Biophysical and network mechanisms of high frequency extracellular potentials in the rat hippocampus

A fundamental question in neuroscience is how distributed networks of neurons communicate and coordinate dynamically and specifically. Several models propose that oscillating local networks can transiently couple to each other through phase-locked firing. Coherent local field potentials (LFP) between synaptically connected regions is often presented as evidence for such coupling. The physiological correlates of LFP signals depend on many anatomical and physiological factors, however, and how the underlying neural processes collectively generate features of different spatiotemporal scales is poorly understood. High frequency oscillations in the hippocampus, including gamma rhythms (30-100 Hz) that are organized by the theta oscillations (5-10 Hz) during active exploration and REM sleep, as well as sharp wave-ripples (SWRs, 140-200 Hz) during immobility or slow wave sleep, have each been associated with various aspects of learning and memory. Deciphering their physiology and functional consequences is crucial to understanding the operation of the hippocampal network.

We investigated the origins and coordination of high frequency LFPs in the hippocampo-entorhinal network using both biophysical models and analyses of large-scale recordings in behaving and sleeping rats. We found that the synchronization of pyramidal cell spikes substantially shapes, or even dominates, the electrical signature of SWRs in area CA1 of the hippocampus. The precise mechanisms coordinating this synchrony are still unresolved, but they appear to also affect CA1 activity during theta oscillations. The input to CA1, which often arrives in the form of gamma-frequency waves of activity from area CA3 and layer 3 of entorhinal cortex (EC3), did not strongly influence the timing of CA1 pyramidal cells. Rather, our data are more consistent with local network interactions governing pyramidal cells' spike timing during the integration of their inputs. Furthermore, the relative timing of input from EC3 and CA3 during the theta cycle matched that found in previous work to engage mechanisms for synapse modification and active dendritic processes. Our work demonstrates how local networks interact with upstream inputs to generate a coordinated hippocampal output during behavior and sleep, in the form of theta-gamma coupling and SWRs.

Morphofunctional changes in a rat model of Parkinson's disease - Effects of neurotrophic factors administration

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Effects of prolonged exposure to context following contextual fear conditioning on synaptic properties in rat hippocampal slices

Acute stressful events enhance plasma corticosterone release and profoundly affect synaptic functions, which are involved in the development of stress-related cognitive and mental disorders. However, how exposure to stressful context immediately after str

Effect of chitin and prawn shell on the growth of albino rat

The effect of addition of pure chitin from prawn shell, deproteinised prawn shell, demineralized prawn shell and dry prawn shell in casein based control diet on albino rats was studied. The diets contained 0.5% chitin and 10% protein. The results obtained in the studies show that the weight gain and feed conversion were maximum in the control diet. While addition of pure chitin slightly brought down the weight gain, addition of deproteinsed prawn shell have the minimum weight gain showing that presence of minerals adversely affects both feed consumption and weight gain in the case of albino rats. Although it was reported that addition of pure chitin at 0.5% in the commercial feed of broiler chicken gave increased weight, in the case of albino rats the weight gain was slightly reduced compared to control diet.

Metabolic changes in rat prefrontal cortex and hippocampus induced by chronic morphine treatment studied ex vivo by high resolution H-1 NMR spectroscopy

Ex vivo H-1 NMR spectroscopy was used to measure changes in the concentrations of cerebral metabolites in the prefrontal cortex (PFC) and hippocampus of rats subjected to repeated morphine treatment known to cause tolerance/dependence. The results show th

Extremely low-frequency electromagnetic field exposure during chronic morphine treatment strengthens downregulation of dopamine D2 receptors in rat dorsal hippocampus after morphine withdrawal

The aim of this study was to investigate the effect of extremely low-frequency electromagnetic field (ELF-EMF) exposure during morphine treatment on dopamine D2 receptor (D2R) density in the rat dorsal hippocampus following withdrawal. Rats were exposed t

KARYOTYPE AND BANDING-PATTERNS OF FEA TREE RAT (CHIROMYSCUS-CHIROPUS)

Fea's tree rat (Chiromyscus chiropus) is a very rare species which there are only a few specimens in the world. The chromosomes of two male specimens, collected from Xishuanbanna, Yunnan, are analysed by several banding technique (G-, C-bands, as well as Ag-staining). The diploid chromosome number is 22, and autosomes comprise 5 pairs of metacentrics, 2 pairs of subacrocentrics, and 3 pairs of acrocentrics. The X chromosome is a acrocentric, and Y is a micro-chromosome, almost a point, which could be a marker chromosome of the species and the genus. The centromeric C-bands are very faint, and C-bands of Nos. 1, 2, 9 and Y chromosome are negative. Only one pair Ag-NORs was found on No. 10 in the silver-stained karyotype. The relationship between morphologic and chromosomal features was discussed, and C-banded karyotype evolutionary trend has also been discussed. Moreover, the conventional karyotype of Niviventer confucianus was described.

Spatial exploration induces a persistent reversal of long-term potentiation in rat hippocampus

Experience-dependent long-lasting increases in excitatory synaptic transmission in the hippocampus are believed to underlie certain types of memory(1-3). Whereas stimulation of hippocampal pathways in freely moving rats can readily elicit a long-term potentiation (LTP) of transmission that may last for weeks, previous studies have failed to detect persistent increases in synaptic efficacy after hippocampus-mediated learning(4-6). As changes in synaptic efficacy are contingent on the history of plasticity at the synapses(7), we have examined the effect of experience-dependent hippocampal activation on transmission after the induction of LTP, We show that exploration of a new, non-stressful environment rapidly induces a complete and persistent reversal of the expression of high-frequency stimulation-induced early-phase LTP in the CA1 area of the hippocampus, without affecting baseline transmission in a control pathway. LTP expression is not affected by exploration of familiar environments. We found that spatial exploration affected LTP within a defined time window because neither the induction of LTP nor the maintenance of long-established LTP was blocked. The discovery of a novelty-induced reversal of LTP expression provides strong evidence that extensive long-lasting decreases in synaptic efficacy may act in tandem with enhancements at selected synapses to allow the detection and storage of new information by the hippocampus.

Mechanisms of H+ modulation of glycinergic response in rat sacral dorsal commissural neurons

Many ionotropic receptors are modulated by extracellular H+. So far, few studies have directly addressed the role of such modulation at synapses. In the present study, we investigated the effects of changes in extracellular pH on glycinergic miniature inhibitory postsynaptic currents (mIPSCs) as well as glycine-evoked currents (I-Gly) in mechanically dissociated spinal neurons with native synaptic boutons preserved. H+ modulated both the mIPSCs and I-Gly, biphasically, although it activated an amiloride-sensitive inward current by itself. Decreasing extracellular pH reversibly inhibited the amplitude of the mIPSCs and I-Gly, while increasing external pH reversibly potentiated these parameters. Blockade of acid-sensing ion channels (ASICs) with amiloride, the selective antagonist of ASICs, or decreasing intracellular pH did not alter the modulatory effect of H+ on either mIPSCs or I-Gly, H+ shifted the EC50 of the glycine concentration-response curve from 49.3 +/- 5.7 muM at external pH 7.4 to 131.5 +/- 8.1 muM at pH 5.5, without altering the Cl- selectivity of the glycine receptor (GlyR), the Hill coefficient and the maximal I-Gly, suggesting a competitive inhibition of I-Gly by H+. Both Zn2+ and H+ inhibited I-Gly. However, H+ induced no further inhibition of I-Gly in the presence of a saturating concentration of Zn2+. In addition, H+ significantly affected the kinetics of glycinergic mIPSCs and I-Gly. It is proposed that H+ and/or Zn2+ compete with glycine binding and inhibit the amplitude of glycinergic mIPSCs and I-Gly. Moreover, binding of H+ induces a global conformational change in GlyR, which closes the GlyR Cl- channel and results in the acceleration of the seeming desensitization of IGly as well as speeding up the decay time constant of glycinergic mIPSCs. However, the deprotonation rate is faster than the unbinding rate of glycine from the GlyR, leading to reactivation of the undesensitized GlyR after washout of agonist and the appearance of a rebound I-Gly. H+ also modulated the glycine cotransmitter, GABA-activated current (I-GABA). Taken together, the results support a 'conformational coupling' model for H+ modulation of the GlyR and suggest that W may act as a novel modulator for inhibitory neurotransmission in the mammalian spinal cord.

Characterization of acid-sensing ion channels in dorsal horn neurons of rat spinal cord

Acid-sensing ion channels (ASICs) are ligand-gated cation channels activated by extracellular protons. In periphery, they contribute to sensory transmission, including that of nociception and pain. Here we characterized ASIC-like currents in dorsal horn neurons of the rat spinal cord and their functional modulation in pathological conditions. Reverse transcriptase-nested PCR and Western blotting showed that three ASIC isoforms, ASIC1a, ASIC2a, and ASIC2b, are expressed at a high level in dorsal horn neurons. Electrophysiological and pharmacological properties of the proton-gated currents suggest that homomeric ASIC1a and/or heteromeric ASIC1a + 2b channels are responsible for the proton-induced currents in the majority of dorsal horn neurons. Acidification-induced action potentials in these neurons were compatible in a pH-dependent manner with the pH dependence of ASIC-like current. Furthermore, peripheral complete Freund's adjuvant-induced inflammation resulted in increased expression of both ASIC1a and ASIC2a in dorsal horn. These results support the idea that the ASICs of dorsal horn neurons participate in central sensory transmission/modulation under physiological conditions and may play important roles in inflammation-related persistent pain.

Long-term depression in rat CA1-subicular synapses depends on the G-protein coupled mACh receptors

The subiculum, which is the primary target of CA1 pyramidal neurons and sending efferent fibres to many brain regions, serves as a hippocampal interface in the neural information processes between hippocampal formation and neocortex. Long-term depression (LTD) is extensively studied in the hippocampus, but not at the CA1-subicular synaptic transmission. Using whole-cell EPSC recordings in the brain slices of young rats, we demonstrated that the pairing protocols of low frequency stimulation (LFS) at 3 Hz and postsynaptic depolarization of -50 mVelicited a reliable LTD in the subiculum. The LTD did not cause the changes of the paired-pulse ratio of EPSC. Furthermore, it did not depend on either NMDA receptors or voltage-gated calcium channels (VGCCs). Bath application of the G-protein coupled muscarinic acetylcholine receptors (mAChRs) antagonists, atropine or scopolamine, blocked the LTD, suggesting that mAChRs are involved in the LTD. It was also completely blocked by either the Ca2+ chelator BAPTA or the G-protein inhibitor GDP-beta-S in the intracellular solution. This type of LTD in the subiculum may play a particular role in the neural information processing between the hippocampus and neocortex. (c) 2005 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

Prenatal stress modifies hippocampal synaptic plasticity and spatial learning in young rat offspring

Clinical studies demonstrate that prenatal stress causes cognitive deficits and increases vulnerability to affective disorders in children and adolescents. The underlying mechanisms are not yet fully understood. Here, we reported that prenatal stress (10

Morphine induces Beclin 1-and ATG5-dependent autophagy in human neuroblastoma SH-SY5Y cells and in the rat hippocampus

Chronic exposure to morphine can induce drug addiction and neural injury, but the exact mechanism is not fully understood. Here we show that morphine induces autophagy in neuroblastoma SH-SY5Y cells and in the rat hippocampus. Pharmacological approach shows that this effect appears to be mediated by PTX-sensitive G protein-coupled receptors signaling cascade. Morphine increases Beclin 1 expression and reduces the interaction between Beclin 1 and Bcl-2, thus releasing Beclin 1 for its pro-autophagic activity. Bcl-2 overexpression inhibits morphine-induced autophagy, whereas knockdown of Beclin 1 or knockout of ATG5 prevents morphine-induced autophagy. In addition, chronic treatment with morphine induces cell death, which is increased by autophagy inhibition through Beclin 1 RNAi. Our data are the first to reveal that Beclin 1 and ATG5 play key roles in morphine-induced autophagy, which may contribute to morphine-induced neuronal injury.