Keeping track of time intervals is a crucial aspect of behavior and cognition. Many theoretical models of how the brain times behavior make predictions for steady-state performance of well-learned intervals, but the rate of learning intervals in these models varies greatly, ranging from one-shot learning to learning over thousands of trials. Here, we explored how quickly rats and mice adapt to changes in interval durations using a serial fixed-interval task. In the first experiment, animals experienced randomly selected fixed-intervals of 12, 24, 36, 48, or 60 s, for blocks ranging from 13 to 21 trials. Consistent with previous work, animals abruptly increased lever pressing as reward availability approached, and these 'start times' scaled with the interval duration for both species. We then quantified the rate of updating to new trial durations and found that rodents consistently updated their start times within 2-3 trials following a change in interval duration, before stabilizing their behavior by the third or fourth trial. To account for repeated exposures to fixed-interval durations, a second set of animals was tested with new fixed-intervals after being trained on the serial fixed-interval task described above. Next, a third group was trained on fixed-interval durations that were generated de novo in each day. In each of these contexts, rodents rapidly increased or decreased their start times to mirror new FI durations following exposure to 1-2 trials of new intervals following block transitions. This work adds to growing evidence for rapid duration learning across species, highlighting the need for timing models to be capable of rapid updating in dynamic temporal scenarios.
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http://dx.doi.org/10.1007/s10071-025-01930-9 | DOI Listing |
Anim Cogn
January 2025
Neuroscience Department, Oberlin College, 173 Lorain St, Oberlin, OH, USA.
Keeping track of time intervals is a crucial aspect of behavior and cognition. Many theoretical models of how the brain times behavior make predictions for steady-state performance of well-learned intervals, but the rate of learning intervals in these models varies greatly, ranging from one-shot learning to learning over thousands of trials. Here, we explored how quickly rats and mice adapt to changes in interval durations using a serial fixed-interval task.
View Article and Find Full Text PDFBr J Anaesth
January 2025
Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. Electronic address:
Background: Chronic neuropathic pain generally has a poor response to treatment with conventional drugs. Sympathectomy can alleviate neuropathic pain in some patients, suggesting that abnormal sympathetic-somatosensory signaling interactions might underlie some forms of neuropathic pain. The molecular mechanisms underlying sympathetic-somatosensory interactions in neuropathic pain remain obscure.
View Article and Find Full Text PDFJ Nucl Med
January 2025
Intramural Research Program, National Institute of Mental Health, Bethesda, Maryland;
Cyclooxygenase-2 (COX-2) is present in a healthy brain at low densities but can be markedly upregulated by excitatory input and by inflammogens. This study evaluated the sensitivity of the PET radioligand [C]-6-methoxy-2-(4-(methylsulfonyl)phenyl)--(thiophen-2-ylmethyl)pyrimidin-4-amine ([C]MC1) to detect COX-2 density in a healthy human brain. The specificity of [C]MC1 was confirmed using lipopolysaccharide-injected rats and transgenic mice expressing the human gene, with 120-min baseline and blocked scans using COX-1 and COX-2 selective agents.
View Article and Find Full Text PDFScience
January 2025
Laboratory of Cerebral Cortex Research, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Rewards are essential for motivation, decision-making, memory, and mental health. We identified the subventricular tegmental nucleus (SVTg) as a brainstem reward center. In mice, reward and its prediction activate the SVTg, and SVTg stimulation leads to place preference, reduced anxiety, and accumbal dopamine release.
View Article and Find Full Text PDFDokl Biochem Biophys
January 2025
Center for Strategic Planning and Management of Biomedical Health Risks, Federal Medical and Biological Agency, Moscow, Russia.
Unlabelled: The association of the pathogenesis of neurodegenerative diseases, depression, anxiety, and cognitive disorders with neurotrophin-3 deficiency determines the prospect of creating drugs with a similar mechanism of action. Since the use of full-length NT-3 is limited by unsatisfactory pharmacokinetic properties, the creation of low-molecular mimetics of neurotrophin-3 that are active when administered systemically is relevant. The Federal Research Center for Innovator and Emerging Biomedical and Pharmaceutical Technologies has created a dimeric dipeptide mimetic of the 4th loop of NT-3, hexamethylenediamide bis-(N-γ-oxybutyryl-L-glutamyl-L-asparagine) with the laboratory code GTS-302, which activates TrkC and TrkB receptors.
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