memory. A priori contrasts indicated that tobacco offset the effects of cannabis on delayed recall. However, this was not supported by linear mixed model analysis. Cannabis load-dependently impaired WM. By contrast, tobacco improved WM across all load levels. The acute Psychotomimetic effects and ratings of ‘stoned’ and ‘dizzy’ induced by cannabis were not altered by tobacco. Cannabis and tobacco had independent effects on increasing heart rate and interacting effects on increasing diastolic blood pressure. Conclusions Relative to placebo, acute cannabis impaired verbal memory and WM. Tobacco enhanced performance on WM, independently of cannabis. Moreover, we found some preliminary evidence that tobacco may offset the effects of cannabis on delayed, but not immediate, verbal recall. In contrast, the Psychotomimetic and subjective effects of cannabis were unaffected by tobacco co-administration. By reducing the cognitive impairment from cannabis, tobacco co-administration may perpetuate use despite adverse health consequences.
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are adolescents more vulnerable to the harmful effects of cannabis than adults a placebo controlled study in human males
Translational Psychiatry, 2016Co-Authors: Claire Mokrysz, S Korkki, Kristi R Griffiths, Tom P Freeman, H. Valerie CurranAbstract:Preclinical research demonstrates that cannabinoids have differing effects in adolescent and adult animals. Whether these findings translate to humans has not yet been investigated. Here we believe we conducted the first study to compare the acute effects of cannabis in human adolescent (n=20; 16–17 years old) and adult (n=20; 24–28 years old) male cannabis users, in a placebo-controlled, double-blind cross-over design. After inhaling vaporized active or placebo cannabis, participants completed tasks assessing spatial working memory, episodic memory and response inhibition, alongside measures of blood pressure and heart rate, Psychotomimetic symptoms and subjective drug effects (for example, ‘stoned’, ‘want to have cannabis’). Results showed that on active cannabis, adolescents felt less stoned and reported fewer Psychotomimetic symptoms than adults. Further, adults but not adolescents were more anxious and less alert during the active cannabis session (both pre- and post-drug administration). Following cannabis, cognitive impairment (reaction time on spatial working memory and prose recall following a delay) was greater in adults than adolescents. By contrast, cannabis impaired response inhibition accuracy in adolescents but not in adults. Moreover, following drug administration, the adolescents did not show satiety; instead they wanted more cannabis regardless of whether they had taken active or placebo cannabis, while the opposite was seen for adults. These contrasting profiles of adolescent resilience (blunted subjective, memory, physiological and Psychotomimetic effects) and vulnerability (lack of satiety, impaired inhibitory processes) show some degree of translation from preclinical findings, and may contribute to escalated cannabis use by human adolescents.
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The Psychotomimetic states inventory (PSI): measuring psychotic-type experiences from ketamine and cannabis.
Schizophrenia research, 2008Co-Authors: Oliver J Mason, Celia J M Morgan, Ana Stefanovic, H. Valerie CurranAbstract:This study reports a new measure of Psychotomimetic states in the context of cannabis and ketamine use. The Psychotomimetic States Inventory (PSI) has sub-scales of Delusory Thinking, Perceptual Distortions, Cognitive Disorganization, Anhedonia, Mania and Paranoia. The PSI was administered in two independent group, repeated measures designs: an experimental study of ketamine and a naturalistic study of cannabis. Both cannabis and ketamine produced reliable increases in ratings of Psychotomimetic state effects across several sub-scales. The PSI is a potentially useful measure of the nature and extent of the phenomenological effects of psychotropic drugs in schizophrenia-related research.
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The Psychotomimetic states inventory (PSI): measuring psychotic-type experiences from ketamine and cannabis.
Schizophrenia Research, 2008Co-Authors: Oliver Mason, Ana Stefanovic, Celia J M Morgan, H. Valerie CurranAbstract:Abstract Background This study reports a new measure of Psychotomimetic states in the context of cannabis and ketamine use. The Psychotomimetic States Inventory (PSI) has sub-scales of Delusory Thinking, Perceptual Distortions, Cognitive Disorganization, Anhedonia, Mania and Paranoia. Methods The PSI was administered in two independent group, repeated measures designs: an experimental study of ketamine and a naturalistic study of cannabis. Results Both cannabis and ketamine produced reliable increases in ratings of Psychotomimetic state effects across several sub-scales. Conclusions The PSI is a potentially useful measure of the nature and extent of the phenomenological effects of psychotropic drugs in schizophrenia-related research.
Toru Nishikawa - One of the best experts on this subject based on the ideXlab platform.
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Psychotomimetic induction of tissue plasminogen activator mrna in corticostriatal neurons in rat brain
European Journal of Neuroscience, 1998Co-Authors: Takanori Hashimoto, Yasushi Kajii, Toru NishikawaAbstract:We have studied in the rat the effects of acute subcutaneous injection of Psychotomimetics including methamphetamine (MAP), cocaine and phencyclidine (PCP) on the expression of a brain plasticity-related molecule, tissue plasminogen activator (tPA) mRNA, using non-radioactive in situ hybridization histochemistry. In addition to the constitutive expression of tPA mRNA in cerebellar Purkinje cells, ventricular ependymal cells and meningeal blood vessel-associated cells, MAP (1-4 mg/kg), cocaine (30 mg/kg) and PCP (1.25-5 mg/kg) caused a transient and dose-dependent induction of the transcript with its peak at 3 h postinjection in a group of neurons of the medial and insular prefrontal cortices, and the piriform cortex. Another indirect dopamine agonist nomifensine (20-40 mg/kg) mimicked the tPA mRNA induction in the prefrontal cortical areas. Moreover, MAP induction of tPA mRNA was markedly inhibited by pretreatment with a D1 (R(+)-SCH23390: R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetra-hydro-1H-3-be nza zepine hydrochloride) or a D2 (haloperidol) dopamine receptor-preferring antagonist. Intramedial striatum, but not intrathalamic, application of a fluorescent tracer, fluorogold, retrogradely labelled the cortical cells expressing tPA mRNA. The present results suggest that acute injections of the above Psychotomimetic drugs may induce tPA mRNA in a group of the prefrontal cortical neurons that project to the medial striatum. This tPA mRNA expression may be due to the activation of the dopamine neurotransmission. Because it is well documented that single or repeated administration of methamphetamine, cocaine and PCP produces enduring changes in responses to these drugs in humans and experimental animals (e.g. behavioural sensitization), the Psychotomimetic-induction of tPA mRNA could be implicated in an initial step in the plastic rearrangements in the neuronal circuits underlying long-lasting changes in behavioural expression.
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Psychotomimetic‐induction of tissue plasminogen activator mRNA in corticostriatal neurons in rat brain
The European journal of neuroscience, 1998Co-Authors: Takanori Hashimoto, Yasushi Kajii, Toru NishikawaAbstract:We have studied in the rat the effects of acute subcutaneous injection of Psychotomimetics including methamphetamine (MAP), cocaine and phencyclidine (PCP) on the expression of a brain plasticity-related molecule, tissue plasminogen activator (tPA) mRNA, using non-radioactive in situ hybridization histochemistry. In addition to the constitutive expression of tPA mRNA in cerebellar Purkinje cells, ventricular ependymal cells and meningeal blood vessel-associated cells, MAP (1-4 mg/kg), cocaine (30 mg/kg) and PCP (1.25-5 mg/kg) caused a transient and dose-dependent induction of the transcript with its peak at 3 h postinjection in a group of neurons of the medial and insular prefrontal cortices, and the piriform cortex. Another indirect dopamine agonist nomifensine (20-40 mg/kg) mimicked the tPA mRNA induction in the prefrontal cortical areas. Moreover, MAP induction of tPA mRNA was markedly inhibited by pretreatment with a D1 (R(+)-SCH23390: R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetra-hydro-1H-3-be nza zepine hydrochloride) or a D2 (haloperidol) dopamine receptor-preferring antagonist. Intramedial striatum, but not intrathalamic, application of a fluorescent tracer, fluorogold, retrogradely labelled the cortical cells expressing tPA mRNA. The present results suggest that acute injections of the above Psychotomimetic drugs may induce tPA mRNA in a group of the prefrontal cortical neurons that project to the medial striatum. This tPA mRNA expression may be due to the activation of the dopamine neurotransmission. Because it is well documented that single or repeated administration of methamphetamine, cocaine and PCP produces enduring changes in responses to these drugs in humans and experimental animals (e.g. behavioural sensitization), the Psychotomimetic-induction of tPA mRNA could be implicated in an initial step in the plastic rearrangements in the neuronal circuits underlying long-lasting changes in behavioural expression.
Hideo Tsukada - One of the best experts on this subject based on the ideXlab platform.
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reduction of dopamine d2 3 receptor binding in the striatum after a single administration of esketamine but not r ketamine a pet study in conscious monkeys
European Archives of Psychiatry and Clinical Neuroscience, 2017Co-Authors: Kenji Hashimoto, Takeharu Kakiuchi, Hiroyuki Ohba, Shingo Nishiyama, Hideo TsukadaAbstract:R-ketamine appears to be a potent, long-lasting and safer antidepressant, relative to esketamine (S-ketamine), since it might be free of Psychotomimetic side effects. Using [11C]raclopride and positron emission tomography (PET), we investigated whether esketamine and R-ketamine can affect dopamine D2/3 receptor binding in the conscious monkey brain. A single infusion of esketamine (0.5 mg/kg), but not R-ketamine (0.5 mg/kg), caused a reduction of binding availability of dopamine D2/3 receptor in the monkey striatum. This study suggests that unlike to R-ketamine, esketamine can cause dopamine release in the striatum, and that its release might be associated with Psychotomimetic effects of esketamine.
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Reduction of dopamine D_2/3 receptor binding in the striatum after a single administration of esketamine, but not R-ketamine: a PET study in conscious monkeys
European Archives of Psychiatry and Clinical Neuroscience, 2017Co-Authors: Kenji Hashimoto, Takeharu Kakiuchi, Hiroyuki Ohba, Shingo Nishiyama, Hideo TsukadaAbstract:R-ketamine appears to be a potent, long-lasting and safer antidepressant, relative to esketamine (S-ketamine), since it might be free of Psychotomimetic side effects. Using [^11C]raclopride and positron emission tomography (PET), we investigated whether esketamine and R-ketamine can affect dopamine D_2/3 receptor binding in the conscious monkey brain. A single infusion of esketamine (0.5 mg/kg), but not R-ketamine (0.5 mg/kg), caused a reduction of binding availability of dopamine D_2/3 receptor in the monkey striatum. This study suggests that unlike to R-ketamine, esketamine can cause dopamine release in the striatum, and that its release might be associated with Psychotomimetic effects of esketamine.
Hweihsien Chen - One of the best experts on this subject based on the ideXlab platform.
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n n dimethylglycine differentially modulates Psychotomimetic and antidepressant like effects of ketamine in mice
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2016Co-Authors: Minghuan Chan, Yichyan Chen, Hweihsien ChenAbstract:Abstract Ketamine, a dissociative anesthetic, produces rapid and sustained antidepressant effects at subanesthtic doses. However, it still inevitably induces Psychotomimetic side effects. N , N -dimethylglycine (DMG) is a derivative of the amino acid glycine and is used as a dietary supplement. Recently, DMG has been found acting at glycine binding site of the N -methyl- d -aspartate receptor (NMDAR). As blockade of NMDARs is one of the main mechanisms responsible for the action of ketamine on central nervous system, DMG might modulate the behavioral responses to ketamine. The present study determined the effects of DMG on the ketamine-induced Psychotomimetic, anesthetic and antidepressant-like effects in mice. DMG pretreatment reversed the ketamine-induced locomotor hyperactivity and impairment in the rotarod performance, novel location and novel object recognition tests, and prepulse inhibition. In addition, DMG alone exhibited antidepressant-like effects in the forced swim test and produced additive effects when combined with ketamine. However, DMG did not affect ketamine-induced anesthesia. These results reveal that DMG could antagonize ketamine's Psychotomimetic effects, yet produce additive antidepressant-like effects with ketamine, suggesting that DMG might have antipsychotic potential and be suitable as an add-on therapy to ketamine for patients with treatment-resistant depression.
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Betaine enhances antidepressant-like, but blocks Psychotomimetic effects of ketamine in mice
Psychopharmacology, 2016Co-Authors: Jen-cheng Lin, Minghuan Chan, Yichyan Chen, Mei-yi Lee, Hweihsien ChenAbstract:Ketamine is emerging as a new hope against depression, but ketamine-associated Psychotomimetic effects limit its clinical use. An adjunct therapy along with ketamine to alleviate its adverse effects and even potentiate the antidepressant effects might be an alternative strategy. Betaine, a methyl derivative of glycine and a dietary supplement, has been shown to have antidepressant-like effects and to act like a partial agonist at the glycine site of N-methyl-D-aspartate receptors (NMDARs). Accordingly, betaine might have potential to be an adjunct to ketamine treatment for depression. The antidepressant-like effects of ketamine and betaine were evaluated by forced swimming test and novelty suppressed feeding test in mice. Both betaine and ketamine produced antidepressant-like effects. Furthermore, we determined the effects of betaine on ketamine-induced antidepressant-like and Psychotomimetic behaviors, motor incoordination, hyperlocomotor activity, and anesthesia. The antidepressant-like responses to betaine combined with ketamine were stronger than their individual effects. In contrast, ketamine-induced impairments in prepulse inhibition, novel object recognition test, social interaction, and rotarod test were remarkably attenuated, whereas ketamine-induced hyperlocomotion and loss of righting reflex were not affected by betaine. These findings revealed that betaine could enhance the antidepressant-like effects, yet block the Psychotomimetic effects of ketamine, suggesting that betaine can be considered as an add-on therapy to ketamine for treatment-resistant depression and suitable for the treatment of depressive symptoms in patients with schizophrenia.
Moskal - One of the best experts on this subject based on the ideXlab platform.
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NMDA Receptor Glycine Site Modulators as Therapeutics for Depression: Rapastinel has Antidepressant Activity without Causing Psychotomimetic Side Effects.
Current Neuropharmacology, 2016Co-Authors: Amin Khan M, Houck D, Yu W, Jeffrey Burgdorf, MoskalAbstract:Abstract Major depressive disorder and related despressive disorders continue to be poorly treated with existing therapies. Most current therapies target biogenic amines, have low efficacy among the depressed population, failing to achieve clinical response (>50% reduction in depression score) in many patients, and often exhibit delayed onset. Since 2000, much attention has focused on ionotropic N-methyl-D-aspartate (NMDA) receptors, resulting from several reports that ketamine, a NMDA receptor noncompetitive antagonist which blocks channel opening, produces a rapid (hours) and large clinical response (effect size >1 in some studies) in a majority of subjects following a single dose, with prolonged duration of action (three days to one week or more) in subjects with treatment-resistant depression. A major shortcoming of ketamine is that it causes Psychotomimetic side effects. Other NMDA receptor full antagonists have also demonstrated efficacy in depressed subjects without Psychotomimetic side effects at relatively low doses, but like ketamine induce Psychotomimetic side effects at high receptor occupancy. It has been suggested that NMDA receptor partial agonists may produce efficacy in affective and neurological disorders without producing Psychotomimetic effects. D-cycloserine, a glycine site partial agonist at some classes of NMDA receptors, has been extensively studied in subjects with affective disorders and has demonstrated efficacy in schizophrenic subjects and in some studies in depressed subjects. More recently, rapastinel, an NMDA receptor modulator that allosterically alters glycine site activity in a partial agonist-like manner but does not actually bind to the glycine site (functional partial agonism), has been found to be antidepressant without inducing Psychotomimetic effects. Here we review glycine site modulation of NMDA receptors and discuss data that support glycine site modulators as antidepressant agents. We focus on recent studies of rapastinel, a glycine site functional partial agonist, as an antidepressant agent.
