Papers by Shweta Tripathi
Oscillating waves during sleep play an essential role in memory consolidation. The cortical slow ... more Oscillating waves during sleep play an essential role in memory consolidation. The cortical slow wave activity (SWA) and sigma waves during NREM sleep and theta waves during REM sleep increase after a variety of memory tasks including declarative, procedural and associative learning tasks. These oscillatory waves during sleep help to promote neural dialog between circuitries, which possibly plays a causal role in memory consolidation. However, the role of sleep-associated oscillating waves in a complex appetitive-conditioning paradigm is not clear. The parietal cortex and amygdala are involved in the cognitive evaluation of the environmental stimuli, and appetitive conditioning. Here, we have studied the changes in sleep architecture and oscillatory waves during NREM and REM sleep in the parietal cortices and amygdalarlocal field potential (A-LFP) after appetitive-conditioning in the rat. We observed that REM sleep increased significantly after appetitive conditioning, which significantly positively correlated with performance on the appetitive-conditioning task. Further, the cortical SWA (0.1-4.5 Hz), and sigma (12-14.25 Hz) waves during NREM sleep, theta (6-9 Hz) waves during REM sleep, the amygdalar SWA (0.1-3.75 Hz) during NREM sleep and theta (6-8.25 Hz) waves during REM sleep significantly increased after appetitive conditioning. Interestingly, the augmented oscillatory waves significantly positively correlated with the performances on the appetitive-conditioning task. Our results suggest that the augmented REM sleep after conditioning may be required for the consolidation of appetitive-conditioned memory. Further, a significant correlation between augmented power in oscillatory waves during sleep and performance suggesting that these waves may be playing a crucial role in the consolidation of appetitive-conditioned memory.
Sleep deprivation (SD) disrupts memory consolidation, including amygdala-dependent processes such... more Sleep deprivation (SD) disrupts memory consolidation, including amygdala-dependent processes such as appetitive delayconditioned memory. SD impairs this form of conditioning by inducing deficits in the formation of associations between conditioned and unconditioned stimuli, likely by reducing cAMP signaling in the amygdala. Rolipram, a phosphodiesterase-4 inhibitor, prevents cAMP breakdown, enhancing PKA and CREB activity, which are vital for long-term memory formation. The reversibility of SD-mediated learning impairment through pharmacological means remains unclear. We hypothesized that rolipram microinjection into the central nucleus of the amygdala (CeA) could alleviate SD-induced memory impairments. Rats were surgically prepared for drug microinjection and sleep-wake recording. The conditioned stimulus, a house light, and the unconditioned stimulus, mango juice, were used to train the animals on an appetitive delay-conditioning task. Mango juice was delivered through a juice dispensing window, and the number of head entries into the window to obtain juice was considered a learning outcome. Rolipram or vehicle was microinjected into the CeA in two independent groups shortly after training, followed by 6 h of SD. The non-SD and SD-Rolipram groups made significantly more head entries than the SD-Vehicle groups. Nevertheless, the SD-Vehicle animals exhibited less number of head entries. These findings indicate that Rolipram mitigated the SD-induced impairment of appetitive delay-conditioned memory, suggesting that it may have therapeutic potential for treating cognitive deficits in conditions like Alzheimer's disease and other forms of dementia. Investigating the long-term impact of sleep deprivation on dementia in humans and the therapeutic potential of phosphodiesterase inhibitors as drugs may provide valuable insights.
• MSO, a glutamine synthetase inhibitor, induced temporal memory deficit. • However, it did not a... more • MSO, a glutamine synthetase inhibitor, induced temporal memory deficit. • However, it did not alter spatial recognition memory. • This suggests that glia also modulates some aspects of mnemonic processes. a b s t r a c t The glutamate neurotransmitter is intrinsically involved in learning and memory. Glial glutamine syn-thetase enzyme synthesizes glutamine, which helps maintain the optimal neuronal glutamate level. However, the role of glutamine synthetase in learning and memory remains unclear. Using associative trace learning task, we investigated the effects of methionine sulfoximine (MSO) (glutamine synthetase inhibitor) on recognition and temporal memories. MSO and vehicle were injected (i.p.) three hours before training in separate groups of male Wistar rats (n = 11). Animals were trained to obtain fruit juice after following a set of sequential events. Initially, house-light was presented for 15 s followed by 5 s trace interval. Thereafter, juice was given for 20 s followed by 20 s inter-presentation interval. A total of 75 presentations were made over five sessions during the training and testing periods. The average number of head entries to obtain juice per session and during individual phases at different time intervals was accounted as an outcome measure of recognition and temporal memories. The total head entries in MSO and vehicle treated animals were comparable on training and testing days. However, it was 174.90% (p = 0.08), 270.61% (p < 0.05), 143.20% (p < 0.05) more on training day and 270.33% (p < 0.05), 157.94% (p < 0.05), 170.42% (p < 0.05) more on testing day, during the house-light, trace-interval and inter-presentation interval phases in MSO animals. Glutamine synthetase inhibition did not induce recognition memory deficit, while temporal memory was altered, suggesting that glutamine synthetase modulates some aspects of mnemonic processes.
• MSO, a glutamine synthetase inhibitor, induced temporal memory deficit. • However, it did not a... more • MSO, a glutamine synthetase inhibitor, induced temporal memory deficit. • However, it did not alter spatial recognition memory. • This suggests that glia also modulates some aspects of mnemonic processes. a b s t r a c t The glutamate neurotransmitter is intrinsically involved in learning and memory. Glial glutamine syn-thetase enzyme synthesizes glutamine, which helps maintain the optimal neuronal glutamate level. However, the role of glutamine synthetase in learning and memory remains unclear. Using associative trace learning task, we investigated the effects of methionine sulfoximine (MSO) (glutamine synthetase inhibitor) on recognition and temporal memories. MSO and vehicle were injected (i.p.) three hours before training in separate groups of male Wistar rats (n = 11). Animals were trained to obtain fruit juice after following a set of sequential events. Initially, house-light was presented for 15 s followed by 5 s trace interval. Thereafter, juice was given for 20 s followed by 20 s inter-presentation interval. A total of 75 presentations were made over five sessions during the training and testing periods. The average number of head entries to obtain juice per session and during individual phases at different time intervals was accounted as an outcome measure of recognition and temporal memories. The total head entries in MSO and vehicle treated animals were comparable on training and testing days. However, it was 174.90% (p = 0.08), 270.61% (p < 0.05), 143.20% (p < 0.05) more on training day and 270.33% (p < 0.05), 157.94% (p < 0.05), 170.42% (p < 0.05) more on testing day, during the house-light, trace-interval and inter-presentation interval phases in MSO animals. Glutamine synthetase inhibition did not induce recognition memory deficit, while temporal memory was altered, suggesting that glutamine synthetase modulates some aspects of mnemonic processes.
Short-term sleep deprivation soon after training may impair memory consolidation. Also, a particu... more Short-term sleep deprivation soon after training may impair memory consolidation. Also, a particular
sleep stage or its components increase after learning some tasks, such as negative and positive
reinforcement tasks, avoidance tasks, and spatial learning tasks, and so forth. It suggests that discrete
memory types may require specific sleep stage or its components for their optimal processing. The
classical conditioning paradigms are widely used to study learning and memory but the role of sleep in
a complex conditioned learning is unclear. Here, we have investigated the effects of short-term sleep
deprivation on the consolidation of delay-conditioned memory and the changes in sleep architecture after
conditioning. Rats were trained for the delay-conditioned task (for conditioning, house-light [conditioned
stimulus] was paired with fruit juice [unconditioned stimulus]). Animals were divided into 3 groups: (a)
sleep deprived (SD); (b) nonsleep deprived (NSD); and (c) stress control (SC) groups. Two-way ANOVA
revealed a significant interaction between groups and days (training and testing) during the conditioned
stimulus– unconditioned stimulus presentation. Further, Tukey post hoc comparison revealed that the
NSD and SC animals exhibited significant increase in performances during testing. The SD animals,
however, performed significantly less during testing. Further, we observed that wakefulness and NREM
sleep did not change after training and testing. Interestingly, REM sleep increased significantly on both
days compared to baseline more specifically during the initial 4-hr time window after conditioning. Our
results suggest that the consolidation of delay-conditioned memory is sleep-dependent and requires
augmented REM sleep during an explicit time window soon after training
Uploads
Papers by Shweta Tripathi
sleep stage or its components increase after learning some tasks, such as negative and positive
reinforcement tasks, avoidance tasks, and spatial learning tasks, and so forth. It suggests that discrete
memory types may require specific sleep stage or its components for their optimal processing. The
classical conditioning paradigms are widely used to study learning and memory but the role of sleep in
a complex conditioned learning is unclear. Here, we have investigated the effects of short-term sleep
deprivation on the consolidation of delay-conditioned memory and the changes in sleep architecture after
conditioning. Rats were trained for the delay-conditioned task (for conditioning, house-light [conditioned
stimulus] was paired with fruit juice [unconditioned stimulus]). Animals were divided into 3 groups: (a)
sleep deprived (SD); (b) nonsleep deprived (NSD); and (c) stress control (SC) groups. Two-way ANOVA
revealed a significant interaction between groups and days (training and testing) during the conditioned
stimulus– unconditioned stimulus presentation. Further, Tukey post hoc comparison revealed that the
NSD and SC animals exhibited significant increase in performances during testing. The SD animals,
however, performed significantly less during testing. Further, we observed that wakefulness and NREM
sleep did not change after training and testing. Interestingly, REM sleep increased significantly on both
days compared to baseline more specifically during the initial 4-hr time window after conditioning. Our
results suggest that the consolidation of delay-conditioned memory is sleep-dependent and requires
augmented REM sleep during an explicit time window soon after training
sleep stage or its components increase after learning some tasks, such as negative and positive
reinforcement tasks, avoidance tasks, and spatial learning tasks, and so forth. It suggests that discrete
memory types may require specific sleep stage or its components for their optimal processing. The
classical conditioning paradigms are widely used to study learning and memory but the role of sleep in
a complex conditioned learning is unclear. Here, we have investigated the effects of short-term sleep
deprivation on the consolidation of delay-conditioned memory and the changes in sleep architecture after
conditioning. Rats were trained for the delay-conditioned task (for conditioning, house-light [conditioned
stimulus] was paired with fruit juice [unconditioned stimulus]). Animals were divided into 3 groups: (a)
sleep deprived (SD); (b) nonsleep deprived (NSD); and (c) stress control (SC) groups. Two-way ANOVA
revealed a significant interaction between groups and days (training and testing) during the conditioned
stimulus– unconditioned stimulus presentation. Further, Tukey post hoc comparison revealed that the
NSD and SC animals exhibited significant increase in performances during testing. The SD animals,
however, performed significantly less during testing. Further, we observed that wakefulness and NREM
sleep did not change after training and testing. Interestingly, REM sleep increased significantly on both
days compared to baseline more specifically during the initial 4-hr time window after conditioning. Our
results suggest that the consolidation of delay-conditioned memory is sleep-dependent and requires
augmented REM sleep during an explicit time window soon after training