Effects of deprivation of oxygen or glucose on the neural activity in the guinea pig hippocampal slice-intracellular recording study of pyramidal neurons in the CA3 area

1994 ◽  
Vol 19 ◽  
pp. S38
Author(s):  
Toshihiro Takata ◽  
Yasuhiro Okada
Keyword(s):  
Guinea Pig ◽  
Neural Activity ◽  
Intracellular Recording ◽  
Hippocampal Slice ◽  
Pyramidal Neurons

Picrotoxin- and 4-aminopyridine-induced activity in hilar neurons in the guinea pig hippocampal slice

1991 ◽  
Vol 65 (1) ◽  
pp. 141-147 ◽  
Author(s):  
W. Muller ◽  
U. Misgeld
Keyword(s):  
Guinea Pig ◽  
Intracellular Recording ◽  
Hippocampal Slice ◽  
Pyramidal Neurons ◽  
Granule Cells ◽  
Field Potential ◽  
Granule Cell Layer ◽  
Perforant Path ◽  
Hilar Region ◽  
Hilar Neurons

1. Paired extra- and intracellular recording was used to study the activity of neurons in the dentate hilus and their interaction with CA3/CA4 pyramidal neurons and granule cells during picrotoxin- or 4-aminopyridine (4-AP)-induced rhythmical activity in the guinea pig hippocampal slice. 2. Picrotoxin induced synchronous repetitive population spikes in the CA3, CA4, and hilar region, but no extracellular activity in the granule cell layer. 4-AP induced rhythmically occurring positive field-potential waves in the CA3, CA4, and granular layer coincident to negative/positive field potentials in the hilus. 3. Picrotoxin-induced activity originated in the CA3 area and subsequently appeared in the CA4 and hilar region, whereas 4-AP-induced activity appeared simultaneously in all subfields. 4. Blockade of fast glutamatergic excitation by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) blocked the picrotoxin-induced activity but not the 4-AP-induced activity. 5. Focal application of tetrodotoxin (TTX) between area CA3 and CA4 blocked picrotoxin-induced activity in the CA4 and hilar region but decoupled 4-AP-induced activity in the CA3 area. 6. Under intracellular recording, picrotoxin induced bursts in CA3, CA4, and hilar neurons but K-dependent slow IPSPs in granule cells. 4-AP induced rhythmically occurring burst in hilar neurons synchronous to Cl- and K-dependent IPSPs in CA3, CA4, and granule cells. 7. Comparison of picrotoxin- and 4-AP-induced rhythmical burst activity reveals that many hilar neurons are excited by CA3/CA4 pyramidal neurons in addition to the well-known excitation by granule cells and perforant path fibers, and that, in turn, many hilar neurons inhibit CA3, CA4, and granule cells.

Inhibitory role of dentate hilus neurons in guinea pig hippocampal slice

1990 ◽  
Vol 64 (1) ◽  
pp. 46-56 ◽  
Author(s):  
W. Muller ◽  
U. Misgeld
Keyword(s):  
Guinea Pig ◽  
Dentate Gyrus ◽  
Hippocampal Slice ◽  
Pyramidal Neurons ◽  
Granule Cells ◽  
Stratum Pyramidale ◽  
Stratum Oriens ◽  
Bath Application ◽  
Ca3 Neurons ◽  
Hilar Neurons

1. Current and voltage-clamp recording of CA3/CA4 pyramidal neurons, hilar neurons, and granule cells or pairs of these neurons were used to study the generation of Cl-dependent and K-dependent inhibitory postsynaptic potentials (IPSPs) in the guinea pig hippocampal slice preparation. 2. A sequence of an early Cl-dependent and a late K-dependent IPSP was evoked in CA3 neurons by electrical stimulation from the stratum moleculare of the dentate gyrus, the hilus, and the stratum oriens/alveus. Blockade of glutamatergic excitation by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and D(-)-2-amino-5-phosphonovaleric acid (APV, 30 microM) abolished IPSPs evoked from the stratum moleculare of the dentate gyrus, but IPSPs could still be evoked from the hilus and the stratum oriens/alveus. 3. Repetitive giant IPSPs, which consisted of Cl-dependent and K-dependent components, were evoked by bath application of 4-aminopyridine (4-AP, 10-50 microM) in CA3 neurons and in granule cells. Giant IPSPs were blocked by bath-applied tetrodotoxin (TTX). In addition, 4-AP hyperpolarized CA3 neurons in a Cl-dependent and picrotoxin-sensitive way. 4. Focal application of TTX to the dentate gyrus or the hilus considerably reduced the amplitude of giant IPSPs evoked by 4-AP in CA3 neurons. In hilar neurons, 4-AP evoked repetitive bursts, eventually, but not necessarily intermingled with giant IPSPs. Bursts were observed in hilar neurons in presence as well as absence of CNQX and APV. 5. In paired recordings, bursts in hilar neurons induced by 4-AP occurred simultaneously to giant IPSPs in granule cells and CA3 neurons, and giant IPSPs in granule cells occurred simultaneously to giant IPSPs in CA3 neurons. Blockade of glutamatergic excitation by CNQX and APV did not abolish this synchrony. 6. 4-AP-evoked Cl- and K-dependent IPSPs were, unlike electrically evoked IPSPs, not strictly coupled: some 20% of large IPSPs and up to 90% of small IPSPs were either Cl or K dependent. In granule cells K-dependent components either preceded or followed Cl-dependent components. 7. K-dependent IPSPs only could be evoked in CA3 neurons by focal application of 4-AP (1 mM) to the hilus, the stratum lacunosum moleculare or the stratum pyramidale. Wash out of Ca for 15–20 min blocked the Cl-dependent but not the K-dependent component of giant IPSPs evoked by bath-applied 4-AP.(ABSTRACT TRUNCATED AT 400 WORDS)

Oxidative damage in the guinea pig hippocampal slice

1989 ◽  
Vol 6 (5) ◽  
pp. 467-472 ◽  
Author(s):  
Terry C. Pellmar ◽  
Kathryn L. Neel
Keyword(s):  
Guinea Pig ◽  
Oxidative Damage ◽  
Hippocampal Slice

scholarly journals Early Life Vitamin C Deficiency Does Not Alter Morphology of Hippocampal CA1 Pyramidal Neurons or Markers of Synaptic Plasticity in a Guinea Pig Model

Nutrients ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 749 ◽  
Author(s):  
Stine Hansen ◽  
Jane Jørgensen ◽  
Jens Nyengaard ◽  
Jens Lykkesfeldt ◽  
Pernille Tveden-Nyborg
Keyword(s):  
Synaptic Plasticity ◽  
Vitamin C ◽  
Guinea Pig ◽  
Early Life ◽  
Pyramidal Neurons ◽  
Pig Model ◽  
Vitamin C Deficiency ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1 ◽  
Guinea Pig Model

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.

Excitatory and inhibitory effects of toluene on neural activity in guinea pig hippocampal slices

1993 ◽  
Vol 158 (1) ◽  
pp. 63-66 ◽  
Author(s):  
Youji Ikeuchi ◽  
Hirokazu Hirai ◽  
Yasuhiro Okada ◽  
Takaya Mio ◽  
Toshiji Matsuda
Keyword(s):  
Guinea Pig ◽  
Neural Activity ◽  
Hippocampal Slices ◽  
Inhibitory Effects

The K+ channel opener diazoxide enhances glutamatergic currents and reduces GABAergic currents in hippocampal neurons

1993 ◽  
Vol 69 (2) ◽  
pp. 494-503 ◽  
Author(s):  
V. Crepel ◽  
C. Rovira ◽  
Y. Ben-Ari
Keyword(s):  
Intracellular Recording ◽  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Reversal Potential ◽  
Input Resistance ◽  
Katp Channels ◽  
K Channel ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials

1. The effect of diazoxide, an opener of ATP-sensitive K+ channels (KATP channels) has been investigated in the rat hippocampal slices by the use of extracellular and intracellular recording techniques. 2. In control solution, diazoxide enhanced the CA1 and CA3 field excitatory postsynaptic potentials (EPSPs) and produced interictal activities in CA3. These effects were neither prevented by KATP blockers, including glibenclamide (3-30 microM) or tolbutamide (500 microM), nor mimicked by another KATP opener such as galanine (1 microM); thus these effects are probably not mediated by KATP channels. 3. Using intracellular recording, we then studied, in CA3 pyramidal neurons, the effect of diazoxide on the EPSPs and the fast and slow inhibitory postsynaptic potentials (IPSPs). 4. In presence of bicuculline (10 microM) and phaclofen (50 microM), to block, respectively, fast and slow IPSPs, diazoxide reversibly enhanced the EPSPs. 5. In presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM), to block EPSPs, diazoxide reversibly decreased both fast and slow IPSPs. 6. These effects of diazoxide on the EPSPs and fast and slow IPSPs were associated neither with a change of the reversal potential of the EPSPs or the fast and slow IPSPs nor with a change of the input resistance and membrane potential. 7. Using single electrode voltage-clamp technique, we then tested the effects of diazoxide on the currents generated by applications of glutamate or gamma-aminobutyric acid (GABA) -A and -B analogues. 8. In presence of tetrodotoxin (TTX; 1 microM), diazoxide reversibly enhanced the peak currents evoked by alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionate (AMPA; 3-5 microM), quisqualate (5-10 microM) and N-methyl-D-aspartate (NMDA; 10 microM), but not those evoked by kainate (1-3 microM). 9. In presence of TTX (1 microM), diazoxide reversibly decreased the GABA- (1-5 mM), isoguvacine- (30-60 microM), and baclofen- (10-30 microM) mediated peak currents. 10. It is concluded that, in the hippocampus, diazoxide enhances the excitatory glutamatergic currents and reduces the GABAergic inhibition, thus generating paroxystic activities. We suggest that these effects are mediated by second messenger cascades.

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