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Central Neuronal Pathways Involved in Psychotic Syndromes
Published in Fuad Lechin, Bertha van der Dijs, Neurochemistry and Clinical Disorders: Circuitry of Some Psychiatric and Psychosomatic Syndromes, 2020
Fuad Lechin, Bertha van der Dijs, Jose Amat, Marcel Lechin
DA-VTA cells have two kind of neurons: lateral DA neurons which innervate mesolimbic structures, and medial-anterior neurons innervating prefrontal cortex. Sufficient evidence exists to support a hypothesis that rewarding is related to septal and other mesolimbic but not cortical DA innervated structures. Furthermore, treatments which interfere with DA metabolism or synaptic action, clearly interfere with brain stimulation reward. Moreover, they do so by reducing the rewarding impact of stimulation and not merely by impairing the response capacity of the animal. Also, neuroleptics (DA blocking agents) have been found to cause major disruption of self-stimulation in every stimulation site thus far reported. All the above leads us to postulate a positive correlation between rewarding and DA mesolimbic but not DA mesocortical system. The latter seems to be closely related to punishment behavior and anxiogenic activity.200,316,317,319-346
Animal Models of Subtypes of Depression
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
Paul Willner, Paul J. Mitchell
In a variant of this procedure, animals self-administer cocaine, rather than being administered amphetamine [131]. In these experiments, the threshold for brain stimulation reward, administered through electrodes in the posterior lateral hypothalamus, was obtained using a discrete trial procedure [133], which is sensitive to changes in reward value, but not to changes in motor performance [167]. Following 24 h of cocaine self-administration, ICSS thresholds were elevated for several hours [131], indicating that cocaine withdrawal induced a state of anhedonia. Acute administration of the DA receptor agonist, bromocriptine, restored ICSS thresholds to normal [166]. Only one conventional antidepressant has been tested in this procedure: repeated administration of the TCA, DMI, was reported to shorten the duration of post-cocaine anhedonia [168].
Drug dependence as a split object: Trajectories of neuroscientification and behavioralization at the Max Planck Institute of Psychiatry
Published in Journal of the History of the Neurosciences, 2023
Overall, there was a great deal of overlap between the different research groups on drug dependence from the clinical and theoretical division at the Institute, and not just in that they were all studying questions of dependence at the same time at the same institution. They used metaphors that were partly similar; they dealt with substance dependence and referred to the WHO definition that stabilized the multiple phenomena of dependence; they all operated under the principle of basic research; they were subject to the same administrative rules; they all worked at an institution with a research clinic that had many addiction patients; and they partly shared similar theoretical and empirical foundations in regard to dependence that were evident, for example, in references to behaviorism or practices of animal experimentation. And, at least in the English-speaking context, the concept of “brain stimulation reward,” which combined behavioral and neuroscientific approaches, began to emerge in the 1970s (Campbell 2019, 242). Against this backdrop, it seems likely that the different groups at the MPIP could have ended up aligning their material, social, and epistemic components; built joint “repertoires” (Ankeny and Leonelli 2016); and started multidisciplinary collaborations. Accordingly, it appears plausible that the common research topic of substance dependence might have acted as a boundary object, at least in some specific research contexts.
Beneficial effects of atypical antipsychotics on object recognition deficits after adolescent toluene exposure in mice: involvement of 5-HT1A receptors
Published in The American Journal of Drug and Alcohol Abuse, 2022
Mei-Yi Lee, Chung-Pin Hsieh, Ming-Huan Chan, Hwei-Hsien Chen
Toluene is inhaled for its capacity to cause euphoria. However, the users do not continuously sniff or huff toluene for a long period of time, but rather prefer to titer their dose by repeatedly sniffing or huffing very-high-exposure concentrations for only seconds to minutes. This is difficult to accomplish in animal models. Intraperitoneal toluene injection produces dose-dependent enhancement of brain-stimulation reward (24–26) and full substitution for inhaled toluene vapor in drug discrimination (27), indicating that toluene is able to produce rewarding effects through this route. The present study further confirmed that intraperitoneal injection of toluene during adolescence can consistently produce enduring deficits in NORT in mice (15,20). Recognition of novel object possesses visual learning and recognition processing, which is an analog of declarative memory (28). This mouse model is suitable for the assessment of the beneficial effects of pharmacological therapy on this type of memory dysfunction after adolescent toluene exposure.
Discovery and development of varenicline for smoking cessation
Published in Expert Opinion on Drug Discovery, 2018
Chloe J. Jordan, Zheng-Xiong Xi
Preclinical studies indicate that varenicline is superior to cytisine in reducing nicotine addiction-related behaviors (Table 1). In rodents, varenicline attenuates nicotine-induced locomotor sensitization, blocks nicotine conditioned place preferences, reduces nicotine self-administration under fixed- and progressive-ratio schedules, and suppresses nicotine-primed as well as cue-induced reinstatement of nicotine seeking following intraperitoneal, subcutaneous, or oral routes of administration [39,42–45]. Varenicline also selectively blocks nicotine’s effects on brain stimulation reward in intracranial self-stimulation (ICSS) paradigms through activity at the α4β2, but not the α7, nAchR [46]. Finally, varenicline attenuates the dysphoria associated with nicotine withdrawal as measured by ICSS thresholds [47]. Taken together, these preclinical findings indicate varenicline may not only attenuate nicotine reward and intake, but could reduce the risk of relapse and mitigate withdrawal symptoms in nicotine-dependent subjects.