scholarly journals Chemokine CCL2 modulation of neuronal excitability and synaptic transmission in rat hippocampal slices

2010 ◽  
Vol 116 (3) ◽  
pp. 406-414 ◽  
Author(s):  
Yan Zhou ◽  
Hongmei Tang ◽  
Jianuo Liu ◽  
Jun Dong ◽  
Huangui Xiong
Keyword(s):  
Synaptic Transmission ◽  
Neuronal Excitability ◽  
Hippocampal Slices

Prolonged Bursts Occur in Normal Calcium in Hippocampal Slices After Raising Excitability and Blocking Synaptic Transmission

2001 ◽  
Vol 86 (5) ◽  
pp. 2625-2628 ◽  
Author(s):  
Zhi-Qi Xiong ◽  
Janet L. Stringer
Keyword(s):  
Synaptic Transmission ◽  
Neuronal Excitability ◽  
Hippocampal Slices ◽  
High Potassium ◽  
Tetraethylammonium Chloride ◽  
Neurotransmitter Receptor ◽  
Long Duration ◽  
Artificial Cerebrospinal Fluid ◽  
Receptor Blockers ◽  
Interictal Discharges

This study examined the conditions that are required for the appearance of the long-duration seizure-like activity that can be recorded in hippocampal slices. Spontaneous interictal activity was induced in CA1 and CA3 by perfusing hippocampal slices with high potassium, cesium, 4-aminopyridine, or tetraethylammonium chloride, in normal levels of calcium. Synaptic transmission was then blocked by the addition of neurotransmitter receptor blockers (6-cyano-7-nitroquinoxaline-2,3-dione,d,l-2-amino-5-phosphonopentanoic acid, and bicuculline) or the calcium channel blocker cadmium, resulting in complete blockade of the interictal discharges and the appearance of spontaneous seizure-like events (ictal-like discharges) primarily in CA1 and the dentate gyrus. Blocking synaptic transmission in normal artificial cerebrospinal fluid did not induce ictal-like discharges in any region. The results demonstrate that ictal-like discharges can appear in normal levels of extracellular calcium when chemical synaptic transmission is blocked pharmacologically. The results suggest that an increase in neuronal excitability and absence of interictal activity promote the appearance of the longer ictal-like discharges.

scholarly journals Metformin Enhances Excitatory Synaptic Transmission onto Hippocampal CA1 Pyramidal Neurons

2020 ◽  
Vol 10 (10) ◽  
pp. 706
Author(s):  
Wen-Bing Chen ◽  
Jiang Chen ◽  
Zi-Yang Liu ◽  
Bin Luo ◽  
Tian Zhou ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Glutamate Release ◽  
Hippocampal Slices ◽  
Hippocampal Pyramidal Neurons ◽  
Beneficial Effects ◽  
Ca1 Pyramidal Neurons ◽  
Postsynaptic Currents ◽  
Hippocampal Ca1

Metformin (Met) is a first-line drug for type 2 diabetes mellitus (T2DM). Numerous studies have shown that Met exerts beneficial effects on a variety of neurological disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). However, it is still largely unclear how Met acts on neurons. Here, by treating acute hippocampal slices with Met (1 μM and 10 μM) and recording synaptic transmission as well as neuronal excitability of CA1 pyramidal neurons, we found that Met treatments significantly increased the frequency of miniature excitatory postsynaptic currents (mEPSCs), but not amplitude. Neither frequency nor amplitude of miniature inhibitory postsynaptic currents (mIPSCs) were changed with Met treatments. Analysis of paired-pulse ratios (PPR) demonstrates that enhanced presynaptic glutamate release from terminals innervating CA1 hippocampal pyramidal neurons, while excitability of CA1 pyramidal neurons was not altered. Our results suggest that Met preferentially increases glutamatergic rather than GABAergic transmission in hippocampal CA1, providing a new insight on how Met acts on neurons.

Methylmercury reduces synaptic transmission and neuronal excitability in rat hippocampal slices

2018 ◽  
Vol 470 (8) ◽  
pp. 1221-1230 ◽  
Author(s):  
J. Gutiérrez ◽  
A. M. Baraibar ◽  
E. Albiñana ◽  
P. Velasco ◽  
J. M. Solís ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Neuronal Excitability ◽  
Hippocampal Slices

scholarly journals Astrocytic Connectivity in the Hippocampus

2004 ◽  
Vol 1 (1) ◽  
pp. 3-11 ◽  
Author(s):  
JAI-YOON SUL ◽  
GEORGE OROSZ ◽  
RICHARD S. GIVENS ◽  
PHILIP G. HAYDON
Keyword(s):  
Synaptic Transmission ◽  
Neuronal Excitability ◽  
Metabotropic Glutamate Receptor ◽  
Hippocampal Slices ◽  
Atp Release ◽  
Flufenamic Acid ◽  
Functional Coupling ◽  
Metabotropic Glutamate ◽  
Exogenous Ligands ◽  
Internal Calcium

Little is known about the functional connectivity between astrocytes in the CNS. To explore this issue we photo-released glutamate onto a single astrocyte in murine hippocampal slices and imaged calcium responses. Photo-release of glutamate causes a metabotropic glutamate receptor (mGluR)-dependent increase in internal calcium in the stimulated astrocyte and delayed calcium elevations in neighboring cells. The delayed elevation in calcium was not caused by either neuronal activity following synaptic transmission or by glutamate released from astrocytes. However, it was reduced by flufenamic acid (FFA), which is consistent with a role for adenosine triphosphate (ATP) release from astrocytes as an intercellular messenger. Exogenous ligands such as ATP (1 µM) increased the number of astrocytes that were recruited into coupled astrocytic networks, indicating that extracellular accumulation of neurotransmitters modulates neuronal excitability, synaptic transmission and functional coupling between astrocytes.

scholarly journals Zinc Enhances the Inhibitory Effects of Strychnine-Sensitive Glycine Receptors in Mouse Hippocampal Neurons

2007 ◽  
Vol 98 (6) ◽  
pp. 3666-3676 ◽  
Author(s):  
Hai Xia Zhang ◽  
Liu Lin Thio
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Neuronal Excitability ◽  
Hippocampal Slices ◽  
Glycine Receptors ◽  
Inhibitory Effects ◽  
Action Potential Firing ◽  
Embryonic Mouse ◽  
Potential Firing

Although extracellular Zn2+ is an endogenous biphasic modulator of strychnine-sensitive glycine receptors (GlyRs), the physiological significance of this modulation remains poorly understood. Zn2+ modulation of GlyR may be especially important in the hippocampus where presynaptic Zn2+ is abundant. Using cultured embryonic mouse hippocampal neurons, we examined whether 1 μM Zn2+, a potentiating concentration, enhances the inhibitory effects of GlyRs activated by sustained glycine applications. Sustained 20 μM glycine (EC25) applications alone did not decrease the number of action potentials evoked by depolarizing steps, but they did in 1 μM Zn2+. At least part of this effect resulted from Zn2+ enhancing the GlyR-induced decrease in input resistance. Sustained 20 μM glycine applications alone did not alter neuronal bursting, a form of hyperexcitability induced by omitting extracellular Mg2+. However, sustained 20 μM glycine applications depressed neuronal bursting in 1 μM Zn2+. Zn2+ did not enhance the inhibitory effects of sustained 60 μM glycine (EC70) applications in these paradigms. These results suggest that tonic GlyR activation could decrease neuronal excitability. To test this possibility, we examined the effect of the GlyR antagonist strychnine and the Zn2+ chelator tricine on action potential firing by CA1 pyramidal neurons in mouse hippocampal slices. Co-applying strychnine and tricine slightly but significantly increased the number of action potentials fired during a depolarizing current step and decreased the rheobase for action potential firing. Thus Zn2+ may modulate neuronal excitability normally and in pathological conditions such as seizures by potentiating GlyRs tonically activated by low agonist concentrations.

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