Behavioural PharmacologyPub Date : 2025-06-01Epub Date: 2024-12-16DOI: 10.1097/FBP.0000000000000809
Ronan Depoortère, Mariusz Papp, Piotr Gruca, Ewa Litwa, Magdalena Lason, Dominika Biała, Adrian Newman-Tancredi
{"title":"The antidepressant-like activity of ketamine in the rat chronic mild stress model requires activation of cortical 5-HT 1A receptors.","authors":"Ronan Depoortère, Mariusz Papp, Piotr Gruca, Ewa Litwa, Magdalena Lason, Dominika Biała, Adrian Newman-Tancredi","doi":"10.1097/FBP.0000000000000809","DOIUrl":"10.1097/FBP.0000000000000809","url":null,"abstract":"<p><p>Ketamine displays efficacious rapid-acting antidepressant (RAAD) activity in the rat chronic mild stress (CMS) model. It rapidly reverses anhedonia (CMS-induced sucrose consumption deficit) and attenuates working memory deficit (novel object recognition: NOR) following both systemic (intraperitoneal, i.p.) administration or local administration in the prefrontal cortex (PFC). However, the receptor mechanisms underlying these effects remain to be clarified and may involve activation of serotonin 5-HT 1A receptors, as previously found in experiments using the forced swim test. The present study explored the contribution of PFC 5-HT 1A receptors in ketamine's RAAD activity in the CMS model. Ketamine (10 mg/kg i.p.) reversed CMS-induced sucrose consumption and working memory (NOR test) deficits. Notably, unilateral PFC microinjections of a 5-HT 1A receptor antagonist, WAY-100635 (2 µg), prevented the antidepressant-like and pro-cognitive activity of systemic ketamine on sucrose consumption and working memory deficits. These data indicate that the RAAD activity of ketamine in the rat CMS model requires activation of PFC 5-HT 1A receptors. They also reinforce the notion that drugs that directly activate PFC 5-HT 1A receptors could constitute an alternative to ketamine as a promising strategy to achieve RAAD effects, with additional benefits against cognitive deficits in depressed patients, but without ketamine's troublesome side-effects and requirements for in-patient supervision.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"182-188"},"PeriodicalIF":1.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881072","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 : 2025-06-01Epub Date: 2025-05-07DOI: 10.1097/FBP.0000000000000827
Samuel Budniok
{"title":"The complexity of socially transmitted food preferences in rodents: a model for human epistemic trust?","authors":"Samuel Budniok","doi":"10.1097/FBP.0000000000000827","DOIUrl":"10.1097/FBP.0000000000000827","url":null,"abstract":"<p><p>Social safety learning refers to the process by which animals indirectly learn about the safety of novel stimuli. This process is critical when rodents decide what to eat since they lack the capacity to vomit, reducing their ability to expel ingested toxins. Consequently, rodents display neophobia when encountering novel food, but are more likely to eat the food when a conspecific signals its safety. This natural behavior is modeled using the social transmission of food preference (STFP) paradigm. Based on behavioral and neural insights into STFP, I argue in the current work that its acquisition may involve cognitive processes that extend beyond social safety learning. Specifically, I argue that STFP acquisition may parallel functional aspects of human epistemic trust. Epistemic trust refers to trust in communicated knowledge, enabling humans to learn from, adapt to, and respond to their (social) environment. This perspective could position the STFP paradigm as a valuable tool to investigate the neurobiology of cognitive processes that may be relevant to human epistemic trust. Given the importance of epistemic trust in therapeutic settings, understanding its neurobiology may have direct clinical implications.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":"36 4","pages":"196-201"},"PeriodicalIF":1.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963828","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 : 2025-06-01Epub Date: 2025-05-07DOI: 10.1097/FBP.0000000000000829
Bart A Ellenbroek, Louk J M J Vanderschuren, Gernot Riedel
{"title":"In memory of Dr Emily Jutkiewicz, 1975-2024.","authors":"Bart A Ellenbroek, Louk J M J Vanderschuren, Gernot Riedel","doi":"10.1097/FBP.0000000000000829","DOIUrl":"https://doi.org/10.1097/FBP.0000000000000829","url":null,"abstract":"","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":"36 4","pages":"161-162"},"PeriodicalIF":1.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953162","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 : 2025-06-01Epub Date: 2025-04-01DOI: 10.1097/FBP.0000000000000826
Justyna K Hinchcliffe, Sarah A Stuart, Emma S J Robinson
{"title":"Investigating the effects of different herbal preparations, 5-hydroxytryptophan and involuntary exercise on affective bias modification in male Lister Hooded rats.","authors":"Justyna K Hinchcliffe, Sarah A Stuart, Emma S J Robinson","doi":"10.1097/FBP.0000000000000826","DOIUrl":"10.1097/FBP.0000000000000826","url":null,"abstract":"<p><p>Mood disorders are a prevalent global health concern with natural health products, including herbal supplements, an increasingly popular choice as an alternative or complementary therapy. Despite their widespread use, few studies have tested the clinical efficacy of natural health products or explored their underlying mechanisms in animal models. Modification of affective biases has been linked to mood in humans and animal models and may provide insights into potential antidepressant effects. In this study, we used a translational rodent model of affective bias modification to investigate the effects of five commonly used supplements: Hypericum perforatum , that is, St. John's Wort (SJW), Mucuna pruriens , Rhodiola rosea root extract, Valerian root extract and 5-hydroxytryptophan. Exercise is also thought to improve mood disorders, but clinical studies reveal mixed results therefore we also tested the effect of involuntary exercise on affective biases. In separate experiments, male Lister Hooded rats were acutely treated with SJW, Mucuna pruriens , Rhodiola rosea root extract, Valerian root extract and 5-hydroxytryptophan, or underwent an involuntary exercise manipulation. Our results showed a significant positive affective bias following treatment with SJW, whilst the involuntary exercise induced a negative affective bias in rats. No effects were found following the other acute treatments. These data suggest SJW has similar effects in terms of affective bias modification as conventional antidepressants. The negative affective bias observed with involuntary exercise suggests the animals experience a negative affective state and suggests exercise-based therapy may be less effective if the patient perceives this as involuntary.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":"189-195"},"PeriodicalIF":1.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762527","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 : 2025-06-01Epub Date: 2025-05-07DOI: 10.1097/FBP.0000000000000819
Emma S J Robinson
{"title":"Delivering a new generation of translational animal models for depression research.","authors":"Emma S J Robinson","doi":"10.1097/FBP.0000000000000819","DOIUrl":"10.1097/FBP.0000000000000819","url":null,"abstract":"<p><p>Early animal models of depression focused on developing methods that could predict treatment efficacy and were validated based on pharmacological responses to known antidepressants. As our understanding of major depressive disorder (MDD) and the pharmacology of antidepressants progressed, so did the need for better animal models. This need was met with the development of new disease models, such as the chronic mild stress model, and behavioural readouts such as the sucrose preference test, which more closely aligned with risk factors and symptoms seen in patients. These approaches have supported huge advances in the understanding of how stress affects the brain and impacts on reward-related behaviours. However, there remain significant challenges when trying to model complex psychiatric symptoms and disorders in non-human animals. In this perspective article, a brief history of animal models of depression and associated readouts is discussed with specific reference to the important contributions from Paul Willner. The main discussion then focuses on translational validity and approaches that may support delivering this objective. This is illustrated with the example of the affective bias test and reward learning assays, which have been developed to recapitulate in animals the neuropsychological impairments observed in MDD and modulation by antidepressants.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":"36 4","pages":"175-181"},"PeriodicalIF":1.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957572","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 : 2025-06-01Epub Date: 2025-05-07DOI: 10.1097/FBP.0000000000000816
Kate M Witt, David N Harper, Bart A Ellenbroek
{"title":"A review on the validity of animal models for neuropsychiatric disorders: an exploration of anhedonia.","authors":"Kate M Witt, David N Harper, Bart A Ellenbroek","doi":"10.1097/FBP.0000000000000816","DOIUrl":"https://doi.org/10.1097/FBP.0000000000000816","url":null,"abstract":"<p><p>Despite major advances in neuroscience, there has been limited progress in improving pharmacological treatment for neuropsychiatric disorders. Neuropsychiatric disorders are heterogeneous with variance in symptoms within disorders and partial overlap in symptoms between disorders, leading to symptoms that remain untreated. To improve treatment outcomes, neuroscience has shifted to examining the neurobiological mechanisms underlying individual components, or dysfunctions, across disorders. Anhedonia, a decreased capacity to experience pleasure from positive stimuli or rewards, is a prominent symptom associated with poor functional outcome across neuropsychiatric disorders. This article reflects on Professor Paul Willner's contributions to the field of behavioural neuroscience, specifically his promotion of validity in animal models of neuropsychiatric disorders. Research can build upon Willner's scholarship by continuing to refine and explore the validity of animal models as our understanding of neuropsychiatric disorders improves. To exemplify this, we discuss current understanding of the neurobiological basis and clinical presentation of the two domains of anhedonia: anticipation and consumption. We argue for the examination of anticipatory anhedonia and consummatory anhedonia within a single paradigm to improve understanding of these domains, aligning animal models to the clinical reality in humans.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":"36 4","pages":"165-170"},"PeriodicalIF":1.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968079","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 : 2025-06-01Epub Date: 2025-05-07DOI: 10.1097/FBP.0000000000000817
Morgane Colom, Amy L Milton, Trevor W Robbins
{"title":"'Only connect': cognition meets motivation as cognitive effort to enhance models of depression.","authors":"Morgane Colom, Amy L Milton, Trevor W Robbins","doi":"10.1097/FBP.0000000000000817","DOIUrl":"https://doi.org/10.1097/FBP.0000000000000817","url":null,"abstract":"","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":"36 4","pages":"171-174"},"PeriodicalIF":1.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972740","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}
{"title":"Neurobehavioral manifestations in female rats after intermittent exposure to an anticancer agent, paclitaxel.","authors":"Deepika Pathak, K P Singh","doi":"10.1097/FBP.0000000000000833","DOIUrl":"https://doi.org/10.1097/FBP.0000000000000833","url":null,"abstract":"<p><p>Paclitaxel (PTX), a widely used chemotherapeutic agent, causes both peripheral and central neurotoxicity, leading to significant behavioral impairments. However, inadequate literature is available on PTX-induced neurobehavioral sequelae associated with anxiety, depression, and cognition in adults during and after chemotherapy. Therefore, the present study aimed to investigate neurobehavioral impairments in adult female rats following PTX exposure, with a specific focus on anxiety-like behaviors and cognitive functions such as learning and memory. In this study, we used adult female Wistar rats aged 10-12 weeks (average weight: 180 ± 5 g) and administered clinically relevant therapeutic doses of PTX (1.6 and 3.2 mg/kg body weight) intravenously once weekly for 6 weeks, simulating the clinical chemotherapy regimen. Neurobehavioral assessments were conducted after the first and sixth doses of PTX using validated mazes, including the photoactometer, open-field maze, elevated plus-maze (EPM; for anxiety-like behaviors), and the step-down latency test (SDL; for cognitive performance). Neurobehavioral patterns were recorded using autotracking software (ANY-maze, Stoelting Co., Wood Dale, Illinois, USA). Our findings revealed substantially reduced locomotor activity in the photoactometer, increased anxiety-like behaviors with amplified fear emotionality in the open-field and EPM tests, and memory impairment in the SDL test. These results suggest that the manifestation of anxiogenic and cognitive behavioral changes is associated with the administration of a higher dose (3.2 mg/kg) of PTX. In conclusion, our study indicates that PTX causes significant neurobehavioral impairments in rats after exposure to equivalent therapeutic doses of PTX.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109587","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}
Ping-Hsun Tsai, Erica R Morales, Yvonne Y Reed, Hasan Qamar, Emily F Jones, Gopika Saji, Christopher P Ward, Ethan S Burstein, Georgina L Moreno, David H Malin
{"title":"5-HT2A receptor inverse agonist attenuates morphine withdrawal syndrome and its aversiveness in rats.","authors":"Ping-Hsun Tsai, Erica R Morales, Yvonne Y Reed, Hasan Qamar, Emily F Jones, Gopika Saji, Christopher P Ward, Ethan S Burstein, Georgina L Moreno, David H Malin","doi":"10.1097/FBP.0000000000000832","DOIUrl":"https://doi.org/10.1097/FBP.0000000000000832","url":null,"abstract":"<p><p>This study explored a potential role for the 5-hydroxytryptamine2A (5-HT2A) serotonin receptor in opiate physical dependence. Rats were rendered opiate-dependent by 7 days of continuous subcutaneous (s.c.) morphine sulfate infusion. Pimavanserin is a selective 5-HT2A receptor inverse agonist in current medical use. A day after termination of drug infusion, rats were injected s.c. with 0.3 or 1.0 mg/kg pimavanserin or saline alone. A nondependent control group was infused with saline alone and injected with saline. One hour after injections, all rats were observed under blind conditions for somatically expressed spontaneous withdrawal signs. While both pimavanserin doses significantly reduced withdrawal signs in the dependent rats, the higher dose reduced those signs to the level exhibited by the nondependent group. In a second experiment, utilizing only nondependent, saline-infused rats, pimavanserin had no significant effect vs. saline injection on overall signs. A third experiment extended these findings to naloxone-precipitated morphine withdrawal. Relative to saline injection, pimavanserin, 1.3 mg/kg s.c., significantly reduced withdrawal signs precipitated by 0.3 mg/kg naloxone 1 h later. This effect was reconfirmed in a separate experiment. The pimavanserin injection also significantly attenuated the aversiveness of morphine withdrawal, as indicated by reduced conditioned avoidance of the chamber where precipitated withdrawal had occurred. These results indicate a major role for the 5-HT2A receptor in opiate physical dependence and withdrawal syndrome, suggesting this receptor as a potential therapeutic target.</p>","PeriodicalId":8832,"journal":{"name":"Behavioural Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109573","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}