Hippocampal CA1 neuronal properties in genetically epilepsyprone rats: Evidence for increased excitation

Verma-Ahuja, Suneeta; Pencek, T.L.

doi:10.1016/0920-1211(94)90041-8

Cited by 18 publications

(6 citation statements)

References 23 publications

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“…In addition to audiogenic seizures, both GEPR-9 and GEPR-3 also exhibited enhanced propensity to seizures induced by non-audiogenic stimuli including limbic kindling (Savage et al 1986). In line with this report, functional ion channel abnormalities were reported in the hippocampus of the GEPR-9, a brain site that is not implicated in the initiation of reflex audiogenic seizures (Evans et al 1994, Verma-Ahuja and Pencek, 1994; Verma-Ahuja et al 1995). The mechanisms underlying the increases in IC neuronal firing and inherited seizure susceptibility in the GEPR-9 and GEPR-3 are not as yet well understood.…”

Section: Discussionsupporting

confidence: 85%

“…The large (BK) and small (SK) conductance, Ca 2+ -activated K + channels are known to play important roles in the control of IC neuronal excitability, and altered expression of these channels therefore may play important roles in seizure susceptibility and seizure generation (Li et al 1998; Sivaramakrishnan and Oliver 2001). In support of this idea, electrophysiological study reported that the amplitude of slow AHP was smaller in hippocampal neurons of the GEPR-9 (Verma-Ahuja and Pencek, 1994; Verma-Ahuja et al 1995; 1998). Such altered slow AHP also was found in human with epilepsy suggesting that abnormal AHP may be a general mechanism underlying neuronal hyperexcitability across species (Williamson et al 1993).…”

Section: Discussionmentioning

confidence: 76%

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Protein expression of small conductance calcium-activated potassium channels is altered in inferior colliculus neurons of the genetically epilepsy-prone rat

2009

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The genetically epilepsy-prone rat (GEPR) exhibits inherited predisposition to sound stimuli-induced generalized tonic-clonic seizures (audiogenic reflex seizures) and is a valid model to study the physiopathology of epilepsy. In this model, the inferior colliculus (IC) exhibits enhanced neuronal firing that is critical in the initiation of reflex audiogenic seizures. The mechanisms underlying IC neuronal hyperexcitability that leads to seizure susceptibility are not as yet fully understood. The present report shows that the levels of protein expression of SK1 and SK3 subtypes of the small conductance Ca 2+ -activated K + channels were significantly decreased, while SK2 channel proteins were increased in IC neurons of seizure-naive GEPR-3s (SN-GEPR-3), as compared to control Sprague-Dawley rats. No significant change was found in the expression of BK channel proteins in IC neurons of SN-GEPR-3s. Single episode of reflex audiogenic seizures in the GEPR-3s did not significantly alter the protein expression of SK1-3 and BK channels in IC neurons compared to SN-GEPR-3s. Thus, downregulation of SK1 and SK3 channels and upregulation of SK2 channels provide direct evidence that these Ca 2+ -activated K + channels play important roles in IC neuronal hyperexcitability that leads to inherited seizure susceptibility in the GEPR.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 76%

Protein expression of small conductance calcium-activated potassium channels is altered in inferior colliculus neurons of the genetically epilepsy-prone rat

2009

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“…For example, 4-AP-induced epileptiform activity in the neocortex increased input resistance of parvalbumin-expressing neurons and reduced the action potential threshold for parvalbumin-expressing and pyramidal neurons both [43]. Apart from the 4-AP model, an increase in input resistance has been observed in the CA1 neurons of genetically epilepsy-prone rats [44], kindled rats [45], and in the pentylenetetrazole model [17]. However, after acute kainate-induced status epilepticus, there were no changes in input resistance in CA1 neurons [46], and the resting membrane potential and input resistance in piriform cortex neurons were not affected by abnormal activity induced by repeatedly applied tetanic stimulation [47].…”

Section: Discussionmentioning

confidence: 99%

Short-Term Epileptiform Activity Potentiates Excitatory Synapses but Does Not Affect Intrinsic Membrane Properties of Pyramidal Neurons in the Rat Hippocampus In Vitro

et al. 2021

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Even brief epileptic seizures can lead to activity-dependent structural remodeling of neural circuitry. Animal models show that the functional plasticity of synapses and changes in the intrinsic excitability of neurons can be crucial for epileptogenesis. However, the exact mechanisms underlying epileptogenesis remain unclear. We induced epileptiform activity in rat hippocampal slices for 15 min using a 4-aminopyridine (4-AP) in vitro model and observed hippocampal hyperexcitability for at least 1 hour. We tested several possible mechanisms of this hyperexcitability, including changes in intrinsic membrane properties of neurons and presynaptic and postsynaptic alterations. Neither input resistance nor other essential biophysical properties of hippocampal CA1 pyramidal neurons were affected by epileptiform activity. The glutamate release probability also remained unchanged, as the frequency of miniature EPSCs and the paired amplitude ratio of evoked responses did not change after epileptiform activity. However, we found an increase in the AMPA/NMDA ratio, suggesting alterations in the properties of postsynaptic glutamatergic receptors. Thus, the increase in excitability of hippocampal neural networks is realized through postsynaptic mechanisms. In contrast, the intrinsic membrane properties of neurons and the probability of glutamate release from presynaptic terminals are not affected in a 4-AP model.

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“…For example, 4-AP-induced epileptiform activity in the neocortex increased input resistance of parvalbumin-expressing neurons and reduced the action potential threshold for parvalbumin-expressing and pyramidal neurons both [42]. Apart from the 4-AP model, an increase in input resistance has been observed in the CA1 neurons of genetically epilepsy-prone rats [43], kindled rats [44], and in the pentylenetetrazole model [17]. However, after acute kainate-induced status epilepticus, there were no changes in input resistance in CA1 neurons [45], resting membrane potential and input resistance in piriform cortex neurons were not affected by abnormal activity induced by repeatedly applied tetanic stimulation [46].…”

Section: Discussionmentioning

confidence: 99%

Short-term Epileptiform Activity Potentiates Excitatory Synapses but does not Affect Intrinsic Membrane Properties of Pyramidal Neurons in the Rat Hippocampus <em>in Vitro</em>

Ergina¹,

Amakhin²,

Postnikova³

et al. 2021

Preprint

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Even brief epileptic seizures can lead to activity-dependent structural remodeling of neural circuitry. Animal models show that the functional plasticity of synapses and changes in the intrinsic excitability of neurons can be crucial for epileptogenesis. However, the exact mechanisms underlying epileptogenesis remain unclear. We induced epileptiform activity in rat hippocampal slices for 15 min using a 4-aminopyridine (4-AP) in vitro model and observed hippocampal hyperexcitability for at least 1 hour. We tested several possible mechanisms of this hyperexcitability, including changes in intrinsic membrane properties of neurons, presynaptic and postsynaptic alterations. Neither input resistance nor other essential biophysical properties of hippocampal CA1 pyramidal neurons were affected by epileptiform activity. The glutamate release probability also remained unchanged, as the frequency of miniature EPSCs and the paired amplitude ratio of evoked responses did not change after epileptiform activity. However, we found an increase in the AMPA/NMDA ratio, suggesting alterations in the properties of postsynaptic glutamatergic receptors. Thus, the increase in excitability of hippocampal neural networks is realized through postsynaptic mechanisms. In contrast, the intrinsic membrane properties of neurons and the probability of glutamate release from presynaptic terminals are not affected in a 4-AP model.

show abstract

Hippocampal CA1 neuronal properties in genetically epilepsyprone rats: Evidence for increased excitation

Cited by 18 publications

References 23 publications

Protein expression of small conductance calcium-activated potassium channels is altered in inferior colliculus neurons of the genetically epilepsy-prone rat

Protein expression of small conductance calcium-activated potassium channels is altered in inferior colliculus neurons of the genetically epilepsy-prone rat

Short-Term Epileptiform Activity Potentiates Excitatory Synapses but Does Not Affect Intrinsic Membrane Properties of Pyramidal Neurons in the Rat Hippocampus In Vitro

Short-term Epileptiform Activity Potentiates Excitatory Synapses but does not Affect Intrinsic Membrane Properties of Pyramidal Neurons in the Rat Hippocampus <em>in Vitro</em>

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