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ABSTRACT: In area CA1 of hippocampal slices, a single 1-sec train of 100-Hz stimulation generally triggers a short-lasting long-term potentiation (S-LTP) of 1-2 h. Here, we found that when such a train was applied 45 min after application of the small conductance Ca(2+)-activated K(+ )(SK) channel blocker apamin, it induced a long-lasting LTP (L-LTP) of several hours, instead of an S-LTP. Apamin-induced SK channel blockage is known to resist washing. Nevertheless, the aforementioned effect is not a mere delayed effect; it is metaplastic. Indeed, when a single train was delivered to the Schaffer's collaterals during apamin application, it induced an S-LTP, like in the control situation. At the moment of this LTP induction (15th min of apamin application), the SK channel blockage was nevertheless complete. Indeed, at that time, under the influence of apamin, the amplitude of the series of field excitatory postsynaptic potentials (fEPSPs) triggered by a stimulation train was increased. We found that the metaplastic effect of apamin on LTP was crucially dependent on the NO-synthase pathway, whereas the efficacy of the NMDA receptors was not modified at the time of its occurrence. We also found that apamin produced an increase in paired-pulse facilitation not during, but after, the application of the drug. Finally, we found that the induction of each of these two metaplastic phenomena was mediated by NMDA receptors. A speculative unitary hypothesis to explain these phenomena is proposed.
Learning & memory (Cold Spring Harbor, N.Y.) 07/2007; 14(6):390-9. · 4.08 Impact Factor
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ABSTRACT: Long-term potentiation (LTP) is a persistent increase in the strength of synaptic transmission triggered by neuronal activity. Here, we submitted hippocampal slices to a perfusion of forskolin and IBMX, which induces a long-lasting LTP (>4 h) (L-LTP). We separated the proteins of the CA1 region by two-dimensional gel electrophoresis (2-DE). We then immunoblotted them using an anti-p-Tyr antibody. We found a protein whose tyrosine phosphorylation was unchanged 10 min after LTP induction but was dramatically increased after 1h, dropping back to its baseline after 4 h. This protein was identified as rabphilin using matrix-assisted laser desorption ionisation-time of flight mass spectrometry (MALDI-TOF MS). We also demonstrated that genistein, an inhibitor of tyrosine phosphorylation, prevented the development of the late phase of electrically-induced L-LTP. Our results suggest that rabphilin, a protein present in presynaptic terminals, could play a role in the late phase of L-LTP.
Neuroscience Letters 04/2007; 414(3):257-62. · 2.11 Impact Factor
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ABSTRACT: In the vestibular nuclei of the awake guinea pig, all neurones are spontaneously active. After unilateral labyrinthectomy, this activity virtually disappears on the ipsilateral side, but is completely restored one week later. In a recent study, we observed that the restoration of spontaneous activity was correlated with an increase in pacemaker activity. In the current study, we found that the ratio of medial vestibular nucleus (MVN) neurones endowed with one of the currents known to play a role in pacemaker activity (i.e. low-threshold calcium current; LTCC) increased from 29% in control guinea pigs to 65% in animals labyrinthectomised on the ipsilateral side one week earlier. Yet this change was not correlated with a modification of the ratio of neurones expressing any of the three related protein-channels (alpha1G, alpha1H and alpha1I).
Neuroreport 09/2003; 14(12):1585-9. · 1.66 Impact Factor
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ABSTRACT: In the guinea pig, unilateral labyrinthectomy causes an immediate and severe depression of the spontaneous activity of the ipsilateral central vestibular neurons, which subsequently recovers completely within one week. A possible underlying mechanism could be an increase in the endogenous activity of the neurons deprived of their labyrinthine input. Here, we addressed this hypothesis. The endogenous activity of the neurons was assessed by their spontaneous activity recorded extracellularly in brainstem slices in the presence of a cocktail of neurotransmitter blockers (CNQX, d-APV, bicuculline and strychnine) which freed them from their main synaptic influences. The left medial vestibular nucleus (MVN) was explored in a very systematic way and strict methodological precautions were taken in order to validate comparisons between the numbers of spontaneously active neurons recorded in the MVN of distinct slices. In the presence of neurotransmitter antagonists, the mean number of spontaneously active neurons detected in a single MVN increased dramatically from 9.5 in slices from control guinea pigs to 26.3 in slices from animals labyrinthectomized on the left side one week beforehand. The mean firing rate of the recorded neurons also increased from 7.5 ± 5.6 spikes/s in slices from control animals to 12.3 ± 7.6 spikes/s in slices from guinea pigs labyrinthectomized one week beforehand. These results show that deprivation of the vestibular neurons of their labyrinthine input caused a change in the deprived neurons themselves. They suggest that an increase in pacemaker activity might be a factor responsible for the restoration of spontaneous activity in the vestibular neurons after labyrinthectomy.
European Journal of Neuroscience 05/2001; 13(12):2234 - 2240. · 3.63 Impact Factor
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ABSTRACT: In the guinea pig, lateral deviation of the head is a cardinal symptom of the vestibular syndrome caused by unilateral labyrinthectomy.
In the course of recovery from this syndrome (vestibular compensation), lateral deviation of the head disappears completely
in 2–3 days. Because this symptom is known to be due to the lesion of the horizontal semicircular canal system, and since
obliquus capitis inferior (OCI) muscle is activated predominantly by yaw rotation (horizontal vestibulocollic reflex), we
hypothesized that changes in the activity of this muscle could be at least in part responsible for the lateral head deviation
caused by unilateral labyrinthectomy. In order to test this hypothesis, electromyographic (EMG) activities of the right and
left OCI muscles, as well as eye movements, were recorded in 12 head-fixed alert guinea pigs at various times after left surgical
labyrinthectomy (performed with the animals under halothane anesthesia). After the operation, a decrease in tonic EMG activity
was observed in the right (contralateral to the lesion) OCI muscle while an increase in tonic EMG activity was detected in
the left (ipsilateral) OCI muscle. In addition, phasic changes in EMG activity associated with ocular nystagmic beats occurred
in the OCI muscles. These phasic changes were in the opposite direction to those of the tonic changes. There were bursts of
activity in the right OCI and pauses in the left OCI. From measurements of rectified averaged EMG activities which took into
account both parts (tonic and phasic) of the phenomenon, it was concluded that the labyrinthectomy-induced asymmetry between
the activities of the left and right OCI muscles was high enough and lasted long enough to be an important mechanism in the
lateral deviation of the head caused by unilateral labyrinthectomy.
Experimental Brain Research 12/1998; 124(2):159-165. · 2.39 Impact Factor
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ABSTRACT: In area CA1 of hippocampal slices which are allowed to recover from slicing "in interface" and where recordings are carried out in interface, a single 1-sec train of 100-Hz stimulation triggers a short-lasting long-term potentiation (S-LTP), which lasts 1-2 h, whereas multiple 1-sec trains induce a long-lasting LTP (L-LTP), which lasts several hours. Moreover, the threshold and the features of these LTP depend on the history of the neurons, a phenomenon known as metaplasticity. Here, where all recordings were performed in interface, we found that allowing the slices to recover "in submersion" had dramatic metaplastic effects. In these conditions, a single 1-sec train at 100 Hz induced an L-LTP which lasted at least 4 h and was dependent on protein synthesis. Interestingly, this type of metaplasticity was observed when the concentration of Mg(++) used was 1.0 mM but not when it was 1.3 mM. The LTP induced by four 1-sec trains at 100 Hz was similar whatever the incubation method. However, the signaling cascades recruited to achieve that pattern were different. In the interface-interface paradigm (recovery and recording both in interface) the four-train induced LTP recruited the PKA signaling pathway but not that of the p42/44MAPK. On the contrary, in the submersion-interface paradigm the four-train induced LTP recruited the p42/44MAPK signaling pathway but not that of the PKA. To our knowledge this is the first example of metaplasticity involving the recruitment of signaling cascades in LTP.
Learning & Memory 13(3):271-7. · 4.22 Impact Factor
