scholarly journals Chondroitin Sulfate Induces Depression of Synaptic Transmission and Modulation of Neuronal Plasticity in Rat Hippocampal Slices

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Elisa Albiñana ◽  
Javier Gutierrez-Luengo ◽  
Natalia Hernández-Juarez ◽  
Andrés M. Baraibar ◽  
Eulalia Montell ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Synaptic Transmission ◽  
Neuronal Plasticity ◽  
Chondroitin Sulphate ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Dependent Manner ◽  
Perineuronal Net ◽  
Concentration Dependent Manner ◽  
Population Spike Amplitude

It is currently known that in CNS the extracellular matrix is involved in synaptic stabilization and limitation of synaptic plasticity. However, it has been reported that the treatment with chondroitinase following injury allows the formation of new synapses and increased plasticity and functional recovery. So, we hypothesize that some components of extracellular matrix may modulate synaptic transmission. To test this hypothesis we evaluated the effects of chondroitin sulphate (CS) on excitatory synaptic transmission, cellular excitability, and neuronal plasticity using extracellular recordings in the CA1 area of rat hippocampal slices. CS caused a reversible depression of evoked field excitatory postsynaptic potentials in a concentration-dependent manner. CS also reduced the population spike amplitude evoked after orthodromic stimulation but not when the population spikes were antidromically evoked; in this last case a potentiation was observed. CS also enhanced paired-pulse facilitation and long-term potentiation. Our study provides evidence that CS, a major component of the brain perineuronal net and extracellular matrix, has a function beyond the structural one, namely, the modulation of synaptic transmission and neuronal plasticity in the hippocampus.

Characterization of dopamine receptors mediating inhibition of excitatory synaptic transmission in the rat hippocampal slice

1996 ◽  
Vol 76 (3) ◽  
pp. 1887-1895 ◽  
Author(s):  
K. S. Hsu
Keyword(s):  
Synaptic Transmission ◽  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Hippocampal Slices ◽  
D2 Receptor ◽  
D1 Receptor ◽  
Excitatory Synaptic Transmission ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Ca1 Neurons

1. The effect of dopamine (DA) on the excitatory synaptic transmission was studied in the CA1 neurons of rat hippocampal slices using intracellular recording technique. 2. Depolarizing excitatory postsynaptic potentials (EPSPs) were evoked by stimulation of the Schaffer collateral-commissural pathway. Superfusion of DA (0.03-1 microM) reversibly decreased the EPSP in a concentration-dependent manner and with an estimated IC50 of 0.3 microM. The sensitivity of postsynaptic neurons to the glutamate-receptor agonists, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid or N-methyl-D-aspartate was unchanged by DA (0.3 microM) pretreatment. In addition, DA (0.3 microM) increased the magnitude of paired-pulse facilitation, a phenomenon attributed to an increase in the amount of transmitter released in response to the second stimulus. 3. The reduction of DA (0.3 microM) on the EPSP was antagonized by sulpiride (1-10 nM), a selective D2-receptor antagonist. However, D1-receptor antagonist, SKF-83566 (1-10 microM), did not significantly affect the reduction of DA (0.3 microM) on the EPSP. 4. (+/-)-2-(N-Phenylethyl-N-propyl)amino-5-hydroxytetralin (1 microM), an agonist of D2 receptor, mimicked the inhibitory effect of DA on the EPSP. However, neither the D1-receptor agonist SKF-38393 (1 microM) nor the D3-receptor agonist (PD-128,907 (1 microM) affected the EPSP. 5. Incubation of hippocampal slices with pertussis toxin (PTX, 5 micrograms/ml) for 12 h prevented the reduction of EPSP induced by DA (0.3 microM). 6. Rp-adenosine-3',5'-cyclic monophosphothioate (25 microM), a potent inhibitor of protein kinase A (PKA), alone decreased the amplitude of EPSP below baseline values and prevented the subsequent reduction by DA (0.3 microM). 7. These results indicate that DA at a low concentration (< or = 0.3 microM) reduces the excitatory response of hippocampal CA1 neurons after synaptic stimulation via the activation of presynaptic D2 receptors. The presynaptic action of DA is mediated by a PTX-sensitive Gi-proteins-coupled to PKA pathway.

Presynaptic Modulation of Synaptic Transmission by Pregnenolone Sulfate as Studied by Optical Recordings

2005 ◽  
Vol 94 (6) ◽  
pp. 4131-4144 ◽  
Author(s):  
Ling Chen ◽  
Masahiro Sokabe
Keyword(s):  
Synaptic Transmission ◽  
Glutamate Release ◽  
Hippocampal Slices ◽  
Receptor Activation ◽  
Optical Recording ◽  
Perforant Path ◽  
Dependent Manner ◽  
Pregnenolone Sulfate ◽  
Voltage Sensitive Dyes ◽  
Dose Dependent

The effects of pregnenolone sulfate (PREGS), a putative neurosteroid, on the transmission of perforant path–granule cell synapses were investigated with an optical recording technique in rat hippocampal slices stained with voltage-sensitive dyes. Application of PREGS to the bath solution resulted in an acute augmentation of EPSP in a dose-dependent manner. The PREGS effect was dependent on the extracellular Ca2+ concentration ([Ca2+]o), but independent of NMDA receptor activation. PREGS caused a decrease in paired-pulse facilitation, which implies that PREGS positively modulates presynaptic neurotransmitter releases. Firmer support for this mechanism was that PREGS augmented the synaptically induced glial depolarization (SIGD) that reflects the activity of electrogenic glutamate transporters in glial cells during the uptake of released glutamate. The selective α7nAChR antagonist α-BGT or MLA prevented the SIGD increase by PREGS. Furthermore DMXB, a selective α7nAChR agonist, mimicked the PREGS effect on SIGD and antagonized the effect of PREGS. The presynaptic effect of PREGS was partially attenuated by the L-type Ca2+ channel (VGCC) blocker nifedipine. Based on these findings, we proposed a novel mechanism underlying the facilitated synaptic transmission by PREGS: this neurosteroid sensitizes presynaptic α7nAChR that is followed by an activation of L-type VGCC to increase the presynaptic glutamate release.

Extracellular matrix in plasticity and epileptogenesis

2008 ◽  
Vol 4 (3) ◽  
pp. 235-247 ◽  
Author(s):  
Alexander Dityatev ◽  
Tommaso Fellin
Keyword(s):  
Extracellular Matrix ◽  
Developmental Plasticity ◽  
Mossy Fibers ◽  
Long Term Potentiation ◽  
Therapeutic Interventions ◽  
Neural Cells ◽  
Dependent Manner ◽  
Extracellular Proteases ◽  
Mature Brain ◽  
The Brain

Extracellular matrix (ECM) in the brain is composed of molecules synthesized and secreted by neurons and glial cells in a cell-type-specific and activity-dependent manner. During development, ECM plays crucial roles in proliferation, migration and differentiation of neural cells. In the mature brain, ECM undergoes a slow turnover and supports multiple physiological processes, while restraining structural plasticity. In the first part of this review, we discuss the contribution of ECM molecules to different forms of plasticity, including developmental plasticity in the cortex, long-term potentiation and depression in the hippocampus, homeostatic scaling of synaptic transmission and metaplasticity. In the second part, we focus on pathological changes associated with epileptogenic mutations in ECM-related molecules or caused by seizure-induced remodeling of ECM. The available data suggest that ECM components regulating physiological plasticity are also engaged in different aspects of epileptogenesis, such as dysregulation of excitatory and inhibitory neurotransmission, sprouting of mossy fibers, granule cell dispersion and gliosis. At the end, we discuss combinatorial approaches that might be used to counteract seizure-induced dysregulation of both ECM molecules and extracellular proteases. By restraining ECM modification and preserving the status quo in the brain, these treatments might prove to be valid therapeutic interventions to antagonize the progression of epileptogenesis.

Sevoflurane Blocks Cholinergic Synaptic Transmission Postsynaptically but Does Not Affect Short-term Potentiation

2005 ◽  
Vol 102 (5) ◽  
pp. 920-928 ◽  
Author(s):  
Hiroaki Naruo ◽  
Shin Onizuka ◽  
David Prince ◽  
Mayumi Takasaki ◽  
Naweed I. Syed
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Fluorescent Imaging ◽  
Posttetanic Potentiation ◽  
Dependent Manner ◽  
General Anesthetics ◽  
Short Term ◽  
Concentration Dependent Manner ◽  
Cholinergic Synaptic Transmission ◽  
Term Potentiation

Background As compared with their effects on both inhibitory and excitatory synapses, little is known about the mechanisms by which general anesthetics affect synaptic plasticity that forms the basis for learning and memory at the cellular level. To test whether clinically relevant concentrations of sevoflurane affect short-term potentiation involving cholinergic synaptic transmission, the soma-soma synapses between identified, postsynaptic neurons were used. Methods Uniquely identifiable neurons visceral dorsal 4 (presynaptic) and left pedal dorsal 1 (postsynaptic) of the mollusk Lymnaea stagnalis were isolated from the intact ganglion and paired overnight in a soma-soma configuration. Simultaneous intracellular recordings coupled with fluorescent imaging of the FM1-43 dye were made in either the absence or the presence of sevoflurane. Results Cholinergic synapses, similar to those observed in vivo, developed between the neurons, and the synaptic transmission exhibited classic short-term, posttetanic potentiation. Action potential-induced (visceral dorsal 4), 1:1 excitatory postsynaptic potentials were reversibly and significantly suppressed by sevoflurane in a concentration-dependent manner. Fluorescent imaging with the dye FM1-43 revealed that sevoflurane did not affect presynaptic exocytosis or endocytosis; instead, postsynaptic nicotinic acetylcholine receptors were blocked in a concentration-dependent manner. To test the hypothesis that sevoflurane affects short-term potentiation, a posttetanic potentiation paradigm was used, and synaptic transmission was examined in either the presence or the absence of sevoflurane. Although 1.5% sevoflurane significantly reduced synaptic transmission between the paired cells, it did not affect the formation or retention of posttetanic potentiation at this synapse. Conclusions This study demonstrates that sevoflurane blocks cholinergic synaptic transmission postsynaptically but does not affect short-term synaptic plasticity at the visceral dorsal 4-left pedal dorsal 1 synapse.

Sleep Deprivation Impairs Long-Term Potentiation in Rat Hippocampal Slices

2002 ◽  
Vol 88 (2) ◽  
pp. 1073-1076 ◽  
Author(s):  
I. G. Campbell ◽  
M. J. Guinan ◽  
J. M. Horowitz
Keyword(s):  
Sleep Deprivation ◽  
Neural Plasticity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Adult Rats ◽  
Cellular Processes ◽  
Term Potentiation ◽  
Population Spike Amplitude ◽  
Specific Factors

To determine if 12-h sleep deprivation disrupts neural plasticity, we compared long-term potentiation (LTP) in five sleep-deprived and five control rats. Thirty minutes after tetanus population spike amplitude increased 101 ± 15% in 16 slices from sleep deprived rats and 139 ± 14% in 14 slices from control rats. This significant ( P < 0.05) reduction of LTP, the first demonstration that the sleep deprivation protocol impairs plasticity in adult rats, may be due to several factors. Reduced LTP may indicate that sleep provides a period of recuperation for cellular processes underlying neural plasticity. Alternatively, the stress of sleep deprivation, as indicated by elevated blood corticosterone levels, or other non-sleep-specific factors of deprivation may contribute to the LTP reduction.

scholarly journals Early low-level developmental arsenic exposure impacts mouse hippocampal synaptic function

2021 ◽  
Author(s):  
Karl F Foley ◽  
Daniel Barnett ◽  
Deborah A Cory-Slechta ◽  
Houhui Xia
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Arsenic Exposure ◽  
Long Term Potentiation ◽  
Epidemiological Studies ◽  
Synaptic Function ◽  
Learning Deficits ◽  
Term Potentiation ◽  
The Impact

Background: Arsenic is a well-established carcinogen known to increase all-cause mortality, but its effects on the central nervous system are less well understood. Recent epidemiological studies suggest that early life exposure to arsenic is associated with learning deficits and behavioral changes, and increased arsenic exposure continues to affect an estimated 200 million individuals worldwide. Previous studies on arsenic exposure and synaptic function have demonstrated a decrease in synaptic transmission and long-term potentiation in adult rodents, but have relied on in vitro or extended exposure in adulthood. Therefore, little is known about the effect of arsenic exposure in development. Objective: Here, we studied the effects of gestational and early developmental arsenic exposure in juvenile mice. Specifically, our objective was to investigate the impact of arsenic exposure on synaptic transmission and plasticity in the hippocampus. Methods: C57BL/6 females were exposed to arsenic (0, 50ppb, 36ppm) in their drinking water two weeks prior to mating and continued to be exposed to arsenic throughout gestation and after parturition. We then performed field recordings in acute hippocampal slices from the juvenile offspring prior to weaning (P17-P23). In this paradigm, the juvenile mice are only exposed to arsenic in utero and via the mothers milk. Results: High (36ppm) and relatively low (50ppb) arsenic exposure both lead to decreased basal synaptic transmission in the hippocampus of juvenile mice. There was a mild decrease in paired-pulse facilitation in juvenile mice exposed to high, but not low, arsenic, suggesting the alterations in synaptic transmission are primarily post-synaptic. Finally, high developmental arsenic exposure led to a significant increase in long-term potentiation. Discussion: These results suggest that indirect, ecologically-relevant arsenic exposure in early development impacts hippocampal synaptic transmission and plasticity that could underlie learning deficits reported in epidemiological studies.

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.

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