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Thalamofrontal synaptic weakening underlies short-term memory deficits from adolescent NMDAR hypofunction.

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Τίτλος: Thalamofrontal synaptic weakening underlies short-term memory deficits from adolescent NMDAR hypofunction.
Συγγραφείς: Yu J; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.; Department of Brain Sciences, Daegu Gyeongbuk Institute of Science & Technology (DGIST), Daegu, Republic of Korea., Choi IS; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea., Kim GH; Neural Circuits Research Group, KBRI, Daegu, Republic of Korea., Bahn S; Cognitive Science Group, KBRI, Daegu, Republic of Korea., Kim J; Department of Electrical Engineering and Computer Science, DGIST, Daegu, Republic of Korea., Bae S; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.; Department of Pharmacology, College of Medicine, Yonsei University, Seoul, Republic of Korea., Lee T; Brain Research Core Facility, KBRI, Daegu, Republic of Korea., Choi JH; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea., Kwon JS; Department of Psychiatry, Hanyang University Hospital, Seoul, Republic of Korea.; Institute of Human Behavioral Medicine, Seoul National University (SNU) Medical Research Center, Seoul, Republic of Korea., Kim M; Institute of Human Behavioral Medicine, Seoul National University (SNU) Medical Research Center, Seoul, Republic of Korea.; Department of Psychiatry, SNU College of Medicine, Seoul, Republic of Korea.; Department of Neuropsychiatry, SNU Hospital, Seoul, Republic of Korea., Choi JW; Department of Electrical Engineering and Computer Science, DGIST, Daegu, Republic of Korea.; Brain Engineering Convergence Research Center, DGIST, Daegu, Republic of Korea.; Biomedical Science and Engineering, DGIST, Daegu, Republic of Korea., Lee KJ; Neural Circuits Research Group, KBRI, Daegu, Republic of Korea., Rah JC; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.; Department of Brain Sciences, Daegu Gyeongbuk Institute of Science & Technology (DGIST), Daegu, Republic of Korea.; Brain Engineering Convergence Research Center, DGIST, Daegu, Republic of Korea.; Biomedical Science and Engineering, DGIST, Daegu, Republic of Korea.
Πηγή: Science advances [Sci Adv] 2026 Sep 25; Vol. 12 (39), pp. eaee2152. Date of Electronic Publication: 2026 Sep 23.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: American Association for the Advancement of Science Country of Publication: United States NLM ID: 101653440 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2375-2548 (Electronic) Linking ISSN: 23752548 NLM ISO Abbreviation: Sci Adv Subsets: MEDLINE
Imprint Name(s): Original Publication: Washington, DC : American Association for the Advancement of Science, [2015]-
Ιατρικοί όροι (MeSH): Receptors, N-Methyl-D-Aspartate*/metabolism , Receptors, N-Methyl-D-Aspartate*/antagonists & inhibitors , Memory, Short-Term*/drug effects , Memory Disorders*/physiopathology , Memory Disorders*/metabolism , Memory Disorders*/etiology , Synapses*/metabolism , Prefrontal Cortex*/physiopathology , Prefrontal Cortex*/metabolism , Thalamus*/physiopathology , Thalamus*/metabolism, Synaptic Transmission/drug effects ; Ketamine/pharmacology ; Animals ; Mice ; Male
Περίληψη: Thalamofrontal (TF) dysconnectivity is one of the most consistent circuit-level abnormalities reported in patients with schizophrenia and is linked to deficits in short-term memory (STM). However, the biological mechanisms underlying TF weakening remain unclear. Here, we show that repeated adolescent N-methyl-d-aspartate receptor (NMDAR) antagonism produces STM deficits by impairing TF synaptic transmission. In mice repeatedly exposed to ketamine, STM impairment coincided with reduced release probability and attenuated short-term depression at mediodorsal thalamus (MD) → dorsomedial prefrontal cortex (dmPFC) synapses, without detectable changes in corticocortical synaptic release probability, intrinsic excitability, or gross synaptic ultrastructure. These presynaptic deficits were accompanied by diminished direction-selective population coding in the dmPFC and impaired delayed alternation performance. Chemogenetically strengthening MD → dmPFC projections restored both neural selectivity and behavior. These findings identify a projection-specific presynaptic mechanism through which adolescent NMDAR hypofunction weakens TF communication and produces cognitive impairment, offering a biological explanation for clinically observed TF dysconnectivity and establishing TF synapses as a therapeutic target.
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Substance Nomenclature: 0 (Receptors, N-Methyl-D-Aspartate)
690G0D6V8H (Ketamine)
Entry Date(s): Date Created: 20260923 Date Completed: 20260923 Latest Revision: 20260925
Update Code: 20260925
PubMed Central ID: PMC13600250
DOI: 10.1126/sciadv.aee2152
PMID: 42777060
Βάση Δεδομένων: MEDLINE
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  Data: Thalamofrontal synaptic weakening underlies short-term memory deficits from adolescent NMDAR hypofunction.
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  Data: <searchLink fieldCode="AU" term="%22Yu+J%22">Yu J</searchLink>; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.; Department of Brain Sciences, Daegu Gyeongbuk Institute of Science & Technology (DGIST), Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Choi+IS%22">Choi IS</searchLink>; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Kim+GH%22">Kim GH</searchLink>; Neural Circuits Research Group, KBRI, Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Bahn+S%22">Bahn S</searchLink>; Cognitive Science Group, KBRI, Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Kim+J%22">Kim J</searchLink>; Department of Electrical Engineering and Computer Science, DGIST, Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Bae+S%22">Bae S</searchLink>; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.; Department of Pharmacology, College of Medicine, Yonsei University, Seoul, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Lee+T%22">Lee T</searchLink>; Brain Research Core Facility, KBRI, Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Choi+JH%22">Choi JH</searchLink>; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Kwon+JS%22">Kwon JS</searchLink>; Department of Psychiatry, Hanyang University Hospital, Seoul, Republic of Korea.; Institute of Human Behavioral Medicine, Seoul National University (SNU) Medical Research Center, Seoul, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Kim+M%22">Kim M</searchLink>; Institute of Human Behavioral Medicine, Seoul National University (SNU) Medical Research Center, Seoul, Republic of Korea.; Department of Psychiatry, SNU College of Medicine, Seoul, Republic of Korea.; Department of Neuropsychiatry, SNU Hospital, Seoul, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Choi+JW%22">Choi JW</searchLink>; Department of Electrical Engineering and Computer Science, DGIST, Daegu, Republic of Korea.; Brain Engineering Convergence Research Center, DGIST, Daegu, Republic of Korea.; Biomedical Science and Engineering, DGIST, Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Lee+KJ%22">Lee KJ</searchLink>; Neural Circuits Research Group, KBRI, Daegu, Republic of Korea.<br /><searchLink fieldCode="AU" term="%22Rah+JC%22">Rah JC</searchLink>; Sensory and Motor Systems Research Group, Korea Brain Research Institute (KBRI), Daegu, Republic of Korea.; Department of Brain Sciences, Daegu Gyeongbuk Institute of Science & Technology (DGIST), Daegu, Republic of Korea.; Brain Engineering Convergence Research Center, DGIST, Daegu, Republic of Korea.; Biomedical Science and Engineering, DGIST, Daegu, Republic of Korea.
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  Data: <searchLink fieldCode="MM" term="%22Receptors%2C+N-Methyl-D-Aspartate%22">Receptors, N-Methyl-D-Aspartate*</searchLink>/<searchLink fieldCode="MM" term="%22Receptors%2C+N-Methyl-D-Aspartate+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Receptors%2C+N-Methyl-D-Aspartate%22">Receptors, N-Methyl-D-Aspartate*</searchLink>/<searchLink fieldCode="MM" term="%22Receptors%2C+N-Methyl-D-Aspartate+antagonists+%26+inhibitors%22">antagonists & inhibitors</searchLink> <br /><searchLink fieldCode="MM" term="%22Memory%2C+Short-Term%22">Memory, Short-Term*</searchLink>/<searchLink fieldCode="MM" term="%22Memory%2C+Short-Term+drug+effects%22">drug effects</searchLink> <br /><searchLink fieldCode="MM" term="%22Memory+Disorders%22">Memory Disorders*</searchLink>/<searchLink fieldCode="MM" term="%22Memory+Disorders+physiopathology%22">physiopathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Memory+Disorders%22">Memory Disorders*</searchLink>/<searchLink fieldCode="MM" term="%22Memory+Disorders+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Memory+Disorders%22">Memory Disorders*</searchLink>/<searchLink fieldCode="MM" term="%22Memory+Disorders+etiology%22">etiology</searchLink> <br /><searchLink fieldCode="MM" term="%22Synapses%22">Synapses*</searchLink>/<searchLink fieldCode="MM" term="%22Synapses+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Prefrontal+Cortex%22">Prefrontal Cortex*</searchLink>/<searchLink fieldCode="MM" term="%22Prefrontal+Cortex+physiopathology%22">physiopathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Prefrontal+Cortex%22">Prefrontal Cortex*</searchLink>/<searchLink fieldCode="MM" term="%22Prefrontal+Cortex+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Thalamus%22">Thalamus*</searchLink>/<searchLink fieldCode="MM" term="%22Thalamus+physiopathology%22">physiopathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Thalamus%22">Thalamus*</searchLink>/<searchLink fieldCode="MM" term="%22Thalamus+metabolism%22">metabolism</searchLink><br /><searchLink fieldCode="MH" term="%22Synaptic+Transmission%22">Synaptic Transmission</searchLink>/<searchLink fieldCode="MH" term="%22Synaptic+Transmission+drug+effects%22">drug effects</searchLink> ; <searchLink fieldCode="MH" term="%22Ketamine%22">Ketamine</searchLink>/<searchLink fieldCode="MH" term="%22Ketamine+pharmacology%22">pharmacology</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Mice%22">Mice</searchLink> ; <searchLink fieldCode="MH" term="%22Male%22">Male</searchLink>
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  Data: Thalamofrontal (TF) dysconnectivity is one of the most consistent circuit-level abnormalities reported in patients with schizophrenia and is linked to deficits in short-term memory (STM). However, the biological mechanisms underlying TF weakening remain unclear. Here, we show that repeated adolescent N-methyl-d-aspartate receptor (NMDAR) antagonism produces STM deficits by impairing TF synaptic transmission. In mice repeatedly exposed to ketamine, STM impairment coincided with reduced release probability and attenuated short-term depression at mediodorsal thalamus (MD) → dorsomedial prefrontal cortex (dmPFC) synapses, without detectable changes in corticocortical synaptic release probability, intrinsic excitability, or gross synaptic ultrastructure. These presynaptic deficits were accompanied by diminished direction-selective population coding in the dmPFC and impaired delayed alternation performance. Chemogenetically strengthening MD → dmPFC projections restored both neural selectivity and behavior. These findings identify a projection-specific presynaptic mechanism through which adolescent NMDAR hypofunction weakens TF communication and produces cognitive impairment, offering a biological explanation for clinically observed TF dysconnectivity and establishing TF synapses as a therapeutic target.
– Name: Ref
  Label: References
  Group: RefInfo
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