scholarly journals Repeated Isoflurane Exposures Impair Long-Term Potentiation and Increase Basal GABAergic Activity in the Basolateral Amygdala

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Robert P. Long II ◽  
Vassiliki Aroniadou-Anderjaska ◽  
Eric M. Prager ◽  
Volodymyr I. Pidoplichko ◽  
Taiza H. Figueiredo ◽  
...  
Keyword(s):  
Basolateral Amygdala ◽  
Long Term Potentiation ◽  
Emotional Disturbances ◽  
Emotional Behavior ◽  
Male Rats ◽  
Isoflurane Anesthesia ◽  
Term Potentiation ◽  
Anesthetic Exposure ◽  
Gabaergic Activity

After surgery requiring general anesthesia, patients often experience emotional disturbances, but it is unclear if this is due to anesthetic exposure. In the present study, we examined whether isoflurane anesthesia produces long-term pathophysiological alterations in the basolateral amygdala (BLA), a brain region that plays a central role in emotional behavior. Ten-week-old, male rats were administered either a single, 1 h long isoflurane (1.5%) anesthesia or three, 1 h long isoflurane exposures, separated by 48 h. Long-term potentiation (LTP) and spontaneous GABAergic activity in the BLA were studied 1 day, 1 week, and 1 month later. Single isoflurane anesthesia had no significant effect on the magnitude of LTP. In contrast, after repeated isoflurane exposures, LTP was dramatically impaired at both 1 day and 1 week after the last exposure but was restored by 1 month after the exposures. SpontaneousGABAAreceptor-mediated IPSCs were increased at 1 day and 1 week after repeated exposures but had returned to control levels by 1 month after exposure. Thus, repeated exposures to isoflurane cause a long-lasting—but not permanent—impairment of synaptic plasticity in the BLA, which could be due to increased basal GABAergic activity. These pathophysiological alterations may produce emotional disturbances and impaired fear-related learning.

The timing of maternal separation affects morris water maze performance and long-term potentiation in male rats

2013 ◽  
Vol 56 (5) ◽  
pp. 1102-1109 ◽  
Author(s):  
Xiujing Cao ◽  
Shenghai Huang ◽  
Jiejie Cao ◽  
Tingting Chen ◽  
Ping Zhu ◽  
...  
Keyword(s):  
Morris Water Maze ◽  
Water Maze ◽  
Maternal Separation ◽  
Long Term Potentiation ◽  
Male Rats ◽  
Maze Performance ◽  
Term Potentiation

Nicotine-induced impairments of spatial cognition and long-term potentiation in adolescent male rats

2013 ◽  
Vol 33 (2) ◽  
pp. 203-213 ◽  
Author(s):  
G Han ◽  
L An ◽  
B Yang ◽  
L Si ◽  
T Zhang
Keyword(s):  
Young Adult ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Male Rats ◽  
Adolescent Male ◽  
Control Group ◽  
Adult Offspring ◽  
Behavioral Impairment ◽  
Term Potentiation

The aim of the present study was to investigate whether cognitive behavioral impairment, induced by nicotine in offspring rats, was associated with the alteration of hippocampal short-term potentiation (STP) and long-term potentiation (LTP) and to discuss the potential underlying mechanism. Young adult offspring rats were randomly divided into three groups. The groups include: control group (CC), nicotine group 1 (NC), in which their mothers received nicotine from gestational day 3 (GD3) to GD18, and nicotine group 2 (CN), in which young adult offspring rats received nicotine from postnatal day 42 (PD42) to PD56. Morris water maze (MWM) test was performed and then field excitatory postsynaptic potentials elicited by the stimulation of perforant pathway were recorded in the hippocampal dentate gyrus region. The results of the MWM test showed that learning and memory were impaired by either prenatal or postnatal nicotine exposure. In addition, it was found that there was no statistical difference of the MWM data between both nicotine treatments. In the electrophysiological test, LTP and STP were significantly inhibited in both NC and CN groups in comparison with the CC group. Notably, STP in CN group was also lower than that in the NC group. These findings suggested that both prenatal and postnatal exposure to nicotine induced learning and memory deficits, while the potential mechanism might be different from each other due to their dissimilar impairments of synaptic plasticity.

scholarly journals Nitric Oxide Donor Prevents Neonatal Isoflurane-induced Impairments in Synaptic Plasticity and Memory

2019 ◽  
Vol 130 (2) ◽  
pp. 247-262 ◽  
Author(s):  
Michele L. Schaefer ◽  
Meina Wang ◽  
Patric J. Perez ◽  
Wescley Coca Peralta ◽  
Jing Xu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Recognition Memory ◽  
Long Term Potentiation ◽  
Nitric Oxide Donor ◽  
Wild Type ◽  
No Donor ◽  
Term Potentiation ◽  
Anesthetic Exposure ◽  
Wild Type Control

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background In humans, multiple early exposures to procedures requiring anesthesia constitute a significant risk factor for development of learning disabilities and disorders of attention. In animal studies, newborns exposed to anesthetics develop long-term deficits in cognition. Previously, our laboratory showed that postsynaptic density (PSD)-95, discs large homolog, and zona occludens-1 (PDZ) domains may serve as a molecular target for inhaled anesthetics. This study investigated a role for PDZ interactions in spine development, plasticity, and memory as a potential mechanism for early anesthetic exposure-produced cognitive impairment. Methods Postnatal day 7 mice were exposed to 1.5% isoflurane for 4 h or injected with 8 mg/kg active PSD-95 PDZ2WT peptide. Apoptosis, hippocampal dendritic spine changes, synapse density, long-term potentiation, and cognition functions were evaluated (n = 4 to 18). Results Exposure of postnatal day 7 mice to isoflurane or PSD-95 PDZ2WT peptide causes a reduction in long thin spines (median, interquartile range [IQR]: wild type control [0.54, 0.52 to 0.86] vs. wild type isoflurane [0.31, 0.16 to 0.38], P = 0.034 and PDZ2MUT [0.86, 0.67 to 1.0] vs. PDZ2WT [0.55, 0.53 to 0.59], P = 0.028), impairment in long-term potentiation (median, IQR: wild type control [123, 119 to 147] and wild type isoflurane [101, 96 to 118], P = 0.049 and PDZ2MUT [125, 119 to 131] and PDZ2WT [104, 97 to 107], P = 0.029), and deficits in acute object recognition (median, IQR: wild type control [79, 72 to 88] vs. wild type isoflurane [63, 55 to 72], P = 0.044 and PDZ2MUT [81, 69 to 84] vs. PDZ2WT [67, 57 to 77], P = 0.039) at postnatal day 21 without inducing detectable differences in apoptosis or changes in synaptic density. Impairments in recognition memory and long-term potentiation were preventable by introduction of a NO donor. Conclusions Early disruption of PDZ domain–mediated protein–protein interactions alters spine morphology, synaptic function, and memory. These results support a role for PDZ interactions in early anesthetic exposure–produced cognitive impairment. Prevention of recognition memory and long-term potentiation deficits with a NO donor supports a role for the N-methyl-d-aspartate receptor/PSD-95/neuronal NO synthase pathway in mediating these aspects of isoflurane-induced cognitive impairment.

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