Paired-pulse facilitation of presynaptic calcium transient at hippocampal mossy fiber synapse

2000 ◽  
Vol 38 ◽  
pp. S42
Author(s):  
H Kamiya
Keyword(s):  
Mossy Fiber ◽  
Calcium Transient ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Mossy Fiber Synapse ◽  
Presynaptic Calcium

Paired-pulse facilitation in the dentate gyrus: a patch-clamp study in rat hippocampus in vitro

1994 ◽  
Vol 72 (1) ◽  
pp. 326-336 ◽  
Author(s):  
M. Andreasen ◽  
J. J. Hablitz
Keyword(s):  
Patch Clamp ◽  
Dentate Gyrus ◽  
Time Constant ◽  
Rise Time ◽  
Time Course ◽  
Nmda Antagonist ◽  
Paired Pulse ◽  
Stimulation Intensity ◽  
Paired Pulse Facilitation ◽  
Epsc Amplitude

1. Whole-cell patch-clamp recordings were used to study paired-pulse facilitation (PPF) of the lateral perforant path input to the dentate gyrus in thin hippocampal slices. 2. Orthodromic stimulation of the lateral perforant pathway evoked a excitatory postsynaptic current (EPSC) with a latency of 3.3 +/- 0.1 ms (mean +/- SE) that fluctuated in amplitude. The EPSC had a rise time (10-90%) of 2.79 +/- 0.06 ms (n = 35) and decayed with a single exponential time course with a time-constant of 9.14 +/- 0.24 ms (n = 35). No correlation was found between the amplitude of the EPSC and the rise time or decay time-constant. The non-N-methyl-D-aspartate (NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione completely blocked the EPSC whereas the NMDA antagonist D-aminophosphonovaleric acid (APV) had modest effects. 3. When a test (T-)EPSC was preceded at an interval of 100 ms by a conditioning (C-)EPSC, a significant increase in the amplitude of the T-EPSC was seen in 38 out of 44 trials analyzed from a total of 27 granule cells. The average amount of PPF was 35.7 +/- 2.1%. There was no apparent correlation between the amount of PPF and the stimulation intensity or mean amplitude of the C-EPSC. The time course of the facilitated T-EPSC was not significantly different from that of the C-EPSC. 4. No correlation was found between the amplitude of the C-EPSC and that of the T-EPSC. Estimates of quantal content (mcv) were determined by calculating the ratio of the squared averaged EPSC amplitude (from 48 responses) to the variance of these responses (M2/sigma 2) whereas quantal amplitudes (qcv) were estimated by calculating the ratio of the response variance to average EPSC amplitude (sigma 2/M). PPF was found to be associated with an average increase in mcv of 64.8 +/- 7.2% (n = 38) whereas qcv was decreased by 12.1 +/- 3.8%. 5. The time course of PPF was studied by varying the interval between the C- and T-pulse from 10 to 400 ms while keeping the stimulation intensity constant. Maximal facilitation of the T-EPSC was obtained with interpulse intervals < or = 25 ms where the average facilitation amounted to approximately 70% (n = 6). The decline of facilitation was nearly exponential and was no longer evident with intervals > 350 ms.(ABSTRACT TRUNCATED AT 400 WORDS

scholarly journals The intellectual disability gene Kirrel3 regulates target-specific mossy fiber synapse development in the hippocampus

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
E Anne Martin ◽  
Shruti Muralidhar ◽  
Zhirong Wang ◽  
Diégo Cordero Cervantes ◽  
Raunak Basu ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Mossy Fiber ◽  
Neuron Activity ◽  
Target Cells ◽  
Synaptic Changes ◽  
Mossy Fiber Synapse ◽  
Ca3 Neurons ◽  
Circuit Function ◽  
Feed Forward Inhibition

Synaptic target specificity, whereby neurons make distinct types of synapses with different target cells, is critical for brain function, yet the mechanisms driving it are poorly understood. In this study, we demonstrate Kirrel3 regulates target-specific synapse formation at hippocampal mossy fiber (MF) synapses, which connect dentate granule (DG) neurons to both CA3 and GABAergic neurons. Here, we show Kirrel3 is required for formation of MF filopodia; the structures that give rise to DG-GABA synapses and that regulate feed-forward inhibition of CA3 neurons. Consequently, loss of Kirrel3 robustly increases CA3 neuron activity in developing mice. Alterations in the Kirrel3 gene are repeatedly associated with intellectual disabilities, but the role of Kirrel3 at synapses remained largely unknown. Our findings demonstrate that subtle synaptic changes during development impact circuit function and provide the first insight toward understanding the cellular basis of Kirrel3-dependent neurodevelopmental disorders.

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