Ethanol inhibits long‐term potentiation in hippocampal CA1 neurons, irrespective of lamina and stimulus strength, through neurosteroidogenesis

Ramachandran, Binu; Ahmed, Saheeb; Zafar, Noman; Dean, Camin

doi:10.1002/hipo.22356

Cited by 20 publications

(20 citation statements)

References 49 publications

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“…4A), as expected based on previous studies of ethanol actions on synaptic plasticity (reviewed in (McCool, 2011; Zorumski et al, 2014)). For example, 60 mM ethanol completely blocked LTP in the non-tg slices, consistent with studies by others (Ramachandran et al, 2015). Exposure to 60 mM ethanol also significantly reduced PTP (~45%) and STP (~40%) in the non-tg slices (Fig.…”

Section: Resultssupporting

confidence: 91%

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

et al. 2016

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A growing body of evidence has revealed that resident cells of the central nervous system (CNS), and particularly the glial cells, comprise a neuroimmune system that serves a number of functions in the normal CNS and during adverse conditions. Cells of the neuroimmune system regulate CNS functions through the production of signaling factors, referred to as neuroimmune factors. Recent studies show that ethanol can activate cells of the neuroimmune system, resulting in the elevated production of neuroimmune factors, including the cytokine interleukin-6 (IL-6). Here we analyzed the consequences of this CNS action of ethanol using transgenic mice that express elevated levels of IL-6 through increased astrocyte expression (IL-6-tg) to model the increased IL-6 expression that occurs with ethanol use. Results show that increased IL-6 expression induces neuroadaptive changes that alter the effects of ethanol. In hippocampal slices from non-transgenic (non-tg) littermate control mice, synaptically evoked dendritic field excitatory postsynaptic potential (fEPSP) and somatic population spike (PS) at the Schaffer collateral to CA1 pyramidal neuron synapse were reduced by acute ethanol (20 or 60 mM). In contrast, acute ethanol enhanced the fEPSP and PS in hippocampal slices from IL-6 tg mice. Long-term synaptic plasticity of the fEPSP (i.e., LTP) showed the expected dose-dependent reduction by acute ethanol in non-tg hippocampal slices, whereas LTP in the IL-6 tg hippocampal slices was resistant to this depressive effect of acute ethanol. Consistent with altered effects of acute ethanol on synaptic function in the IL-6 tg mice, EEG recordings showed a higher level of CNS activity in the IL-6 tg mice than in the non-tg mice during the period of withdrawal from an acute high dose of ethanol. These results suggest a potential role for neuroadaptive effects of ethanol-induced astrocyte production of IL-6 as a mediator or modulator of the actions of ethanol on the CNS, including persistent changes in CNS function that contribute to cognitive dysfunction and the development of alcohol dependence.

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Section: Resultssupporting

confidence: 91%

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

et al. 2016

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“…Notably, several studies identified long-term potentiation (LTP) differences in the CA1 SO and SR (Cavus and Teyler, 1998; Fan, 2013; Kramár and Lynch, 2003; Navakkode et al, 2012; Ramachandran et al, 2014). The most striking difference is that the magnitude of LTP is significantly higher in SO compared to SR in acute slices and in vivo (Arai et al, 1994; Kaibara and Leung, 1993).…”

Section: Introductionmentioning

confidence: 99%

Heterophilic Type II Cadherins Are Required for High-Magnitude Synaptic Potentiation in the Hippocampus

Basu

Duan

Taylor

et al. 2017

Neuron

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Summary Hippocampal CA3 neurons form synapses with CA1 neurons in two layers, stratum oriens (SO) and stratum radiatum (SR). Each layer develops unique synaptic properties but molecular mechanisms that mediate these differences are unknown. Here, we show SO synapses normally have significantly more mushroom spines and higher magnitude long-term potentiation (LTP) than SR synapses. Further, we discovered these differences require the Type II classic cadherins, cadherins-6, 9, and 10. Though cadherins typically function via trans-cellular homophilic interactions, our results suggest presynaptic cadherin-9 binds postsynaptic cadherins-6 and 10 to regulate mushroom spine density and high magnitude LTP in the SO layer. Loss of these cadherins has no effect on the lower magnitude LTP typically observed in the SR layer, demonstrating that cadherins-6, 9, and 10 are gatekeepers for high magnitude LTP. Thus, Type II cadherins may uniquely contribute to the specificity and strength of synaptic changes associated with learning and memory.

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“…Studies demonstrate a role of anabolic steroids in serotonin modulation, resulting in a reduction of 5HT1B receptors density and alterations in the GABAergic hippocampal system [40,41]. Since AAS can cause a decrease in the receptors and change essential systems, it is believed that high doses, chronically administered can lead to cell death in Ca1 and not only receptors loss [42,43].…”

Section: Discussionmentioning

confidence: 99%

Chronic Use of Anabolic Steroids and the Effects on the Neuronal Density of the Cerebral Cortex and Hippocampus in Mice

Silva¹

2018

AJSS

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This study analyzed the effects of the chronic use of these drugs on the neuronal density of mice cerebral cortex and hippocampus. Materials and methods: 40 male Swiss mice were used, divided into 4 groups (n=10): GI-Control (0,02ml/Kg/week of saline solution), GII-treated with anabolic steroid Durateston® (83,3mg/Kg/week) GIII-treated with anabolic steroid Deca Durabolin® (16,6mg/Kg/week) e GIV-treated with the two anabolic steroids, concomitantly. The mice were treated for sixty days (60) and practiced swimming three times a week. The brain fragments were processed following the standardized sequence in conventional histological procedures and stained using cresyl violet. For the neuronal density analysis, the simple random count methodology was used. Results: Data revealed a significant reduction in the neuronal density of the groups treated with anabolic steroids, the limbic area had an estimated decrease of 16.44% in group III and 29.21% in group IV; the motor area the groups II, III, and IV presented a reduction of 17.63%, 15.35%, and 12.23%, and in the sensory area 15.22%, 16.41% and 21.59%, respectively; the groups II, III, and IV of the Ca1 area of the hippocampus showed a neuronal loss of 23.5%, 27.8%, and 36.36%, while groups II, III and IV of the Ca2 area there was a reduction of 10.37%, 11.83%, and 16.34%. In conclusion, the chronic use of AAS can be harmful to the nervous system since the neuronal reduction can bring structural and functional damages with possible consequences the whole organism.

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Ethanol inhibits long‐term potentiation in hippocampal CA1 neurons, irrespective of lamina and stimulus strength, through neurosteroidogenesis

Cited by 20 publications

References 49 publications

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

Heterophilic Type II Cadherins Are Required for High-Magnitude Synaptic Potentiation in the Hippocampus

Chronic Use of Anabolic Steroids and the Effects on the Neuronal Density of the Cerebral Cortex and Hippocampus in Mice

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