Effects of phencyclidines on signal transfer from the entorhinal cortex to the hippocampus in rats

Dugladze, Tamar; Lepsveridze, Eka; Breustedt, Jörg; Kehrer, Colin; Heinemann, Uwe; Gloveli, Tengis

doi:10.1016/j.neulet.2003.10.008

Cited by 9 publications

(9 citation statements)

References 9 publications

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“…In these studies, it had been shown that high‐frequency stimulation (HFS) of the dCI could interfere with plasticity in area CA1. However, under physiological conditions high‐frequency activation is an unlikely event in this pathway as the cells of origin for this pathway, EC layer III pyramidal cells, display strong frequency adaptation due to intrinsic properties (Erchova et al ., 2004) and due to synaptic interactions (Gloveli et al ., 1997a), which is only overcome under pathological conditions (Gloveli et al ., 2003; Dugladze et al ., 2004). In this study we therefore investigated the effects of low‐frequency stimulation (LFS) usually employed for induction of long‐term depression (LTD) applied to the dCI.…”

Section: Introductionsupporting

confidence: 64%

Low‐frequency stimulation of the direct cortical input to area CA1 induces homosynaptic LTD and heterosynaptic LTP in the rat hippocampal–entorhinal cortex slice preparation

Wöhrl

Haebler

Heinemann

2007

Eur J of Neuroscience

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The entorhinal cortex (EC) innervates area CA1 and the subiculum directly via the portion of the perforant path, which originates from EC layer III cells referred to as direct cortical input (dCI), and indirectly via the trisynaptic loop through the dentate gyrus and area CA3. The dCI is of great importance as it mediates positional information for activation of place cells that is not prevented after interrupting information flow from area CA3 to CA1. In this study, we investigated the effects of low-frequency stimulation of the dCI on homo- and heterosynaptic plasticity in area CA1 and tested for the contribution of NMDA, GABA(A), GABA(B), kainate and group I mGlu receptors. We demonstrate that 1 Hz stimulation of the dCI induces homosynaptic long-term depression (LTD) and that 1 Hz stimulation of the dCI induces a long-lasting augmentation of stratum radiatum-induced population spikes in area CA1 (heterosynaptic long-term potentiation). Additionally we show that homosynaptic effects depend on activation of GABA(B) and kainate receptors, whereas the heterosynaptic effects are GABA(A) and mGlu receptor dependent.

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Section: Introductionsupporting

confidence: 64%

Low‐frequency stimulation of the direct cortical input to area CA1 induces homosynaptic LTD and heterosynaptic LTP in the rat hippocampal–entorhinal cortex slice preparation

Wöhrl

Haebler

Heinemann

2007

Eur J of Neuroscience

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“…Blockade of NMDA receptors with ketamine reduces the output from superficial basket cells concurrently with a selective drop in gamma power in superficial layers. Disinhibition of the entorhinal cortex also has been reported in slices from rats pretreated with NMDA receptor antagonists (Dugladze et al, 2004). It is not clear why ketamine produces a similar pattern of selective reduction of gamma power in superficial layers.…”

Section: Discussionmentioning

confidence: 97%

Region-Specific Reduction in Entorhinal Gamma Oscillations and Parvalbumin-Immunoreactive Neurons in Animal Models of Psychiatric Illness

et al. 2006

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Psychiatric illnesses, particularly schizophrenia, are associated with disrupted markers for interneuronal function and interneuronmediated brain rhythms such as gamma frequency oscillations. Here we investigate a possible link between these two observations in the entorhinal cortex and hippocampus by using a genetic and an acute model of psychiatric illness. Lysophosphatidic acid 1 receptordeficient (LPA1-deficient) mice show psychomotor-gating deficits and neurochemical changes resembling those seen in postmortem schizophrenia studies. Similar deficits are seen acutely with antagonism of the NMDA subtype of glutamate receptor. Neither model induced any change in power or frequency of gamma rhythms generated by kainate in hippocampal slices. In contrast, a dramatic decrease in the power of gamma oscillations was seen in superficial, but not deep, medial entorhinal cortex layers in both models. Immunolabeling for GABA, parvalbumin, and calretinin in medial entorhinal cortex from LPA1-deficient mice showed an ϳ40% reduction in total GABA-and parvalbumin-containing neurons, but no change in the number of calretinin-positive neurons. This deficit was specific for layer II (LII). No change in the number of neurons positive for these markers was seen in the hippocampus. Acute NMDA receptor blockade, which selectively reduces synaptic drive to LII entorhinal interneurons, also disrupted gamma rhythms in a similar manner in superficial entorhinal cortex, but not in hippocampus. These data demonstrate an area-specific deficit in gamma rhythmogenesis in animal models of psychiatric illness and suggest that loss, or reduction in function, of interneurons having a large NMDA receptor expression may underlie the network dysfunction that is seen.

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“…We addressed alterations in the dCI‐induced synaptic plasticity in MK‐801‐treated animals, as previous studies in the same model had shown that stimulus‐evoked field potentials in layer III of the EC, which directly projects to CA1, were altered, whereas those in other layers were unaffected, suggesting an alteration in synaptic transmission in this pathway. High‐frequency input to layer III cells in MK‐801‐treated rats led to reduced frequency habituation as compared to control animals (Dugladze et al ., 2004), suggesting that high‐frequency activation of this pathway may occur in MK‐801‐treated rats and that high‐frequency synaptic input can reach the hippocampus, where, in normal animals, it would induce LTP (Wohrl et al ., 2007). Furthermore, MK‐801‐treated rats show alterations of synaptic plasticity in the subiculum that, like the CA1, receives an important input via dCI (Buck et al ., 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, MK‐801 interferes with frequency adaptation in EC layer III pyramidal cells, which form the dCI to CA1 (Gloveli et al ., 1997; Erchova et al ., 2004). Thus, high‐frequency activation of the dCI is likely in the presence of MK‐801 that, under physiological conditions, would be blocked during high‐frequency stimulation (HFS) (Gloveli et al ., 2003; Dugladze et al ., 2004).…”

Section: Introductionmentioning

confidence: 99%

Acute and long‐term effects of MK‐801 on direct cortical input evoked homosynaptic and heterosynaptic plasticity in the CA1 region of the female rat

Wöhrl

Eisenach

Manahan‐Vaughan

et al. 2007

Eur J of Neuroscience

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We analysed acute and long-term effects of the N-methyl-d-aspartate receptor antagonist MK-801 on long-term heterosynaptic population spike depression (LTHPSD) evoked by high-frequency stimulation of the direct cortical input in female rat hippocampal slices to understand disturbances in cognitive functions associated with an acute phencyclidine-induced psychosis. High-frequency stimulation (HFS) of the direct cortical input (dCI) to cornu ammonis area 1 (CA1) induced homosynaptic long-term potentiation (LTP) while simultaneously evoking LTHPSD at the Schaffer collateral input. Animals treated with a single intraperitoneal application of MK-801 (5 mg/kg body weight) showed severe behavioural alterations for 24 h, although histological examination of CA1 did not reveal any morphological changes. However, after application of MK-801, homosynaptic LTP of the dCI was suppressed for up to 7 days and recovered within 4 weeks. Likewise, LTHPSD in response to HFS of the dCI to CA1 was abolished for at least 1 week post-treatment, with partial recovery occurring after 4 weeks. Homosynaptic LTP, induced by HFS of Schaffer collaterals, was also disturbed for at least 24 h, with recovery after 7 days. Remarkably, bath application of MK-801 (50 microM) converted LTHPSD, induced by dCI HFS, into persistent heterosynaptic long-term enhancement of stratum radiatum-evoked responses. The acute effects of MK-801 on synaptic plasticity seen in this study may contribute to the observed severe behavioural alterations and long-term effects and may explain some of the long-lasting symptoms remaining after an acute psychotic episode in humans.

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Effects of phencyclidines on signal transfer from the entorhinal cortex to the hippocampus in rats

Cited by 9 publications

References 9 publications

Low‐frequency stimulation of the direct cortical input to area CA1 induces homosynaptic LTD and heterosynaptic LTP in the rat hippocampal–entorhinal cortex slice preparation

Low‐frequency stimulation of the direct cortical input to area CA1 induces homosynaptic LTD and heterosynaptic LTP in the rat hippocampal–entorhinal cortex slice preparation

Region-Specific Reduction in Entorhinal Gamma Oscillations and Parvalbumin-Immunoreactive Neurons in Animal Models of Psychiatric Illness

Acute and long‐term effects of MK‐801 on direct cortical input evoked homosynaptic and heterosynaptic plasticity in the CA1 region of the female rat

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