An in vivo model for investigating bilateral synaptic plasticity across CA3/CA1 synapses in guinea pig dorsal hippocampus

Chirwa, Sanika; Mack, Janea; Dennis, K. W.; Aduonum, Adwoa

doi:10.1016/s0165-0270(01)00413-7

Cited by 4 publications

(2 citation statements)

References 29 publications

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“…Our results showed that a stable, robust LTP in the Dm divisions of both the ipsilateral and contralateral sides can be induced by stimulation from either the left or right Dl. Similar results of LTP induction in the contralateral hippocampus of other species have been observed, including in guinea pigs 12 and mice 13 , implying a high degree of evolutionary conservation in the neural mechanism of neuroplasticity among different species. Most previous studies of neuronal transduction between the two hemispheres have used in vivo experiments due to limitations related to brain slice preparation.…”

Section: Discussionsupporting

confidence: 81%

Unilateral stimulation of the lateral division of the dorsal telencephalon induces synaptic plasticity in the bilateral medial division of zebrafish

Chen

Tang

et al. 2017

Sci Rep

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This study was aimed to evaluate the synaptic plasticity in projections from the dorsal lateral region (Dl) to the bilateral dorsal medial region (Dm) of the zebrafish telencephalon. The results showed that unilateral electrical stimulation of the Dl evokes a negative field potential (FP) in both the contralateral and ipsilateral side of the Dm. We tested synaptic plasticity, including high-frequency stimulation-induced LTP (HFS-LTP) and low-frequency stimulation-induced LTD (LFS-LTD). We demonstrated that HFS-induced bilateral LTP is NMDAR-dependent by the application of an NMDAR antagonist, DL-AP5 (30 μM, suprafused for 10 min), which blocked the HFS-induced LTP in both the contralateral and ipsilateral Dm. In addition, LTP was restored after DL-AP5 was washed out by continuous aCSF suprafusion. These results suggested that the potentiation is NMDAR-dependent. Either LFS (1 Hz for 20 min) or applying the mGluR agonist, DHPG (40 μM, suprafused for 10 min) successfully induced bilateral LTD for at least 1 h. Furthermore, both the contralateral fEPSP and LTP vanished after ablation of the anterior commissure. In conclusion, the results of the present study suggested that the projection between the Dl and contralateral Dm in the telencephalon of zebrafish is via the anterior commissure and possesses synaptic plasticity.

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Section: Discussionsupporting

confidence: 81%

Unilateral stimulation of the lateral division of the dorsal telencephalon induces synaptic plasticity in the bilateral medial division of zebrafish

Chen

Tang

et al. 2017

Sci Rep

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“…The jugular vein was cannulated for fluid and drug administration, and the animal was placed in a stereotaxic apparatus. Two holes (3 mm in diameter) were drilled in the skull, overlying the dorsal part of the hippocampus, to provide access for placement of electrodes to the stimulated CA3 and record from CA1 electrodes (Rapisarda and Bacchelli, 1977;Chirwa et al, 2001). After completion of all surgical procedures, alpha-chloralose (60 mg/kg, i.v.)…”

Section: Surgical Preparationmentioning

confidence: 99%

Apnea promotes glutamate-induced excitotoxicity in hippocampal neurons

Fung¹,

Xi²,

Zhang³

et al. 2007

Brain Research

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Patients with obstructive sleep apnea (OSA) exhibit hippocampal damage and cognitive deficits. To determine the effect of apnea on the synaptic transmission in the hippocampus, we performed electrophysiological studies in an in vivo guinea pig model of OSA. Specifically, we determined the cornu ammonis region 1 (CA1) field excitatory postsynaptic potential (fEPSP) response to cornu ammonis region 3 (CA3) stimulation and examined the presynaptic mechanisms underlying the changes in the fEPSP. Single episodes of apnea resulted in a maximal potentiation of the fEPSPs at 1 to 3 min after the termination of each episode of apnea. The mean amplitude and slope of the post-apneic fEPSP was significantly larger compared with the pre-apneic control. These changes were accompanied by a significant decrease in the paired-pulse facilitation ratio during the post-apneic period compared with the pre-apneic control. The N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK-801, when applied locally to the CA1 recording site by pressure ejection, blocked the apnea-induced potentiation of the fEPSP. In the experimental animals that were subjected to extended periods of recurrent apnea, CA1 neurons exhibited positive immunoreactivity for fragmented DNA strands, which indicates apoptotic cell death. The present results demonstrate that apnea-induced potentiation of the hippocampal CA1 fEPSP is mediated by an NMDA receptor mechanism. We therefore conclude that recurrent apnea produces abnormally high levels of glutamate that results in the apoptosis of CA1 neurons. We hypothesize that this damage is reflected by the cognitive deficits that are commonly observed in patients with breathing disorders such as OSA.

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Dopaminergic DA1 signaling couples growth-associated protein-43 and long-term potentiation in guinea pig hippocampus

Chirwa

Aduonum

Pizarro

et al. 2005

Brain Research Bulletin

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An in vivo model for investigating bilateral synaptic plasticity across CA3/CA1 synapses in guinea pig dorsal hippocampus

Cited by 4 publications

References 29 publications

Unilateral stimulation of the lateral division of the dorsal telencephalon induces synaptic plasticity in the bilateral medial division of zebrafish

Unilateral stimulation of the lateral division of the dorsal telencephalon induces synaptic plasticity in the bilateral medial division of zebrafish

Apnea promotes glutamate-induced excitotoxicity in hippocampal neurons

Dopaminergic DA1 signaling couples growth-associated protein-43 and long-term potentiation in guinea pig hippocampus

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