Neuronal firing in guinea pig neocortical slices surviving in vitro during adenosine-induced blockade of synaptic transmission

1988 ◽  
Vol 19 (6) ◽  
pp. 599-605 ◽  
Author(s):  
S. V. Karnup ◽  
A. V. Kolomoets
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Neuronal Firing

Substance P stimulates inhibitory synaptic transmission in the guinea pig basolateral amygdala in vitro

2001 ◽  
Vol 40 (6) ◽  
pp. 806-817 ◽  
Author(s):  
Karen A Maubach ◽  
Karine Martin ◽  
David W Smith ◽  
Louise Hewson ◽  
Robert A Frankshun ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Synaptic Transmission ◽  
Basolateral Amygdala ◽  
Inhibitory Synaptic Transmission

Cholinergic modulation of synaptic inhibition in the guinea pig hippocampus in vitro: excitation of GABAergic interneurons and inhibition of GABA-release

1993 ◽  
Vol 69 (2) ◽  
pp. 626-629 ◽  
Author(s):  
J. C. Behrends ◽  
G. ten Bruggencate
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Pyramidal Neurons ◽  
Gaba Release ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Release Mechanism ◽  
Gabaergic Interneurons ◽  
Gamma Aminobutyric Acid

1. The effect of cholinergic receptor activation on gamma-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission was investigated in voltage-clamped CA1 pyramidal neurons (HPNs) in the guinea pig hippocampal slice preparation. 2. The cholinergic agonist carbachol (1-10 microM) induced a prominent and sustained increase in the frequency and amplitudes of spontaneous inhibitory postsynaptic currents (IPSCs) in Cl(-)-loaded HPNs. The potentiation of spontaneous IPSCs was not dependent on excitatory synaptic transmission but was blocked by atropine (1 microM). 3. Monosynaptically evoked IPSCs were reversibly depressed by carbachol (10 microM). 4. The frequency of miniature IPSCs recorded in the presence of tetrodotoxin (0.6 or 1.2 microM) was reduced by carbachol (10 or 20 microM) in an atropine-sensitive manner. 5. We conclude that, while cholinergic receptor activation directly excites hippocampal GABAergic interneurons, it has, in addition, a suppressant effect on the synaptic release mechanism at GABAergic terminals. This dual modulatory pattern could explain the suppression of evoked IPSCs despite enhanced spontaneous transmission.

scholarly journals Reversible Loss of Hippocampal Function in a Mouse Model of Demyelination/Remyelination

2019 ◽  
Author(s):  
Aniruddha Das ◽  
Chinthasagar Bastian ◽  
Lexie Trestan ◽  
Jason Suh ◽  
Tanujit Dey ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Neurons ◽  
Brain Activity ◽  
Neuronal Firing ◽  
Demyelinating Diseases ◽  
Therapeutic Interventions ◽  
Electrophysiological Recordings ◽  
Nonlinear Imaging

AbstractDemyelination of axons in the central nervous system (CNS) is a hallmark of multiple sclerosis (MS) and other demyelinating diseases. Cycles of demyelination, followed by remyelination, appear in the majority of MS patients, and are associated with the onset and quiescence of disease-related symptoms, respectively. Previous studies have shown in human patients and animal models that vast demyelination is accompanied by wide-scale changes to brain activity, but details of this process are poorly understood. We use electrophysiological recordings and nonlinear imaging of fluorescence from genetically-encoded calcium indicators to monitor the activity of hippocampal neurons during demyelination and remyelination processes over a period of 100 days. We find in vitro that synaptic transmission in CA1 neurons is diminished, and in vivo both CA1 and dentate gyrus (DG) neuronal firing rates are substantially reduced during demyelination and partially recover after a short remyelination period. This new approach allows monitoring how synaptic transmission changes, induced by cuprizone diet, are affecting neuronal activity, and can potentially be used to study the effects of therapeutic interventions in protecting the functionality of CNS neurons.

Slow synaptic transmission in myenteric AH neurons from the inflamed guinea pig ileum

2009 ◽  
Vol 297 (3) ◽  
pp. G582-G593 ◽  
Author(s):  
Kulmira Nurgali ◽  
Trung V. Nguyen ◽  
Michelle Thacker ◽  
Louise Pontell ◽  
John B. Furness
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Intestinal Inflammation ◽  
Enteric Neurons ◽  
Type I ◽  
Type Ii ◽  
Guinea Pig Ileum ◽  
In Vitro Investigation ◽  
Lower Amplitude

We investigated the effect of inflammation on slow synaptic transmission in myenteric neurons in the guinea pig ileum. Inflammation was induced by the intraluminal injection of trinitrobenzene sulfonate, and tissues were taken for in vitro investigation 6–7 days later. Brief tetanic stimulation of synaptic inputs (20 Hz, 1 s) induced slow excitatory postsynaptic potentials (EPSPs) in 49% and maintained postsynaptic excitation that lasted from 27 min to 3 h in 13% of neurons from the inflamed ileum. These neurons were classified electrophysiologically as AH neurons; 10 were morphological type II neurons, and one was type I. Such long-term hyperexcitability after a brief stimulus is not encountered in enteric neurons of normal intestine. Electrophysiological properties of neurons with maintained postsynaptic excitation were similar to those of neurons with slow EPSPs. Another form of prolonged excitation, sustained slow postsynaptic excitation (SSPE), induced by 1-Hz, 4-min stimulation, in type II neurons from the inflamed ileum reached its peak earlier but had lower amplitude than that in control. Unlike slow EPSPs and similar to SSPEs, maintained excitation was not inhibited by neurokinin-1 or neurokinin-3 receptor antagonists. Maintained postsynaptic excitation was not influenced by PKC inhibitors, but the PKA inhibitor, H-89, caused further increase in neuronal excitability. In conclusion, maintained excitation, observed only in neurons from the inflamed ileum, may contribute to the dysmotility, pain, and discomfort associated with intestinal inflammation.

Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial parasympathetic ganglia neurons

2003 ◽  
Vol 284 (4) ◽  
pp. L581-L587 ◽  
Author(s):  
Radhika Kajekar ◽  
Bradley J. Undem ◽  
Allen C. Myers
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Synaptic Transmission ◽  
Cyclooxygenase Inhibitors ◽  
Antigen Challenge ◽  
Parasympathetic Nerve ◽  
Parasympathetic Ganglia ◽  
Parasympathetic Ganglion ◽  
Ganglion Neurons

In vitro antigen challenge has multiple effects on the excitability of guinea pig bronchial parasympathetic ganglion neurons, including depolarization, causing phasic neurons to fire with a repetitive action potential pattern and potentiating synaptic transmission. In the present study, guinea pigs were passively sensitized to the antigen ovalbumin. After sensitization, the bronchi were prepared for in vitro electrophysiological intracellular recording of parasympathetic ganglia neurons to investigate the contribution of cyclooxygenase activation and prostanoids on parasympathetic nerve activity. Cyclooxygenase inhibition with either indomethacin or piroxicam before in vitro antigen challenge blocked the change in accommodation. These cyclooxygenase inhibitors also blocked the release of prostaglandin D2 (PGD2) from bronchial tissue during antigen challenge. We also determined that PGE2 and PGD2 decreased the duration of the action potential after hyperpolarization, whereas PGF2α potentiated synaptic transmission. Thus prostaglandins released during antigen challenge have multiple effects on the excitability of guinea pig bronchial parasympathetic ganglia neurons, which may consequently affect the output from these neurons and thereby alter parasympathetic tone in the lower airways.

The nature of adrenoceptors in the guinea pig cerebral cortex: a microiontophoretic study

1977 ◽  
Vol 55 (6) ◽  
pp. 1400-1404 ◽  
Author(s):  
T. W. Stone ◽  
D. A. Taylor
Keyword(s):  
Cerebral Cortex ◽  
Guinea Pig ◽  
Neuronal Firing ◽  
Neuronal Excitation ◽  
Single Receptor

1. Noradrenaline, isoprenaline, and phenylephrine have been applied my microiontophoresis to neurones in the guinea pig cerebral cortex. All three compounds produced depression of neuronal firing, and all could be antagonized to some extent by phentolamine or propranolol.2. The responses to isoprenaline were substantially reduced in size after a few applications. Noradrenaline and phenylephrine responses were partially reduced at the time of isoprenaline insensitivity, and the responses could now be blocked completely by phentolamine.3. The results suggest that two kinds of receptors are present in the guinea pig cerebral cortex, with properties similar to α and β receptors in the periphery. A single receptor with intermediate properties would not readily explain the present results.4. The results are not consistent with the proposal that α receptors mediate neuronal excitation, and β receptors inhibition in the cerebral cortex.5. It is also suggested that the failure of some previous studies on guinea pig cortex in vitro to demonstrate the presence of β receptors may be due to the particularly rapid desensitization of these receptors.

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