Allyson Gill, Madison Gill, Rahul Mittal, Khemraj Hirani, Ajay Sharma
{"title":"Leptin-dopamine interactions: unveiling the common link between type-2 diabetes and neuropsychiatric comorbidities.","authors":"Allyson Gill, Madison Gill, Rahul Mittal, Khemraj Hirani, Ajay Sharma","doi":"10.1097/FBP.0000000000000820","DOIUrl":"https://doi.org/10.1097/FBP.0000000000000820","url":null,"abstract":"<p><p>Clinical evidence highlights the central nervous system as a key target in type-2 diabetes-related complications, yet the mechanisms underlying the increased prevalence of mood disorder issues, mainly depression, in patients with diabetes remain poorly understood. Leptin, an adiposity hormone known for its role in energy homeostasis, has been shown to improve insulin sensitivity and regulate blood glucose levels in diabetic populations. Beyond its metabolic effects, leptin also has the potential to mitigate psychiatric complications such as depression and anxiety. Notably, leptin receptors are predominantly expressed on dopamine (DA) neurons in the brain, hinting that leptin may orchestrate DA activity by serving as its endogenous modulator. This review examines the role of leptin as a potential common link between type-2 diabetes and mood disorders, particularly through its effects on DA function. This article proposes defective leptin signaling as a vital mechanism contributing to psychiatric complications and compromised DA functions in type-2 diabetes, highlighting leptin as a promising therapeutic target for addressing metabolic and psychiatric comorbidities.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2025-02-01Epub Date: 2024-12-24DOI: 10.1097/FBP.0000000000000808
Cailin van Staden, David Weinshenker, Karin Finger-Baier, Tarryn L Botha, Linda Brand, De Wet Wolmarans
{"title":"Posttraumatic anxiety-like behaviour in zebrafish is dose-dependently attenuated by the alpha-2A receptor agonist, guanfacine.","authors":"Cailin van Staden, David Weinshenker, Karin Finger-Baier, Tarryn L Botha, Linda Brand, De Wet Wolmarans","doi":"10.1097/FBP.0000000000000808","DOIUrl":"10.1097/FBP.0000000000000808","url":null,"abstract":"<p><p>Traumatic stress exposure increases noradrenaline (NA) release, which contributes to anxiety and impaired risk-appraisal. Guanfacine, a selective alpha-2A adrenergic receptor agonist, has been used to treat stress-related disorders characterised by impaired prefrontal cortex function. By acting on both presynaptic inhibitory autoreceptors and postsynaptic heteroreceptors, guanfacine attenuates stress reactivity and enhances cognition. However, its effectiveness in treating trauma-related anxiety and risk-taking behaviour remains unclear. Leveraging the advantages of zebrafish (Danio rerio ) as a sensitive and efficient preclinical model which is ideal for stress research, we explored the impact of traumatic stress exposure combined with varying concentrations of guanfacine in adult zebrafish. Zebrafish were evaluated for trauma-related anxiety using both the novel tank test (NTT) and a novel version of the open-field test (nOFT), the latter which was also used to investigate risk-taking behaviour. We found that (1) traumatic stress exposure led to heightened risk-taking behaviour in the nOFT, and (2) low-to-moderate concentrations of guanfacine (3-20 µg/L) attenuated anxiety-like, but not risk-taking behaviour, with the highest concentration (40 µg/L), showing no effect. These results highlight the complex role of NA in modulating dysregulated behaviours during traumatic events and indicate the potential of guanfacine for improving trauma-related anxiety and risk-taking behaviour.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"47-59"},"PeriodicalIF":1.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2025-02-01Epub Date: 2024-12-12DOI: 10.1097/FBP.0000000000000806
Caitlin A Madison, Roanna A Debler, Paula L Gallegos, Lauren Hillbrick, Robert S Chapkin, Stephen Safe, Shoshana Eitan
{"title":"1,4-dihydroxy-2-naphthoic acid prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced motor function deficits.","authors":"Caitlin A Madison, Roanna A Debler, Paula L Gallegos, Lauren Hillbrick, Robert S Chapkin, Stephen Safe, Shoshana Eitan","doi":"10.1097/FBP.0000000000000806","DOIUrl":"10.1097/FBP.0000000000000806","url":null,"abstract":"<p><p>Parkinson's disease (PD), characterized by death of dopaminergic neurons in the substantia nigra, is the second most prevalent progressive neurodegenerative disease. However, the etiology of PD is largely elusive. This study employed the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) rodent model to examine the effectiveness of 1,4-dihydroxy-2-naphthoic acid (1,4-DHNA), an aryl hydrocarbon receptor (AhR) active gut bacteria-derived metabolite, in mitigating MPTP's motoric deficits, and the role of AhR in mediating these effects. Male C57BL/6 mice were fed daily with vehicle, 20 mg/kg 1,4-DHNA, or AhR-inactive isomer 3,7-DHNA, for 3 weeks before administration of 80 mg/kg MPTP or vehicle. Four weeks later, mice were assessed for motoric functions. Both 1,4-DHNA and 3,7-DHNA prevented MPTP-induced deficits in the motor pole test and in the adhesive strip removal test. Additionally, 1,4-DHNA improved balance beam performance and completely prevented MPTP-induced reduction in stride length. In contrast, 3,7-DHNA, an AhR-inactive compound, did not improve balance beam performance and had only a partial effect on stride length. This study suggests that natural metabolites of gut microbiota, such as 1,4-DHNA, could be beneficial to counteract the development of motor deficits observed in PD. Thus, this study further supports the hypothesis that pathological and mitigating processes in the gut could play an essential role in PD development. Moreover, this indicates that 1,4-DHNA's ability to combat various motor deficits is likely mediated via multiple underlying molecular mechanisms. Specifically, AhR is involved, at least partially, in control of gait and bradykinesia, but it likely does not mediate the effects on fine motor skills.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"40-46"},"PeriodicalIF":1.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2025-02-01Epub Date: 2024-12-24DOI: 10.1097/FBP.0000000000000810
Diba Shirmohammadi, Homayoon Golmohammadi, Fatemehsadat Seyedaghamiri, Abbas Haghparast
{"title":"Role of D1- and D2-like dopamine receptors within the CA1 hippocampal region in the stress-induced antinociceptive response in the exposure to acute pain.","authors":"Diba Shirmohammadi, Homayoon Golmohammadi, Fatemehsadat Seyedaghamiri, Abbas Haghparast","doi":"10.1097/FBP.0000000000000810","DOIUrl":"10.1097/FBP.0000000000000810","url":null,"abstract":"<p><p>Exposure to stressful conditions such as forced swim stress (FSS) induces antinociception. Previous reports determined that dopamine receptors in the CA1 hippocampal area are important in chronic pain processing. Considering that neural mechanisms behind acute and chronic pain differ significantly, in this study, we have investigated the role of dopamine receptors within the CA1 region in the FSS-induced antinociceptive response in the acute pain induced by the tail-flick test in the rat. The cannula was implanted unilaterally in the CA1 region of the animal brain. Animals received drugs or vehicles 5 min before FSS exposure. SCH23390 as the D1-like dopamine receptor (D1R) antagonist and Sulpiride as the D2-like dopamine receptor (D2R) antagonist were microinjected into the CA1 area at three doses (0.25, 1, and 4 μg/0.5 μl vehicle); the vehicle groups received saline instead of SCH23390 and dimethyl sulfoxide instead of Sulpiride. After exposure to FSS, the tail-flick test was done. The findings of this study revealed that FSS significantly attenuates nociceptive response during the tail-flick test ( P < 0.0001). Moreover, intra-CA1 microinjection of SCH23390 and Sulpiride significantly reduces the FSS-induced antinociception in the inducing acute pain ( P < 0.0001). The comparison of effective dose of 50% for D1R and D2R antagonists showed that both receptors in the CA1 almost equally reduce the FSS-induced antinociception in the tail-flick test. The result of this study supports the hypothesis, that the dopaminergic system in CA1 is involved in triggering a stress-induced antinociceptive response in acute pain conditions.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"30-39"},"PeriodicalIF":1.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2025-02-01Epub Date: 2024-12-24DOI: 10.1097/FBP.0000000000000805
Luke A Urbanik, Jennifer L Booth, Nikhil K Acharya, Brianna B Evans, Patricia S Grigson
{"title":"Effect of acute treatment with the glucagon-like peptide-1 receptor agonist, liraglutide, and estrus phase on cue- and drug-induced fentanyl seeking in female rats.","authors":"Luke A Urbanik, Jennifer L Booth, Nikhil K Acharya, Brianna B Evans, Patricia S Grigson","doi":"10.1097/FBP.0000000000000805","DOIUrl":"10.1097/FBP.0000000000000805","url":null,"abstract":"<p><p>Opioid use disorder (OUD) is a crisis in the USA. Despite advances with medications for OUD, overdose deaths have continued to rise and are largely driven by fentanyl. We have previously found that male rats readily self-administer fentanyl, with evident individual differences in fentanyl taking, seeking, and reinstatement behaviors. We also have shown that acute treatment with the glucagon-like peptide-1 receptor (GLP-1R) agonist, liraglutide, can reduce fentanyl seeking behavior in male rats. However, given that females are significantly more vulnerable to drug-related cues, drug cravings, and to the development of OUD compared to males, it is imperative that we investigate the biological risk factors on fentanyl use disorder. Further, preclinical models report that females in estrus have increased fentanyl intake, more rapid development of OUD, and enhanced relapse vulnerability compared to those in a non-estrus phase. Thus, we aimed here to understand the effect of estrus phase on our model of OUD and on the effectiveness of acute liraglutide treatment. Herein, we show that female rats readily self-administer fentanyl (1.85 μg/infusion) intravenously, with marked individual differences in fentanyl taking behavior. Additionally, rats in the estrus phase exhibited greater fentanyl intake compared with those in a non-estrus phase, greater cue-induced fentanyl seeking, and greater drug-induced reinstatement of fentanyl seeking. Finally, acute liraglutide treatment (0.3 mg/kg s.c.) reduced cue-induced fentanyl seeking and blocked drug-induced reinstatement of fentanyl seeking, particularly when tested in estrus. Overall, these data support the broad effectiveness of acute GLP-1R agonists as a promising non-opioid treatment for OUD.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"16-29"},"PeriodicalIF":1.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2025-02-01Epub Date: 2024-12-24DOI: 10.1097/FBP.0000000000000803
Carlos Henrique Alves Jesus, Jaqueline Volpe, Bruna Bittencourt Sotomaior, Maria Augusta Ruy Barbosa, Matheus Vinicius Ferreira, Fernanda Fiatcoski, Karina Genaro, José Alexandre de Souza Crippa, Dênio Emanuel Pires Souto, Joice Maria da Cunha
{"title":"Morphine-induced side effects can be differentially modulated by cannabidiol in male and female rats.","authors":"Carlos Henrique Alves Jesus, Jaqueline Volpe, Bruna Bittencourt Sotomaior, Maria Augusta Ruy Barbosa, Matheus Vinicius Ferreira, Fernanda Fiatcoski, Karina Genaro, José Alexandre de Souza Crippa, Dênio Emanuel Pires Souto, Joice Maria da Cunha","doi":"10.1097/FBP.0000000000000803","DOIUrl":"10.1097/FBP.0000000000000803","url":null,"abstract":"<p><p>Opioid use disorder is a public health problem that includes symptoms such as withdrawal syndrome and opioid-induced hyperalgesia. Currently, drugs to treat side effects of opioids also have undesirable effects, which lead to limitations. This study investigated the effect of a treatment with cannabidiol in morphine-induced hyperalgesia and withdrawal behavior in morphine-dependent rats. Male and female rats were submitted to a morphine-induced physical dependence protocol consisting of a twice daily treatment with morphine (filtered solution, dose of 7.89 mg/kg, 1 ml/kg, s.c.) for 10 days. Nociception was measured using the hot plate test and morphine-induced thermal hyperalgesia was equally achieved following 7-10 days of morphine administration in male and female rats. Repeated treatment with cannabidiol (30 mg/kg) was sufficient to prevent thermal hyperalgesia in male and female rats. Subsequently, rats received an acute administration of naloxone (2 mg/kg. s.c.), 90 min after the morphine treatment on day 11, the number of withdrawal behaviors was scored. Rats that received treatment exclusively with morphine presented significant withdrawal behaviors compared to control (Water). Morphine-dependent female rats showed a prevalent stereotyped behavior of rearing, whereas male rats had teeth chattering behavior as the most preeminent. Treatment with cannabidiol on day 11 partially attenuated withdrawal behavior in morphine-dependent male rats, with mild effects in female rats (high withdrawal responders only). Altogether, our data provide evidence of an anti-hyperalgesic effect of cannabidiol in rats. Male and female rats treated chronically with morphine exhibited withdrawal behaviors in different ratios, and cannabidiol treatment attenuated withdrawal behavior in a sex-dependent manner.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"1-15"},"PeriodicalIF":1.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2025-02-01Epub Date: 2024-12-12DOI: 10.1097/FBP.0000000000000804
Carlos Novoa, Prescilla Garcia-Trevizo, Thomas J Gould
{"title":"Age is associated with altered locomotor and hypothermic response to acute nicotine.","authors":"Carlos Novoa, Prescilla Garcia-Trevizo, Thomas J Gould","doi":"10.1097/FBP.0000000000000804","DOIUrl":"10.1097/FBP.0000000000000804","url":null,"abstract":"<p><p>Cigarette smoking is at an all-time low. However, nicotine consumption has diversified with the introduction of commercial tobacco products that include Electronic Nicotine Delivery Systems. Nicotine is the main psychoactive component of tobacco and contributes to the addictive properties of tobacco products. Prolonged nicotine exposure induces neural adaptations that promote addiction-related behaviors in an age-dependent manner. Here, we investigated nicotine sensitivity among young adult and middle-aged male mice by comparing initial responses to nicotine tartrate from different suppliers. We observed that all nicotine compounds tested in the present study induced a robust reduction in locomotor activity and body temperature, and nicotine exposure resulted in increased serum cotinine concentration. We observed age-related differences in the magnitude and the time course of nicotine responses for locomotor and hypothermic effects. Reduction in locomotor activity was larger among young adult mice, but the time course of this response was similar for both age groups. Nicotine-induced reduction in body temperature was of a comparable magnitude for both age groups but young adults showed a faster decrease than middle-aged mice. These results suggest that age of exposure is a key factor contributing to nicotine sensitivity and its potential addictive effects. These responses were consistently produced for nicotine tartrate from different sources. Our findings reveal distinct responses between young adults and middle-aged mice, suggesting that age-specific neurobiological mechanisms in nicotine sensitivity continue developing into adulthood. These age-related variations in nicotine response are crucial for developing targeted interventions and understanding the risk factors for nicotine dependence across the lifespan.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"60-69"},"PeriodicalIF":1.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11836891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2024-12-01Epub Date: 2024-10-22DOI: 10.1097/FBP.0000000000000796
Ali Dehghani, Gholam Hossein Meftahi, Hedayat Sahraei
{"title":"The administration of a phentolamine infusion into the basolateral amygdala enhances long-term memory and diminishes anxiety-like behavior in stressed rats.","authors":"Ali Dehghani, Gholam Hossein Meftahi, Hedayat Sahraei","doi":"10.1097/FBP.0000000000000796","DOIUrl":"10.1097/FBP.0000000000000796","url":null,"abstract":"<p><p>The basolateral amygdala (BLA) contains adrenergic receptors, which are known to be involved in stress, anxiety, and memory. The objective of this study was to explore whether inhibition of α-adrenergic receptors (by phentolamine, an α-adrenergic receptor antagonist) in the BLA can reduce foot-shock stress-induced anxiety-like behavior, memory deficits, and long-term potentiation (LTP) deficits within the CA1 region of the rat hippocampus. Forty male Wistar rats were assigned to the intact, control, stress (Str), Phent (phentolamine), and Phent + Str groups. Animals were subjected to six shocks on 4 consecutive days, and phentolamine was injected into BLA 20 min before the animals were placed in the foot-shock stress apparatus. Results from the elevated plus maze test (EPM) revealed a reduction in anxiety-like behaviors (by an increased number of entries into the open arm, percentage of time spent in the open arm, and rearing and freezing) among stressed animals upon receiving injections of phentolamine into the BLA. The open-field test results (increased rearing, grooming, and freezing behaviors) were consistent with the EPM test results. Phentolamine infusion into the BLA enhanced spatial memory, reducing errors in finding the target hole and decreasing latency time in the Barnes maze test for stress and nonstress conditions. Injecting phentolamine into the BLA on both sides effectively prevented LTP impairment in hippocampal CA1 neurons after being subjected to foot-shock stress. It has been suggested that phentolamine in the BLA can effectively improve anxiety-like behaviors and memory deficits induced by foot-shock stress.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"419-431"},"PeriodicalIF":1.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142457075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2024-12-01Epub Date: 2024-10-08DOI: 10.1097/FBP.0000000000000797
Ismail Akgoz, Huseyin Kara, Ozgen Ozcelik, Levent Donmez, Mehmet Eryilmaz, Gul Ozbey
{"title":"Evaluation of akathisia in patients receiving selective serotonin reuptake inhibitors/serotonin and noradrenaline reuptake inhibitors.","authors":"Ismail Akgoz, Huseyin Kara, Ozgen Ozcelik, Levent Donmez, Mehmet Eryilmaz, Gul Ozbey","doi":"10.1097/FBP.0000000000000797","DOIUrl":"10.1097/FBP.0000000000000797","url":null,"abstract":"<p><p>Akathisia is an underestimated but disturbing extrapyramidal side effect of antidepressants, which could reduce treatment compliance in mood disorders. This study aimed to investigate the frequency and risk factors in patients treated with selective serotonin reuptake inhibitors/serotonin and noradrenaline reuptake inhibitors (SSRI/SNRI). In addition, we assessed the impact of akathisia on the quality of life (QoL). Patients were aged between 18 and 75 years, receiving an SSRI/SNRI for 4-8 weeks, and were diagnosed with anxiety, depression, or obsessive-compulsive disorder. The Barnes Akathisia Rating Scale was used to assess the severity of the akathisia. QoL was evaluated using the Short Form 36 (SF-36) questionnaire. Akathisia was observed in 25% (50/198) of patients. Smokers and younger patients were more frequent among patients with akathisia. Physical functioning, physical role, vitality, and mental health domains of the SF-36 were reduced in the presence of akathisia. In conclusion, our results suggest that akathisia is not a rare side effect of SSRI/SNRI in patients with mood disorders, especially in smokers and younger patients. In addition, akathisia may reduce treatment compliance owing to a reduction in QoL. Further investigations are needed to confirm the risk factors, frequency, and consequences of treatment compliance for SSRI/SNRI-induced akathisia in patients with mood disorders.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"460-463"},"PeriodicalIF":1.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Behavioural PharmacologyPub Date : 2024-12-01Epub Date: 2024-10-04DOI: 10.1097/FBP.0000000000000794
Fatemeh Khakpai
{"title":"Norharmane potentiated anxiolytic- and antidepressant-like responses induced by imipramine and citalopram: an isobologram analysis.","authors":"Fatemeh Khakpai","doi":"10.1097/FBP.0000000000000794","DOIUrl":"10.1097/FBP.0000000000000794","url":null,"abstract":"<p><p>β-carboline compounds display a therapeutic property for treating depression and anxiety behaviors. Imipramine and citalopram play an important role in the modulation of anxiety and depression behaviors. We investigated the effects of norharmane, imipramine, and citalopram on anxiety- and depression-like effects and their interactions. Elevated plus maze and forced swimming test were used for the assessment of anxiety- and depression-like behaviors in male mice. The results revealed that intraperitoneal (i.p.) administration of norharmane (10 mg/kg) increased percentage of open arm time (%OAT) in the elevated plus maze test and decreased immobility time in the forced swimming test, proposing anxiolytic- and antidepressant-like effects. Injection of imipramine (5 mg/kg; i.p.) enhanced %OAT and decreased immobility time, suggesting anxiolytic- and antidepressant-like effects. Moreover, norharmane potentiated the anxiolytic- and antidepressant-like responses induced by imipramine by increasing %OAT and decreasing immobility time. The results revealed additive anxiolytic- and antidepressant-like effects between norharmane and imipramine in mice. Alone, the administration of citalopram (5 mg/kg; i.p.) enhanced %OAT and reduced immobility time, causing anxiolytic- and antidepressant-like effects. When citalopram and norharmane were coinjected, norharmane augmented the anxiolytic- and antidepressant-like effects induced by citalopram by increasing %OAT and reducing immobility time. These results indicated additive anxiolytic- and antidepressant-like effects between norharmane and antidepressant drugs such as imipramine and citalopram on the modulation of anxiety and depression processes in mice.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"432-441"},"PeriodicalIF":1.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}