scholarly journals Fimbria-Fornix Lesions Compromise the Induction of Long-Term Potentiation at the Schaffer Collateral-CA1 Synapse in the Rat In Vivo

2005 ◽  
Vol 93 (5) ◽  
pp. 3001-3006 ◽  
Author(s):  
Chaoying Li ◽  
Donna L. Maier ◽  
Ben Cross ◽  
James J. Doherty ◽  
Edward P. Christian
Keyword(s):  
Long Term Potentiation ◽  
Lesion Group ◽  
Excitatory Postsynaptic Potential ◽  
Schaffer Collateral ◽  
Term Potentiation ◽  
Significant Deficit ◽  
Theta Burst ◽  
Fepsp Slope

Although bilateral fimbria-fornix (FF) lesioning impairs spatial performance in animals, the literature is equivocal regarding its effects on hippocampal long-term potentiation (LTP). We examined the effects of FF lesioning on LTP induction in the Schaffer collateral–CA1 pathway in vivo with a protocol that delivered theta burst stimulation (TBS) trains of increasing length until a sufficient length was reached to induce LTP of the monosynaptic field excitatory postsynaptic potential (fEPSP). Experiments were performed in urethan-anesthetized Long-Evans rats either 4 or 12–16 wk after lesioning. In sham-operated controls, TBS trains ranging from 4 to 12 bursts were sufficient to induce robust LTP [170 ± 10% (mean ± SF) of control fEPSP slope; n = 8]. Four-week post -FF-lesioned animals also displayed clear LTP (167 ± 12% of control fEPSP slope; n = 4) that did not differ from the shams ( P > 0.05). In contrast, animals in the 12- to 16-wk post-lesion group showed a highly significant deficit in LTP induction (95 ± 3% of control fEPSP slope; n = 8; ≤28 burst TBS trains tested; P < 0.001 vs. sham- and 4-wk post-FF-lesion groups). Other quantitative measures of synaptic excitability (i.e., baseline fEPSP slope and input-output relation) did not differ between the sham- and the 12- to 16-wk post-FF-lesion groups. These results indicate that the FF lesion leads to an enduring defect in hippocampal long-term synaptic plasticity that may relate mechanistically to the cognitive deficits characterized in this model.

scholarly journals Metabotropic Glutamate Receptor Antagonist AIDA Blocks Induction of Mossy Fiber-CA3 LTP In Vivo

2005 ◽  
Vol 93 (5) ◽  
pp. 2668-2673 ◽  
Author(s):  
Kenira J. Thompson ◽  
Mario L. Mata ◽  
James E. Orfila ◽  
Edwin J. Barea-Rodriguez ◽  
Joe L. Martinez
Keyword(s):  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Initial Slope ◽  
Maximal Response ◽  
Excitatory Postsynaptic Potential ◽  
Sprague Dawley ◽  
Metabotropic Glutamate ◽  
Term Potentiation

Metabotropic glutamate receptors (mGluR) are implicated in long-term memory storage. mGluR-I and mGluR-II antagonists impede various forms of learning and long-term potentiation (LTP) in animals. Despite the evidence linking mGluR to learning mechanisms, their role in mossy fiber-CA3 long-term potentiation (LTP) is not yet clear. To explain the involvement of mGluR-I in memory mechanisms, we examined the function of the mGluR-I antagonist 1-aminoindan-1, 5-dicarboxylic acid (AIDA) on the induction of mossy fiber-CA3 LTP in vivo in male Sprague Dawley and Fischer 344 (F344) rats. Acute extracellular mossy fiber (MF) responses were evoked by stimulation of the MF bundle and recorded in the stratum lucidum of CA3. The excitatory postsynaptic potential (EPSP) magnitude was measured by using the initial slope of the field EPSP slope measured 2–3 ms after response onset. After collection of baseline MF-CA3 responses at 0.05 Hz, animals received either ((±))-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid ( N-methyl-d-aspartate-R antagonist, 10 mg/kg ip), naloxone (opioid-R antagonist, 10 mg/kg ip), or AIDA (mGluR antagonist, 1 mg/kg ip or 37.5 nmol ic). LTP was induced by two 100-Hz trains at the intensity sufficient to evoke 50% of the maximal response. Responses were collected for an additional 1 h. AIDA blocked induction of LTP in the mossy fiber pathway ( P < 0.05) in both strains of rats after systemic and in Sprague Dawley rats after intrahippocampal injection.

Blockade of Long-Term Potentiation by β-Amyloid Peptides in the CA1 Region of the Rat Hippocampus In Vivo

2001 ◽  
Vol 85 (2) ◽  
pp. 708-713 ◽  
Author(s):  
Darragh B. Freir ◽  
Christian Holscher ◽  
Caroline E. Herron
Keyword(s):  
Long Term Potentiation ◽  
Amyloid Peptide ◽  
Excitatory Postsynaptic Potential ◽  
Dependent Manner ◽  
Aβ Peptides ◽  
Ca1 Region ◽  
Term Potentiation ◽  
Β Amyloid

The effect of intracerebroventricular (icv) injections of β-amyloid peptide fragments Aβ[15–25], Aβ[25–35], and Aβ[35–25] were examined on synaptic transmission and long-term potentiation (LTP) in the hippocampal CA1 region in vivo. Rats were anesthetized using urethan, and changes in synaptic efficacy were determined from the slope of the excitatory postsynaptic potential (EPSP). Baseline synaptic responses were monitored for 30 min prior to icv injection of Aβ peptides or vehicle. High-frequency stimulation (HFS) to induce LTP was applied to the Schaffer-collateral pathway 5 min or 1 h following the icv injection. HFS comprised 3 episodes of 10 stimuli at 200 Hz, 10 times, applied at 30-s intervals. Normal LTP measured 30 min following HFS, was produced following icv injection of vehicle (191 ± 17%, mean ± SE, n = 6) or Aβ[15–25; 100 nmol] (177 ± 6%, n = 6) 1 h prior to HFS. LTP was, however, markedly reduced by Aβ[25–35; 10 nmol] (129 ± 9%, n = 6, P < 0.001) and blocked by Aβ[25–35; 100 nmol] (99 ± 6%, n = 6, P < 0.001). Injection of the reverse peptide, Aβ[35–25], also impaired LTP at concentrations of 10 nmol (136 ± 3%, n = 6, P < 0.01) and 100 nmol (144 ± 7, n = 8, P < 0.05). Using a different protocol, HFS was delivered 5 min following Aβ injections, and LTP was measured 1 h post HFS. Stable LTP was produced in the control group (188 ± 15%, n = 7) and blocked by Aβ[25–35, 100 nmol] (108 ± 15%, n = 6, P < 0.001). A lower dose of Aβ[25–35; 10 nmol] did not significantly impair LTP (176 ± 30%, n = 4). The Aβ-peptides tested were also shown to have no significant effect on paired pulse facilitation (interstimulus interval of 50 ms), suggesting that neither presynaptic transmitter release or activity of interneurons in vivo are affected. The effects of Aβ on LTP are therefore likely to be mediated via a postsynaptic mechanism. This in vivo model of LTP is extremely sensitive to Aβ-peptides that can impair LTP in a time- ([25–35]) and concentration-dependent manner ([25–35] and [35–25]). These effects of Aβ-peptides may then contribute to the cognitive deficits associated with Alzheimer's disease.

scholarly journals Relief of Synaptic Depression Produces Long-Term Enhancement in Thalamocortical Networks

2006 ◽  
Vol 95 (4) ◽  
pp. 2479-2491 ◽  
Author(s):  
Akio Hirata ◽  
Manuel A. Castro-Alamancos
Keyword(s):  
Field Potential ◽  
Long Term Potentiation ◽  
Spontaneous Firing ◽  
Highly Active ◽  
Term Potentiation ◽  
Activity Dependent ◽  
Spontaneous Firing Rate ◽  
Theta Burst

Thalamocortical synapses may be able to undergo activity-dependent long-term changes in efficacy, such as long-term potentiation. Indeed, studies conducted in vivo have found that theta-burst stimulation (TBS) of the thalamus induces a long-term enhancement (LTE) of field potential responses evoked in the neocortex of adult rodents. Because the thalamus and neocortex form a complex interconnected network that is highly active in vivo, it is possible that a change in thalamic excitability would be reflected in the neocortex. To test this possibility, we recorded from barrel neocortex and applied TBS to the thalamic radiation while the somatosensory thalamus was inactivated with muscimol. Thalamocortical LTE was absent when the thalamus was inactivated, suggesting that changes in thalamic excitability are involved. Single-unit recordings from thalamocortical cells revealed that TBS causes a significant reduction in the spontaneous firing rate of thalamocortical cells. Reducing the spontaneous firing of thalamocortical cells directly enhances the efficacy of the thalamocortical pathway because it relieves the tonic depression of the thalamocortical connection caused by thalamocortical activity. Because these changes in thalamic excitability are triggered by corticothalamic activity, this may be a useful top-down mechanism to regulate afferent sensory input to the neocortex during behavior as a function of experience.

scholarly journals Sensitivity to theta-burst timing permits LTP in dorsal striatal adult brain slice

2013 ◽  
Vol 110 (9) ◽  
pp. 2027-2036 ◽  
Author(s):  
Sarah L. Hawes ◽  
Fawad Gillani ◽  
Rebekah C. Evans ◽  
Elizabeth A. Benkert ◽  
Kim T. Blackwell
Keyword(s):  
Brain Slice ◽  
Dorsal Striatum ◽  
Long Term Potentiation ◽  
Adult Brain ◽  
Memory Storage ◽  
Future Application ◽  
Term Potentiation ◽  
Theta Burst

Long-term potentiation (LTP) of excitatory afferents to the dorsal striatum likely occurs with learning to encode new skills and habits, yet corticostriatal LTP is challenging to evoke reliably in brain slice under physiological conditions. Here we test the hypothesis that stimulating striatal afferents with theta-burst timing, similar to recently reported in vivo temporal patterns corresponding to learning, evokes LTP. Recording from adult mouse brain slice extracellularly in 1 mM Mg2+, we find LTP in dorsomedial and dorsolateral striatum is preferentially evoked by certain theta-burst patterns. In particular, we demonstrate that greater LTP is produced using moderate intraburst and high theta-range frequencies, and that pauses separating bursts of stimuli are critical for LTP induction. By altering temporal pattern alone, we illustrate the importance of burst-patterning for LTP induction and demonstrate that corticostriatal long-term depression is evoked in the same preparation. In accord with prior studies, LTP is greatest in dorsomedial striatum and relies on N-methyl-d-aspartate receptors. We also demonstrate a requirement for both Gq- and Gs/olf-coupled pathways, as well as several kinases associated with memory storage: PKC, PKA, and ERK. Our data build on previous reports of activity-directed plasticity by identifying effective values for distinct temporal parameters in variants of theta-burst LTP induction paradigms. We conclude that those variants which best match reports of striatal activity during learning behavior are most successful in evoking dorsal striatal LTP in adult brain slice without altering artificial cerebrospinal fluid. Future application of this approach will enable diverse investigations of plasticity serving striatal-based learning.

scholarly journals Impairment of in vivo theta-burst long-term potentiation and network excitability in the dentate gyrus of synaptopodin-deficient mice lacking the spine apparatus and the cisternal organelle

Hippocampus ◽  
2009 ◽  
Vol 19 (2) ◽  
pp. 130-140 ◽  
Author(s):  
Peter Jedlicka ◽  
Stephan W. Schwarzacher ◽  
Raphael Winkels ◽  
Friederike Kienzler ◽  
Michael Frotscher ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Spine Apparatus ◽  
Theta Burst ◽  
Deficient Mice

Brivaracetam Prevents the Over-expression of Synaptic Vesicle Protein 2A and Rescues the Deficits of Hippocampal Long-term Potentiation In Vivo in Chronic Temporal Lobe Epilepsy Rats

2020 ◽  
Vol 17 (4) ◽  
pp. 354-360 ◽  
Author(s):  
Yu-Xing Ge ◽  
Ying-Ying Lin ◽  
Qian-Qian Bi ◽  
Yu-Juan Chen
Keyword(s):  
Synaptic Plasticity ◽  
Temporal Lobe Epilepsy ◽  
Synaptic Vesicle ◽  
Long Term Potentiation ◽  
Synaptic Dysfunction ◽  
Over Expression ◽  
Term Potentiation ◽  
Synaptic Vesicle Protein 2A

Background: Patients with temporal lobe epilepsy (TLE) usually suffer from cognitive deficits and recurrent seizures. Brivaracetam (BRV) is a novel anti-epileptic drug (AEDs) recently used for the treatment of partial seizures with or without secondary generalization. Different from other AEDs, BRV has some favorable properties on synaptic plasticity. However, the underlying mechanisms remain elusive. Objective: The aim of this study was to explore the neuroprotective mechanism of BRV on synaptic plasticity in experimental TLE rats. Methods: The effect of chronic treatment with BRV (10 mg/kg) was assessed on Pilocarpine induced TLE model through measurement of the field excitatory postsynaptic potentials (fEPSPs) in vivo. Differentially expressed synaptic vesicle protein 2A (SV2A) were identified with immunoblot. Then, fast phosphorylation of synaptosomal-associated protein 25 (SNAP-25) during long-term potentiation (LTP) induction was performed to investigate the potential roles of BRV on synaptic plasticity in the TLE model. Results: An increased level of SV2A accompanied by a depressed LTP in the hippocampus was shown in epileptic rats. Furthermore, BRV treatment continued for more than 30 days improved the over-expression of SV2A and reversed the synaptic dysfunction in epileptic rats. Additionally, BRV treatment alleviates the abnormal SNAP-25 phosphorylation at Ser187 during LTP induction in epileptic ones, which is relevant to the modulation of synaptic vesicles exocytosis and voltagegated calcium channels. Conclusion: BRV treatment ameliorated the over-expression of SV2A in the hippocampus and rescued the synaptic dysfunction in epileptic rats. These results identify the neuroprotective effect of BRV on TLE model.

Sign in / Sign up

Export Citation Format

Share Document