scholarly journals Dual Electrophysiological Recordings of Synaptically-evoked Astroglial and Neuronal Responses in Acute Hippocampal Slices

Author(s):  
Ulrike Pannasch ◽  
Jérémie Sibille ◽  
Nathalie Rouach
2021 ◽  
Author(s):  
Yi-Ling Lu ◽  
Helen E Scharfman

Spreading depolarization (SD) is a sudden and synchronized depolarization of principal cells followed by depression of activity, which slowly propagates across brain regions like cortex or hippocampus. SD is considered to be mechanistically relevant to migraine, epilepsy, and traumatic brain injury. Interestingly, research into SD typically uses SD triggered immediately after a focal stimulus. Here we optimize an in vitro experimental model allowing us to record SD without focal stimulation. This method uses electrophysiological recordings and intrinsic optical imaging in slices. The method is also relatively easy and inexpensive. Acute hippocampal slices from mice or rats were prepared and used for extracellular and whole-cell recordings. Recordings were made in a submerged-style chamber with flow of artificial cerebrospinal fluid (aCSF) above and below the slices. Flow was fast (> 5ml/min), and temperature was 32°C. As soon as slices were placed in the chamber, aCSF containing 0 mM Mg2+ and 5 mM K+ (0 Mg2+/5 K+ aCSF) was used. Two major types of activity were observed: SD and seizure-like events (SLEs). Both occurred after many minutes of recording. Although both mouse and rat slices showed SLEs, only mouse slices developed SD and did so in the first hour of 0 Mg2+/5 K+ aCSF exposure. Intrinsic optical imaging showed that most SDs initiated in CA3 and could propagate into CA1 and dentate gyrus. In dentate gyrus, SD propagated in two separate waves: (1) into the hilus and (2) into granule cell and molecular layers simultaneously. This in vitro model can be used to better understand the mechanisms and relationship between SD and SLEs. It could also be useful in preclinical drug screening.


2021 ◽  
Vol 14 ◽  
Author(s):  
Patrycja Orlowska-Feuer ◽  
Magdalena Kinga Smyk ◽  
Anna Alwani ◽  
Marian Henryk Lewandowski

The amount and spectral composition of light changes considerably during the day, with dawn and dusk being the most crucial moments when light is within the mesopic range and short wavelength enriched. It was recently shown that animals use both cues to adjust their internal circadian clock, thereby their behavior and physiology, with the solar cycle. The role of blue light in circadian processes and neuronal responses is well established, however, an unanswered question remains: how do changes in the spectral composition of light (short wavelengths blocking) influence neuronal activity? In this study we addressed this question by performing electrophysiological recordings in image (dorsal lateral geniculate nucleus; dLGN) and non-image (the olivary pretectal nucleus; OPN, the suprachiasmatic nucleus; SCN) visual structures to determine neuronal responses to spectrally varied light stimuli. We found that removing short-wavelength from the polychromatic light (cut off at 525 nm) attenuates the most transient ON and sustained cells in the dLGN and OPN, respectively. Moreover, we compared the ability of different types of sustained OPN neurons (either changing or not their response profile to filtered polychromatic light) to irradiance coding, and show that both groups achieve it with equal efficacy. On the other hand, even very dim monochromatic UV light (360 nm; log 9.95 photons/cm2/s) evokes neuronal responses in the dLGN and SCN. To our knowledge, this is the first electrophysiological experiment supporting previous behavioral findings showing visual and circadian functions disruptions under short wavelength blocking environment. The current results confirm that neuronal activity in response to polychromatic light in retinorecipient structures is affected by removing short wavelengths, however, with type and structure – specific action. Moreover, they show that rats are sensitive to even very dim UV light.


2019 ◽  
Vol 122 (2) ◽  
pp. 721-728 ◽  
Author(s):  
Masahito Kawamura ◽  
David N. Ruskin ◽  
Susan A. Masino

Adenosine receptors are widely expressed in the brain, and adenosine is a key bioactive substance for neuroprotection. In this article, we clarify systematically the role of adenosine A1 receptors during a range of timescales and conditions when a significant amount of adenosine is released. Using acute hippocampal slices obtained from mice that were wild type or null mutant for the adenosine A1 receptor, we quantified and characterized the impact of varying durations of experimental ischemia, hypoxia, and hypoglycemia on synaptic transmission in the CA1 subregion. In normal tissue, these three stressors rapidly and markedly reduced synaptic transmission, and only treatment of sufficient duration led to incomplete recovery. In contrast, inactivation of adenosine A1 receptors delayed and/or lessened the reduction in synaptic transmission during all three stressors and reduced the magnitude of the recovery significantly. We reproduced the responses to hypoxia and hypoglycemia by applying an adenosine A1 receptor antagonist, validating the clear effects of genetic receptor inactivation on synaptic transmission. We found activation of adenosine A1 receptor inhibited hippocampal synaptic transmission during the acute phase of ischemia, hypoxia, or hypoglycemia and caused the recovery from synaptic impairment after these three stressors using genetic mutant. These studies quantify the neuroprotective role of the adenosine A1 receptor during a variety of metabolic stresses within the same recording system. NEW & NOTEWORTHY Deprivation of oxygen and/or glucose causes a rapid adenosine A1 receptor-mediated decrease in synaptic transmission in mouse hippocampus. We quantified adenosine A1 receptor-mediated inhibition during and synaptic recovery after ischemia, hypoxia, and hypoglycemia of varying durations using a genetic mutant and confirmed these findings using pharmacology. Overall, using the same recording conditions, we found the acute response and the neuroprotective ability of the adenosine A1 receptor depended on the type and duration of deprivation event.


1993 ◽  
Vol 50 (3) ◽  
pp. 341-351 ◽  
Author(s):  
Patrizia Casaccia-Bonnefil ◽  
Eirikur Benedikz ◽  
Hong Shen ◽  
Armin Stelzer ◽  
Diane Edelstein ◽  
...  

2011 ◽  
Vol 25 (7) ◽  
pp. 1468-1474 ◽  
Author(s):  
Vesna A. Eterović ◽  
Dinely Pérez ◽  
Antonio H. Martins ◽  
Brenda L. Cuadrado ◽  
Marimée Carrasco ◽  
...  

2014 ◽  
Vol 112 (2) ◽  
pp. 263-275 ◽  
Author(s):  
Hayley A. Mattison ◽  
Ashish A. Bagal ◽  
Michael Mohammadi ◽  
Nisha S. Pulimood ◽  
Christian G. Reich ◽  
...  

GluA2-lacking, calcium-permeable α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors (AMPARs) have unique properties, but their presence at excitatory synapses in pyramidal cells is controversial. We have tested certain predictions of the model that such receptors are present in CA1 cells and show here that the polyamine spermine, but not philanthotoxin, causes use-dependent inhibition of synaptically evoked excitatory responses in stratum radiatum, but not s. oriens, in cultured and acute hippocampal slices. Stimulation of single dendritic spines by photolytic release of caged glutamate induced an N-methyl-d-aspartate receptor-independent, use- and spermine-sensitive calcium influx only at apical spines in cultured slices. Bath application of glutamate also triggered a spermine-sensitive influx of cobalt into CA1 cell dendrites in s. radiatum. Responses of single apical, but not basal, spines to photostimulation displayed prominent paired-pulse facilitation (PPF) consistent with use-dependent relief of cytoplasmic polyamine block. Responses at apical dendrites were diminished, and PPF was increased, by spermine. Intracellular application of pep2m, which inhibits recycling of GluA2-containing AMPARs, reduced apical spine responses and increased PPF. We conclude that some calcium-permeable, polyamine-sensitive AMPARs, perhaps lacking GluA2 subunits, are present at synapses on apical dendrites of CA1 pyramidal cells, which may allow distinct forms of synaptic plasticity and computation at different sets of excitatory inputs.


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