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Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury.

Cao L, Bie X, Huo S, Du J, Liu L, Song W - Neural Regen Res (2014)

Bottom Line: Diazepam significantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 μmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus.Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release.These data suggest that diazepam could decrease the fluid percussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.

View Article: PubMed Central - PubMed

Affiliation: Department of Functional Neurosurgery, Xi'an Red Cross Hospital, Xi'an, Shaanxi Province, China ; Department of Rehabilitation Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.

ABSTRACT
The activity of the Schaffer collaterals of hippocampal CA3 neurons and hippocampal CA1 neurons has been shown to increase after fluid percussion injury. Diazepam can inhibit the hyperexcitability of rat hippocampal neurons after injury, but the mechanism by which it affects excitatory synaptic transmission remains poorly understood. Our results showed that diazepam treatment significantly increased the slope of input-output curves in rat neurons after fluid percussion injury. Diazepam significantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 μmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus. Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release. These data suggest that diazepam could decrease the fluid percussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.

No MeSH data available.


Related in: MedlinePlus

Effects of diazepam (DZ) on the excitatory postsynaptic potential paired-pulse facilitation of fluid percussion injury (FPI) rat hippocampal CA1 neurons.The two consecutive excitatory postsynaptic potentials were evoked by paired-pulse stimuli with intervals from 50 to 160 ms repeated every 10 seconds in the presence of bicuculline (15 μmol/L). Sample records (average of six consecutive pairs) of excitatory postsynaptic potential pairs (stimulus interval is 60 ms) were obtained in the control, DZ, FPI and FPI + DZ groups. P1 and P2 indicate the first and second excitatory postsynaptic potentials, respectively. The figure shows pooled data for the effect of DZ on the P2/P1 ratio with stimulation intervals from 50 ms to 160 ms on the FPI ipsilateral side. n: Number of rats. Quantitative data were expressed as the mean ± SD and analyzed by one-way analysis of variance. Student-Newman-Keuls tests were used for specific comparisons. *P < 0.05, vs. other groups.
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Figure 2: Effects of diazepam (DZ) on the excitatory postsynaptic potential paired-pulse facilitation of fluid percussion injury (FPI) rat hippocampal CA1 neurons.The two consecutive excitatory postsynaptic potentials were evoked by paired-pulse stimuli with intervals from 50 to 160 ms repeated every 10 seconds in the presence of bicuculline (15 μmol/L). Sample records (average of six consecutive pairs) of excitatory postsynaptic potential pairs (stimulus interval is 60 ms) were obtained in the control, DZ, FPI and FPI + DZ groups. P1 and P2 indicate the first and second excitatory postsynaptic potentials, respectively. The figure shows pooled data for the effect of DZ on the P2/P1 ratio with stimulation intervals from 50 ms to 160 ms on the FPI ipsilateral side. n: Number of rats. Quantitative data were expressed as the mean ± SD and analyzed by one-way analysis of variance. Student-Newman-Keuls tests were used for specific comparisons. *P < 0.05, vs. other groups.

Mentions: The results described above revealed the preservation of inhibitory pathways; therefore, we concluded that fluid percussion injury directly enhanced the function of the glutamatergic excitatory pathway in the hippocampal CA1 area. To test this, Schaffer collaterals were stimulated by a pair of electrical pulses at 50–160-ms intervals, repeated every 10 seconds. As shown in Figure 2, the paired-pulse facilitation ratio (P1/P2 ratio) decreased with prolonged stimulus interval. P2/P1 ratios were significantly increased in the fluid percussion injury + diazepam group compared with the fluid percussion injury group (P < 0.05), to a level that showed no significant difference from the control group (P > 0.05). These results suggested that diazepam effectively diminishes the probability of action-potential-dependent glutamine release from the terminals of Schaffer collateral terminals in the ipsilateral hippocampus CA1 area following fluid percussion injury.


Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury.

Cao L, Bie X, Huo S, Du J, Liu L, Song W - Neural Regen Res (2014)

Effects of diazepam (DZ) on the excitatory postsynaptic potential paired-pulse facilitation of fluid percussion injury (FPI) rat hippocampal CA1 neurons.The two consecutive excitatory postsynaptic potentials were evoked by paired-pulse stimuli with intervals from 50 to 160 ms repeated every 10 seconds in the presence of bicuculline (15 μmol/L). Sample records (average of six consecutive pairs) of excitatory postsynaptic potential pairs (stimulus interval is 60 ms) were obtained in the control, DZ, FPI and FPI + DZ groups. P1 and P2 indicate the first and second excitatory postsynaptic potentials, respectively. The figure shows pooled data for the effect of DZ on the P2/P1 ratio with stimulation intervals from 50 ms to 160 ms on the FPI ipsilateral side. n: Number of rats. Quantitative data were expressed as the mean ± SD and analyzed by one-way analysis of variance. Student-Newman-Keuls tests were used for specific comparisons. *P < 0.05, vs. other groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4281428&req=5

Figure 2: Effects of diazepam (DZ) on the excitatory postsynaptic potential paired-pulse facilitation of fluid percussion injury (FPI) rat hippocampal CA1 neurons.The two consecutive excitatory postsynaptic potentials were evoked by paired-pulse stimuli with intervals from 50 to 160 ms repeated every 10 seconds in the presence of bicuculline (15 μmol/L). Sample records (average of six consecutive pairs) of excitatory postsynaptic potential pairs (stimulus interval is 60 ms) were obtained in the control, DZ, FPI and FPI + DZ groups. P1 and P2 indicate the first and second excitatory postsynaptic potentials, respectively. The figure shows pooled data for the effect of DZ on the P2/P1 ratio with stimulation intervals from 50 ms to 160 ms on the FPI ipsilateral side. n: Number of rats. Quantitative data were expressed as the mean ± SD and analyzed by one-way analysis of variance. Student-Newman-Keuls tests were used for specific comparisons. *P < 0.05, vs. other groups.
Mentions: The results described above revealed the preservation of inhibitory pathways; therefore, we concluded that fluid percussion injury directly enhanced the function of the glutamatergic excitatory pathway in the hippocampal CA1 area. To test this, Schaffer collaterals were stimulated by a pair of electrical pulses at 50–160-ms intervals, repeated every 10 seconds. As shown in Figure 2, the paired-pulse facilitation ratio (P1/P2 ratio) decreased with prolonged stimulus interval. P2/P1 ratios were significantly increased in the fluid percussion injury + diazepam group compared with the fluid percussion injury group (P < 0.05), to a level that showed no significant difference from the control group (P > 0.05). These results suggested that diazepam effectively diminishes the probability of action-potential-dependent glutamine release from the terminals of Schaffer collateral terminals in the ipsilateral hippocampus CA1 area following fluid percussion injury.

Bottom Line: Diazepam significantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 μmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus.Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release.These data suggest that diazepam could decrease the fluid percussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.

View Article: PubMed Central - PubMed

Affiliation: Department of Functional Neurosurgery, Xi'an Red Cross Hospital, Xi'an, Shaanxi Province, China ; Department of Rehabilitation Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.

ABSTRACT
The activity of the Schaffer collaterals of hippocampal CA3 neurons and hippocampal CA1 neurons has been shown to increase after fluid percussion injury. Diazepam can inhibit the hyperexcitability of rat hippocampal neurons after injury, but the mechanism by which it affects excitatory synaptic transmission remains poorly understood. Our results showed that diazepam treatment significantly increased the slope of input-output curves in rat neurons after fluid percussion injury. Diazepam significantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 μmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus. Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release. These data suggest that diazepam could decrease the fluid percussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.

No MeSH data available.


Related in: MedlinePlus