scholarly journals Shortened tethering filaments stabilize presynaptic vesicles in support of elevated release probability during LTP in rat hippocampus

2021 ◽  
Vol 118 (17) ◽  
pp. e2018653118
Author(s):  
Jae Hoon Jung ◽  
Lyndsey M. Kirk ◽  
Jennifer N. Bourne ◽  
Kristen M. Harris
Keyword(s):  
Active Zone ◽  
Spatial Relationship ◽  
Long Term Potentiation ◽  
Presynaptic Membrane ◽  
Electron Microscopic ◽  
Release Probability ◽  
Adult Rat ◽  
Attachment Sites ◽  
Term Potentiation ◽  
Hippocampal Area

Long-term potentiation (LTP) is a cellular mechanism of learning and memory that results in a sustained increase in the probability of vesicular release of neurotransmitter. However, previous work in hippocampal area CA1 of the adult rat revealed that the total number of vesicles per synapse decreases following LTP, seemingly inconsistent with the elevated release probability. Here, electron-microscopic tomography (EMT) was used to assess whether changes in vesicle density or structure of vesicle tethering filaments at the active zone might explain the enhanced release probability following LTP. The spatial relationship of vesicles to the active zone varies with functional status. Tightly docked vesicles contact the presynaptic membrane, have partially formed SNARE complexes, and are primed for release of neurotransmitter upon the next action potential. Loosely docked vesicles are located within 8 nm of the presynaptic membrane where SNARE complexes begin to form. Nondocked vesicles comprise recycling and reserve pools. Vesicles are tethered to the active zone via filaments composed of molecules engaged in docking and release processes. The density of tightly docked vesicles was increased 2 h following LTP compared to control stimulation, whereas the densities of loosely docked or nondocked vesicles congregating within 45 nm above the active zones were unchanged. The tethering filaments on all vesicles were shorter and their attachment sites shifted closer to the active zone. These findings suggest that tethering filaments stabilize more vesicles in the primed state. Such changes would facilitate the long-lasting increase in release probability following LTP.

Stereotypical changes in the pattern and duration of long-term potentiation expressed at postnatal days 11 and 15 in the rat hippocampus

1993 ◽  
Vol 70 (4) ◽  
pp. 1412-1419 ◽  
Author(s):  
P. S. Jackson ◽  
T. Suppes ◽  
K. M. Harris
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Developmental Changes ◽  
Cellular Mechanisms ◽  
Adult Rat ◽  
Term Potentiation ◽  
Hippocampal Area ◽  
Pharmacological Manipulations

1. Extracellular recordings from hippocampal area CA1 lasting 2-8 h posttetanus were used to evaluate the duration of long-term potentiation (LTP) at two key developmental ages. 2. At day 11 LTP consistently endured for approximately 1 h before declining to baseline by 2.5 h posttetanus. The response could then be repotentiated, and in some cases, the repotentiation lasted longer than the original potentiation. 3. At day 15 two patterns of potentiation were observed. The first pattern was similar to that observed at day 11 in that the potentiation did not persist; however, it did endure for approximately 2-2.5 h before declining to baseline by 4 h posttetanus. In the second pattern the potentiation persisted indefinitely; these responses were monitored for 6-8 h posttetanus. 4. These patterns are similar to the temporal phases of LTP that have been revealed in adult rat hippocampus through pharmacological manipulations. They may reflect developmental changes during which the different cellular mechanisms underlying LTP become sequentially activated. 5. These findings are important for several reasons. First, because the different temporal phases of LTP seem to be added stepwise during development, animals of different ages could be used explicitly to elucidate the underlying cellular mechanisms of these phases in LTP. Second, because LTP is a candidate mechanism for some forms of learning and memory, these results have implications for sequential steps in the ontogeny of learning and memory. Finally, because studies of LTP have used animals of widely varying ages, including these two ages, it is important to consider whether differences in the developmental properties of LTP could influence experimental observations.

scholarly journals Local resources of polyribosomes and SER promote synapse enlargement and spine clustering after long-term potentiation in adult rat hippocampus

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Michael A. Chirillo ◽  
Mikayla S. Waters ◽  
Laurence F. Lindsey ◽  
Jennifer N. Bourne ◽  
Kristen M. Harris
Keyword(s):  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Adult Rat ◽  
Local Resources ◽  
Term Potentiation

The projection from hippocampal area CA1 to the subiculum sustains long-term potentiation

Neuroreport ◽  
1998 ◽  
Vol 9 (5) ◽  
pp. 847-850 ◽  
Author(s):  
Sean Commins ◽  
John Gigg ◽  
Michael Anderson ◽  
Shane M. OʼMara
Keyword(s):  
Long Term Potentiation ◽  
Area Ca1 ◽  
Term Potentiation ◽  
Hippocampal Area

scholarly journals Neuronal NT-3 Is not Required For Synaptic Transmission or Long-Term Potentiation in Area CA1 of the Adult Rat Hippocampus

1999 ◽  
Vol 6 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Long Ma ◽  
Gerald Reis ◽  
Luis F. Parada ◽  
Erin M. Schuman
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Early Death ◽  
Long Term Potentiation ◽  
Wild Type ◽  
Adult Rat ◽  
Term Potentiation ◽  
Knockout Animals

Neurotrophic factors, including BDNF and NT-3, have been implicated in the regulation of synaptic transmission and plasticity. Previous attempts to analyze synaptic transmission and plasticity in mice lacking the NT-3 gene have been hampered by the early death of the NT-3 homozygous knockout animals. We have bypassed this problem by examining synaptic transmission in mice in which the NT-3 gene is deleted in neurons later in development, by crossing animals expressing the CRE recombinase driven by the synapsin I promoter to animals in which the NT-3 gene is floxed. We conducted blind field potential recordings at the Schaffer collateral–CA1 synapse in hippocampal slices from homozygous knockout and wild-type mice. We examined the following indices of synaptic transmission: (1) input-output relationship; (2) paired-pulse facilitation; (3) post-tetanic potentiation; and (4) long-term potentiation: induced by two different protocols: (a) two trains of 100-Hz stimulation and (b) theta burst stimulation. We found no difference between the knockout and wild-type mice in any of the above measurements. These results suggest that neuronal NT-3 does not play an essential role in normal synaptic transmission and some forms of plasticity in the mouse hippocampus.

scholarly journals Long-term population spike-timing-dependent plasticity promotes synaptic tagging but not cross-tagging in rat hippocampal area CA1

2019 ◽  
Vol 116 (12) ◽  
pp. 5737-5746 ◽  
Author(s):  
Karen Ka Lam Pang ◽  
Mahima Sharma ◽  
Kumar Krishna-K. ◽  
Thomas Behnisch ◽  
Sreedharan Sajikumar
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Neuronal Population ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Adult Rat ◽  
Term Potentiation ◽  
Hippocampal Ca3

In spike-timing-dependent plasticity (STDP), the direction and degree of synaptic modification are determined by the coherence of pre- and postsynaptic activities within a neuron. However, in the adult rat hippocampus, it remains unclear whether STDP-like mechanisms in a neuronal population induce synaptic potentiation of a long duration. Thus, we asked whether the magnitude and maintenance of synaptic plasticity in a population of CA1 neurons differ as a function of the temporal order and interval between pre- and postsynaptic activities. Modulation of the relative timing of Schaffer collateral fibers (presynaptic component) and CA1 axons (postsynaptic component) stimulations resulted in an asymmetric population STDP (pSTDP). The resulting potentiation in response to 20 pairings at 1 Hz was largest in magnitude and most persistent (4 h) when presynaptic activity coincided with or preceded postsynaptic activity. Interestingly, when postsynaptic activation preceded presynaptic stimulation by 20 ms, an immediate increase in field excitatory postsynaptic potentials was observed, but it eventually transformed into a synaptic depression. Furthermore, pSTDP engaged in selective forms of late-associative activity: It facilitated the maintenance of tetanization-induced early long-term potentiation (LTP) in neighboring synapses but not early long-term depression, reflecting possible mechanistic differences with classical tetanization-induced LTP. The data demonstrate that a pairing of pre- and postsynaptic activities in a neuronal population can greatly reduce the required number of synaptic plasticity-evoking events and induce a potentiation of a degree and duration similar to that with repeated tetanization. Thus, pSTDP determines synaptic efficacy in the hippocampal CA3–CA1 circuit and could bias the CA1 neuronal population toward potentiation in future events.

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