Evoked potential changes in rat hippocampal slices under helium pressure

Fagni, Laurent; Zinebi, Fatiha; Hugon, M

doi:10.1007/bf00235974

Cited by 37 publications

(34 citation statements)

References 19 publications

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“…However, decreased slow after-hyperpolarization following the firing of action potentials, and a reduced accommodation of firing rate were observed at high pressure. Field potential measurements from the same region show that there is a decrease in the population excitatory postsynaptic potential at pressure but a facilitation of its transfer to a population spike [8]. While this study also showed reduced orthodromic and antidromic population spike responses, conflicting data have been recently reported [29].…”

Section: Introductionmentioning

confidence: 42%

Spontaneous Na + and Ca 2+ spike firing of cerebellar Purkinje neurons at high pressure

Etzion

Grossman

1999

Pfl�gers Archiv European Journal of Physiology

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The effects of high pressure (up to 10.1 MPa) on the spontaneous firing of Purkinje neurons in guinea-pig cerebellar slices were studied using the macropatch clamp technique. Pressure did not significantly alter the single somatic Na+ spike parameters or the frequency of regular Na+ spike firing. When Na+ currents were blocked by 0.5-1 microM tetrodotoxin (TTX), a pressure of 10.1 MPa slightly reduced the dendritic Ca2+ spike amplitude to 90.2+/-3.1% of its control value, and slowed its kinetics. The effects of pressure on the single Ca2+ spike were even less prominent when K+ currents were blocked by 5 mM 4-aminopyridine (4-AP). Pressure prolonged the active period of Ca2+ spike firing to 152.2+/-10.4% of the control value. Within the active period pressure increased the inter-spike interval to 164.9+/-8.7% and suppressed the typical firing of doublets. The latter changes were reversed by a high extracellular potassium concentration ([K+]o) and 1 microM 4-AP, whereas in the presence of 5 mM 4-AP the pattern was insensitive to pressure. A high [Ca2+]o reduced the firing frequency and suppressed doublet firing in a manner reminiscent of the pressure effect, but these changes could not be reversed by 4-AP. A low [Ca2+]o slightly increased the firing of doublets. These results show that the single somatic Na+ spike is insensitive and the dendritic Ca2+ spike is only mildly sensitive to pressure. However, alterations in Ca2+ spike firing pattern suggest that modulation of dendritic K+ currents induce depression of dendritic excitability at pressure.

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Section: Introductionmentioning

confidence: 42%

Spontaneous Na + and Ca 2+ spike firing of cerebellar Purkinje neurons at high pressure

Etzion

Grossman

1999

Pfl�gers Archiv European Journal of Physiology

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“…Moreover, both the extracellular action potential (EAP) amplitude, which measures the synaptic current, and the EAP slope, which measures the rate of activation of synaptic receptors, were used for the evaluation of the efficacy of synaptic transmission. We measured both parameters in all the protocols, and we showed in the Results only EAPs' slopes and EAPs' amplitude under electrical stimulation (Fagni et al 1987). The slope was calculated between 20% and 80% of maximal EAPs' amplitude, normalized to the average slope recorded during a 15 min baseline interval and measured in milliVolt/milliseconds (mV/ms).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Genetic deletion of monoacylglycerol lipase leads to impaired cannabinoid receptor CB₁R signaling and anxiety‐like behavior

Imperatore

Morello

Luongo

et al. 2015

Journal of Neurochemistry

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Endocannabinoids (eCB) are key regulators of excitatory/ inhibitory neurotransmission at cannabinoid-1-receptor (CB 1 R)-expressing axon terminals. The most abundant eCB in the brain, that is 2-arachidonoylglycerol (2-AG), is hydrolyzed by the enzyme monoacylglycerol lipase (MAGL), whose chronic inhibition in the brain was reported to cause CB 1 R desensitization. We employed the MAGL knock-out mouse (MAGLÀ/À), a genetic model of congenital and sustained elevation of 2-AG levels in the brain, to provide morphological and biochemical evidence for b-arrestin2-mediated CB 1 R desensitization in brain regions involved in the control of emotional states, that is, the prefrontal cortex (PFC), amygdala, hippocampus and cerebellar cortex. We found a widespread CB 1 R/b-arrestin2 co-expression in the mPFC, amygdala and hippocampus accompanied by impairment of extracellular signal-regulated kinase signaling and elevation of vesicular glutamate transporter (VGluT1) at CB 1 R-positive excitatory terminals in the mPFC, or vesicular GABA transporter (VGAT) at CB 1 R-positive inhibitory terminals in the amygdala and hippocampus. The impairment of CB 1 R signaling in MAGLÀ/À mice was also accompanied by enhanced excitatory drive in the basolateral amygdala (BLA)-mPFC circuit, with subsequent elevation of glutamate release to the mPFC and anxiety-like and obsessive-compulsive behaviors, as assessed by the light/dark box and marble burying tests, respectively. Collectively, these data provide evidence for a barrestin2-mediated desensitization of CB 1 R in MAGLÀ/À mice, with impact on the synaptic plasticity of brain circuits involved in emotional functions.

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“…This effect was specific because no change in the apparent R in (100 Ϯ 1%; n ϭ 6) was observed when external saline was applied. Because local positive pressure depresses synaptic transmission (Fagni et al, 1987), we used dynamic clamp to reduce electronically G h in the dendrite and determine integration of evoked EPSPs.…”

Section: H-channels Determine Synaptic Integrationmentioning

confidence: 99%

Downregulation of DendriticI_hin CA1 Pyramidal Neurons after LTP

Campanac¹,

Daoudal²,

Ankri³

et al. 2008

J. Neurosci.

108

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Hyperpolarization-activated (h)-channels occupy a central position in dendritic function. Although it has been demonstrated that these channels are upregulated after large depolarizations to reduce dendritic excitation, it is not clear whether they also support other forms of long-term plasticity. We show here that nearly maximal long-term potentiation (LTP) induced by theta-burst pairing produced upregulation in h-channel activity in CA1 pyramidal neurons. In contrast, moderate LTP induced by spike-timing-dependent plasticity or high-frequency stimulation (HFS) downregulated the h-current (Ih) in the dendrites. After HFS-induced LTP, the h-conductance (Gh) was reduced without changing its activation. Pharmacological blockade ofIhhad no effect on LTP induction, but occluded EPSP-to-spike potentiation, an input-specific facilitation of dendritic integration. Dynamic-clamp reduction ofGhlocally in the dendrite mimicked the effects of HFS and enhanced synaptic integration in an input-selective way. We conclude that dendriticIhis locally downregulated after induction of nonmaximal LTP, thus facilitating integration of the potentiated input.

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Evoked potential changes in rat hippocampal slices under helium pressure

Cited by 37 publications

References 19 publications

Spontaneous Na + and Ca 2+ spike firing of cerebellar Purkinje neurons at high pressure

Spontaneous Na + and Ca 2+ spike firing of cerebellar Purkinje neurons at high pressure

Genetic deletion of monoacylglycerol lipase leads to impaired cannabinoid receptor CB₁R signaling and anxiety‐like behavior

Downregulation of DendriticI_hin CA1 Pyramidal Neurons after LTP

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Evoked potential changes in rat hippocampal slices under helium pressure

Cited by 37 publications

References 19 publications

Spontaneous Na + and Ca 2+ spike firing of cerebellar Purkinje neurons at high pressure

Spontaneous Na + and Ca 2+ spike firing of cerebellar Purkinje neurons at high pressure

Genetic deletion of monoacylglycerol lipase leads to impaired cannabinoid receptor CB1R signaling and anxiety‐like behavior

Downregulation of DendriticIhin CA1 Pyramidal Neurons after LTP

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Product

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Genetic deletion of monoacylglycerol lipase leads to impaired cannabinoid receptor CB₁R signaling and anxiety‐like behavior

Downregulation of DendriticI_hin CA1 Pyramidal Neurons after LTP