Optical Recording of the Spatiotemporal Propagation of Neuronal Excitation in the Rat Hippocampal CA2-CA1 Pathway.

Takeya, Mitsue; Hasuo, Hiroshi; Muraoka, Norihiro; Akasu, Takashi

doi:10.2739/kurumemedj.48.205

Cited by 8 publications

(8 citation statements)

References 13 publications

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“…Neuronal activity of CA1 and DG neurons after FPI It has been shown that the optical response of hippocampal neurons mainly reflects Na -dependent action potentials and excitatory postsynaptic potentials in hippocampal slice preparations [20,23,24]. The present study showed that there was no significant difference in the neuronal activity between ipsilateral and contralateral hippocampal neurons in either coronal or horizontal slice in sham-operated rats.…”

Section: Discussionmentioning

confidence: 48%

“…However, it is not clear whether the application of moderate impact indeed facilitates the propagation of neuronal excitation in multiple neuron networks of the hippocampas. Recently, optical recording with voltage-sensitive dye has been developed to simultaneously monitor the spatiotemporal propagation of the action potential and excitatory synaptic response from multiple sites in hippocampal brain slice preparations [19][20][21][22][23][24]. The purpose of the present study is 1) to establish FPI in rats as an experimental animal model for the head trauma and 2) to investigate the effect of moderate percussion head injury on the propagation of neuronal excitation in the hippocampal CA l region and the DG.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Fluid Percussion Injury on the Neuronal Activity in the Hippocampal CA1 Area and the Dentate Gyrus of the Rat.

Muraoka

2002

Kurume Med. J.

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Summary: The effect of fluid percussion injury (FPI) on the propagation of neuronal activity in the rat hippocampus was investigated by using optical and extracellular recording techniques. Under anesthesia with pentobarbital sodium, a moderate impact (1.5-2.0 atm) was applied to the parietal cerebral cortex of the left hemisphere at -3 mm (i.e. caudal) from bregma, 3.5 mm lateral from the sagittal suture. Systemic oxygenation remained normal during the anesthesia. The rats recovered fully from anesthesia within 30-60 min, and their subsequent behavior, such as feeding and grooming, was normal. After a survival period of 1 week from the FPI or sham-operation, neuronal activities were recorded from the hippocampal CA1 region and the dentate gyrus (DG) in either coronal or horizontal brain slice preparations. In sham-operated rats, there was no significant difference in the neuronal activity between contralateral and ipsilateral hippocampal CA1 areas and DG. In corona) slices (-5.6--6.4 mm from bregma), moderate impact (1.5-2.0 atm) markedly depressed the neuronal activity of the ipsilateral (impact side) CA1 region and of the DG directly under the cerebral cortex that received the impact. In horizontal slices, on the other hand, the neuronal activity was markedly enhanced in the ipsilateral hippocampal CA1 region and the DG adjacent the temporal lobe of the cerebral cortex. Field potentials were recorded from the dentate granule cell layer and the hippocampal CA1 pyramidal cell layer in either coronal or horizontal slice. Moderate impact strongly depressed the field potential in the ipsilateral CA1 region and DG directly under the injured cerebral cortex. In horizontal slices, the field potential was followed by multiple population spikes in ipsilateral hippocampal CA1 and the DG neurons. Bicuculline (15 pM) increased the number of spikes of the field potential even after the brain injury. These results suggest that FPI depresses the neuronal activity in the ipsilateral hippocampus directly under the injured parietal cortex, while it enhances the neuronal activity of the ipsilateral hippocampus adjacent to the temporal cortex. The facilitation of neuronal activity following FPI is not due to disinhibition resulting from depression of GABAergic interneuron activity.

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Section: Discussionmentioning

confidence: 48%

Section: Introductionmentioning

confidence: 99%

Effects of Fluid Percussion Injury on the Neuronal Activity in the Hippocampal CA1 Area and the Dentate Gyrus of the Rat.

Muraoka

2002

Kurume Med. J.

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“…It has been shown that the fast and slow optical responses correspond to both presynaptic action potentials and excitatory synaptic responses in the hippocampal CAl region [20,25,28]. Figure 2A shows the fast and slow optical responses separately recorded at (#1) and (#2) on the hippocampal CA1 area, 100 and 500 μm away from the stimulation electrode, respectively [22].…”

Section: Neuronal Activities In the Hippocampal Ca1 Area In Fpi Ratsmentioning

confidence: 99%

“…1Aa). Neuronal activity can be detected as the ratio of absorption signals due to neuronal excitation to the background light signals taken before stimulation [25,26]. The fractional change in the optical signal was coded in color or gray scale.…”

Section: Optical Recordings From Hippocampal Brain Slice Preparationsmentioning

confidence: 99%

“…The composition of the ACSF was as follows (in mM): 117 NaCl, 4.7 KCl, 2.5 CaCl 2 , 12 MgCl 2 , 25 NaHCO 3 , 1.2 NaHPO 4 , and 11 d-glucose (294 mOsm). Neuronal activities from the hippocampal CA1 areas were measured by optical recording methods described previously [24][25][26]. Horizontal sections of the brain slices (400 μm) were cut at -5.6-6.4 mm from the bregma near the temporal lobe of the cerebral cortex ( Fig.…”

Section: Optical Recordings From Hippocampal Brain Slice Preparationsmentioning

confidence: 99%

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Mild Hypothermia Prevents Post-Traumatic Hyperactivity of Excitatory Synapses in Rat Hippocampal CA1 Pyramidal Neurons

et al. 2009

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Monocarboxylate transporters contribute to the adaptation of neuronal activity to repeated glucose deprivation in the rat lateral septal nucleus

Hasuo

Akasu

2003

Synapse

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Using optical recording methods in the rat lateral septal nucleus (LSN) slice, we examined the question of whether antecedent hypoglycemia protects neurons from the adverse effects of subsequent hypoglycemic stimuli. The first exposure of LSN neurons to glucose deprivation for 15 min produced a marked depression of neuronal activity. The neuronal activity recovered by reapplication of glucose to the neurons. In neurons previously exposed to glucose deprivation, subsequent applications of glucose-free artificial cerebrospinal fluid (ACSF) produced only weak depression of the neuronal activity. The contribution of monocarboxylate transporters to this adaptation of neuronal activity to repeated glucose deprivation was examined in LSN neurons. alpha-Cyano-4-hydroxycinnamate (4-CIN, 100 microM), an inhibitor of the monocarboxylate transporters, did not significantly affect the depression of the neuronal activity induced by the first glucose deprivation. However, in the presence of 4-CIN (100 microM), a second glucose deprivation produced a typical depression of the neuronal activity, indicating that 4-CIN had nullified the adaptation of neuronal activity to a second glucose deprivation. Cytochalasin B (CCB, 20 microM), an inhibitor of glucose transporters, depressed the neuronal activity in the presence of 11 mM glucose. Pyruvate (11 mM) partially restored the neuronal activity depressed by pretreatment with CCB (20 microM) for 30-40 min. These results suggest that antecedent glucose deprivation stimulates monocarboxylate-transporters to supply energy substrates to LSN neurons, thus protecting the neurons against subsequent glucose deprivation. .

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Optical Recording of the Spatiotemporal Propagation of Neuronal Excitation in the Rat Hippocampal CA2-CA1 Pathway.

Cited by 8 publications

References 13 publications

Effects of Fluid Percussion Injury on the Neuronal Activity in the Hippocampal CA1 Area and the Dentate Gyrus of the Rat.

Effects of Fluid Percussion Injury on the Neuronal Activity in the Hippocampal CA1 Area and the Dentate Gyrus of the Rat.

Mild Hypothermia Prevents Post-Traumatic Hyperactivity of Excitatory Synapses in Rat Hippocampal CA1 Pyramidal Neurons

Monocarboxylate transporters contribute to the adaptation of neuronal activity to repeated glucose deprivation in the rat lateral septal nucleus

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