Role of the anterior cingulate cortex in the retrieval of novel object recognition memory after a long delay

Pezze, Marie A.; Marshall, Hayley J.; Fone, Kevin C. F.; Cassaday, Helen J.

doi:10.1101/lm.044784.116

Cited by 29 publications

(27 citation statements)

References 47 publications

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“…The novel object recognition task is the ability to distinguish the novel from familiar stimuli which is directly dependent on the prefrontal cortex and hippocampus function ( Banks et al, 2012 ; Pezze et al, 2017 ). In Figure 3A , the data obtained analyzed using paired t -test exhibited that animals spent equal time to explore both object A1 and A2 and there were not any significant preference in exploring two objects in familiarization phase in the M/N-Day 1 [ t (6) = 0.7381, P = 0.4883; ns], Day 5 [ t (6) = 0.5558, P = 0.5984; ns] and Day 10 [ t (6) = 0.5176, P = 0.6109; ns] groups as compared with their respective Saline control groups (right panel).…”

Section: Resultsmentioning

confidence: 99%

“…The long-lasting impairment in learning or memory after acute or chronic opioid administration might be associated with the persistent impairment of different brain functions through several mechanisms, including changes in central signaling proteins ( Lou et al, 1999 ), activation of apoptosis signaling pathway ( Emeterio et al, 2006 ) or impaired synaptic plasticity ( Pu et al, 2002 ). Previous results suggest that the hippocampus and prefrontal cortex are involved in the NOR task ( Banks et al, 2012 ; Pezze et al, 2017 ). The current findings indicate impairment of short-term memory in the NOR task on days 3, 7, and 12 (timeline was shown in Figure 1 ) after methadone overdose.…”

Section: Discussionmentioning

confidence: 99%

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Delay-Dependent Impairments in Memory and Motor Functions After Acute Methadone Overdose in Rats

et al. 2018

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Methadone is used as a substitution drug for the treatment of opioid dependence and chronic pain. Despite its widespread use and availability, there is a serious concern with respect to the relative safety of methadone. The purpose of this study was to characterize how acute methadone overdose affects the cognitive and motor performance of naïve healthy rats. The methadone overdose was induced by administering an acute toxic dose of methadone (15 mg/kg; ip; the equivalent dose of 80% of LD50) to adolescent rats. Resuscitation using a ventilator pump along with a single dose of naloxone (2 mg/kg; ip) was administered following the occurrence of apnea. The animals which were successfully resuscitated divided randomly into three apnea groups that evaluated either on day 1, 5, or 10 post-resuscitation (M/N-Day 1, M/N-Day 5, and M/N-Day 10 groups) in the Y-maze and novel object memory recognition tasks as well as pole and rotarod tests. The data revealed that a single toxic dose of methadone had an adverse effect on spontaneous behavior. In addition, Recognition memory impairment was observed in the M/N-Day 1, 5, and 10 groups after methadone-induced apnea. Further, descending time in the M/N-Day 5 group increased significantly in comparison with its respective Saline control group. The overall results indicate that acute methadone-overdose-induced apnea produced delay-dependent cognitive and motor impairment. We suggest that methadone poisoning should be considered as a possible cause of delayed neurological disorders, which might be transient, in some types of memory or motor performance in naïve healthy rats.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Delay-Dependent Impairments in Memory and Motor Functions After Acute Methadone Overdose in Rats

et al. 2018

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“…We extended the analysis and found that NSPA-KO mice also have an impaired LTP in MPP-DG synapses of dorsal hippocampus and performed poorly in object recognition tests, while open field assays did not detect anxiety-like behaviors. Object recognition tests not only reflect dysfunction in the hippocampus, as the memory flexibility test, but also in other brain regions such as the amygdala and cingulate cortex [ 51 , 52 ], where NSPA is also expressed [ 18 , 20 ]. All these results highlight a role of NSPA in glutamatergic synaptic plasticity associated with memory processes in the hippocampus and suggest other functional alterations remaining to be defined at different brain regions.…”

Section: Discussionmentioning

confidence: 99%

Neuronal surface P antigen (NSPA) modulates postsynaptic NMDAR stability through ubiquitination of tyrosine phosphatase PTPMEG

et al. 2020

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Background Cognitive dysfunction (CD) is common among patients with the autoimmune disease systemic lupus erythematosus (SLE). Anti-ribosomal P autoantibodies associate with this dysfunction and have neuropathogenic effects that are mediated by cross-reacting with neuronal surface P antigen (NSPA) protein. Elucidating the function of NSPA can then reveal CD pathogenic mechanisms and treatment opportunities. In the brain, NSPA somehow contributes to glutamatergic NMDA receptor (NMDAR) activity in synaptic plasticity and memory. Here we analyze the consequences of NSPA absence in KO mice considering its structural features shared with E3 ubiquitin ligases and the crucial role of ubiquitination in synaptic plasticity. Results Electrophysiological studies revealed a decreased long-term potentiation in CA3-CA1 and medial perforant pathway-dentate gyrus (MPP-DG) hippocampal circuits, reflecting glutamatergic synaptic plasticity impairment in NSPA-KO mice. The hippocampal dentate gyrus of these mice showed a lower number of Arc-positive cells indicative of decreased synaptic activity and also showed proliferation defects of neural progenitors underlying less adult neurogenesis. All this translates into poor spatial and recognition memory when NSPA is absent. A cell-based assay demonstrated ubiquitination of NSPA as a property of RBR-type E3 ligases, while biochemical analysis of synaptic regions disclosed the tyrosine phosphatase PTPMEG as a potential substrate. Mice lacking NSPA have increased levels of PTPMEG due to its reduced ubiquitination and proteasomal degradation, which correlated with lower levels of GluN2A and GluN2B NMDAR subunits only at postsynaptic densities (PSDs), indicating selective trafficking of these proteins out of PSDs. As both GluN2A and GluN2B interact with PTPMEG, tyrosine (Tyr) dephosphorylation likely drives their endocytic removal from the PSD. Actually, immunoblot analysis showed reduced phosphorylation of the GluN2B endocytic signal Tyr1472 in NSPA-KO mice. Conclusions NSPA contributes to hippocampal plasticity and memory processes ensuring appropriate levels of adult neurogenesis and PSD-located NMDAR. PTPMEG qualifies as NSPA ubiquitination substrate that regulates Tyr phosphorylation-dependent NMDAR stability at PSDs. The NSPA/PTPMEG pathway emerges as a new regulator of glutamatergic transmission and plasticity and may provide mechanistic clues and therapeutic opportunities for anti-P-mediated pathogenicity in SLE, a still unmet need.

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“…pointing the nose to the object at a distance of <1 cm and/or touching it with the nose (Leger et al, 2013;Okuda et al, 2004). Turning around, climbing or sitting on an object per se was not included in exploration times as the animals then often are not actively engaged in exploring the object but rather exhibit grooming behavior or are using the object to scan the environment (Bianchi et al, 2006;Leger et al, 2013;Li et al, 2011;Pezze et al, 2017;Roozendaal et al, 2006;Vogel-Ciernia & Wood, 2014;Wimmer et al, 2012). In order to analyze memory performance, a discrimination index was calculated as the difference in time exploring the novel and familiar object (or location), expressed as the ratio of the total time spent exploring both objects (i.e.…”

Section: Experimental Apparatus and Behavioral Proceduresmentioning

confidence: 99%

Noradrenergic enhancement of object recognition and object location memory in mice

Bolsius

Ronzoni

et al. 2020

Stress

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Extensive evidence indicates that noradrenergic activation is essentially involved in mediating the enhancing effects of emotional arousal on memory consolidation. Our current understanding of the neurobiological mechanisms underlying the memory-modulatory effects of the noradrenergic system is primarily based on pharmacological studies in rats, employing targeted administration of noradrenergic drugs into specific brain regions. However, the further delineation of the specific neural circuitry involved would benefit from experimental tools that are currently more readily available in mice. Previous studies have not, as yet, investigated the effect of noradrenergic enhancement of memory in mice, which show different cognitive abilities and higher endogenous arousal levels induced by a training experience compared to rats. In the present study, we investigated the effect of posttraining noradrenergic activation in male C57BL/6J mice on the consolidation of object recognition and object location memory. We found that the noradrenergic stimulant yohimbine (0.3 or 1.0 mg/kg) administered systemically immediately after an object training experience dose-dependently enhanced 24-h memory of both the identity and location of the object. Thus, these findings indicate that noradrenergic activation also enhances memory consolidation processes in mice, paving the way for a systematic investigation of the neural circuitry underlying these emotional arousal effects on memory. LAY SUMMARY: The current study successfully validated the effect of noradrenergic activation on both object recognition and object location memory in mice. This study thereby provides a fundamental proof-of-principle for the investigation of the neural circuitry underlying noradrenergic and arousal effects on long-term memory in mice.

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Role of the anterior cingulate cortex in the retrieval of novel object recognition memory after a long delay

Cited by 29 publications

References 47 publications

Delay-Dependent Impairments in Memory and Motor Functions After Acute Methadone Overdose in Rats

Delay-Dependent Impairments in Memory and Motor Functions After Acute Methadone Overdose in Rats

Neuronal surface P antigen (NSPA) modulates postsynaptic NMDAR stability through ubiquitination of tyrosine phosphatase PTPMEG

Noradrenergic enhancement of object recognition and object location memory in mice

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