Identification and two-photon imaging of oligodendrocyte in CA1 region of hippocampal slices

Oligodendrocyte (OL) plays a critical role in myelination and axon maintenance in central nervous system. Recent studies show that OL can also express NMDA receptors in development and pathological situations in white matter. There is still lack of studies about OL properties and function in gray matter of brain. Here we reported that some glial cells in CA1 region of rat hippocampal slices (P15-23) had distinct electrophysiological characteristics from the other glia cells in this region, while they displayed uniform properties with OL from white matter in previous report; therefore, they were considered as OL in hippocampus. By loading dye in recording pipette and imaging with two-photon laser scanning microscopy, we acquired the high spatial resolution, three-dimension images of these special cells in live slices. The OL in hippocampus shows a complex process-bearing shape and the distribution of several processes is parallel to Schaffer fiber in CA1 region. When stimulating Schaffer fiber, OL displays a long duration depolarization mediated by inward rectifier potassium channel. This suggested that the OL in CA1 region could sense the neuronal activity and contribute to potassium clearance.     

The excitation wave returning to the hippocampus through the entorhinal cortex can reactivate the populations of "trained" CA1 neurons during deep sleep

It is suggested that the information about a new stimulus from the neocortex is transferred to the hippocampus and forms there a transient trace in the form of a distributed pattern of modified synapses. During sleep, the neuronal populations which store this trace are reactivated and return to the neocortex the information necessary for consolidation of the permanent memory trace. A possible mechanism of the reactivation of the "learned" hippocampal neurons during memory consolidation is the reverberation of excitation in the neuronal circuits connecting the hippocampus and the entorhinal cortex. In rats, we recorded responses in hippocampal field CA1 to stimulation of the Schaffer collaterals with potentiated synapses during wakefulness and sleep. We showed that in the periods of deep sleep, after the discharge of CA1 neurons, the wave of excitation passes through the entorhinal cortex and via the perforant path fibers enters the hippocampus and the dentate gyrus, causing in the latter the discharge of neurons. The repeated discharge of the CA1 neurons develops as the result of interaction of the early wave which is returned directly via the perforant path fibers and the late wave which is returned via the Schaffer collaterals, but not through the dentate gyrus and hippocampal field CA3 (trisynaptic pathway), but, probably, through the field CA2.     

Theta oscillations in the hippocampus

Theta oscillations represent the "on-line" state of the hippocampus. The extracellular currents underlying theta waves are generated mainly by the entorhinal input, CA3 (Schaffer) collaterals, and voltage-dependent Ca(2+) currents in pyramidal cell dendrites. The rhythm is believed to be critical for temporal coding/decoding of active neuronal ensembles and the modification of synaptic weights. Nevertheless, numerous critical issues regarding both the generation of theta oscillations and their functional significance remain challenges for future research.     

应激诱发的海马神经元突触增强参与大鼠的新环境学习

本文旨在研究应激对海马新环境空间学习记忆的损伤作用机制.在大鼠海马CA1区埋植电极,刺激schaffer侧枝记录CA1区树突层的兴奋性突触后场电位(field excitatory postsynaptic potential,fEPSP),探索应激对火鼠新环境空间学习的突触可塑性的影响.同时研究了再次新环境空间学习时...     

Increased expression of phospho-cofilin in CA1 and subiculum areas after theta-burst stimulation of Schaffer collateral-commissural fibers in rat hippocampal slices

Activity-dependent structural plasticity of dendritic spines of pyramidal neurons in the central neuron system has been proposed to be a cellular basis of learning and memory. Long-term potentiation (LTP) is accompanied by changes in synaptic morphology and structural remodeling of dendritic spines. However, there is considerable uncertainty as to the nature of the adjustment. The present study tested whether immunoreactive phospho-cofilin, an index of altered actin filament assembly, could be increased by theta-burst stimulations (TBS), which is an effective stimulation pattern for inducing LTP in the hippocampus. The slope of fEPSPs evoked by TBS to Schaffer collateral-commissural fibers in hippocampal slices was measured, and p-cofilin expression was examined using immunofluorescence techniques. Results indicated that saturated L-LTP was produced by multiple TBS episodes to Schaffer collateral-commissural fibers in the hippocampal CA1 area, and TBSs also increased immunoreactive p-cofilin expression in the stratum radiatum of the hippocampal CA1 area and pyramidal layer of the subiculum. D-2-amino-5-phosphonovalerate (D-APV) prevented LTP and expression of p-cofilin immunoreactive induced by multiple TBS episodes in the stratum radiatum of the hippocampal CA1 area. Two paired-pulse low-frequency stimulation (PP-LFS) episodes to Schaffer collateral-commissural fibers induced long-term depression (LTD), and did not affect p-cofilin expression in the stratum radiatum of the hippocampal CA1 area. These results suggest that LTP induction is associated with altered actin filament assembly. Moreover, the CA1 and subiculum areas of the hippocampal formation possibly cooperate with each other in important physiological functions, such as learning and memory, or in pathological diseases, such as epilepsy.     

Release of Glutamate and Aspartate from CA1 Synaptosomes: Selective Modulation of Aspartate Release by Ionotropic Glutamate Receptor Ligands

Abstract: Synaptosomes prepared from area CA1 of the rat hippocampus were used to determine (a) whether Schaffer collateral-commissural-ipsilateral associational terminals release both aspartate and glutamate in a Ca²⁺-dependent manner when reuptake of released glutamate is minimal and (b) whether autoreceptor mechanisms described in CA1 or hippocampal slices could reflect direct actions of glutamate receptor ligands on the synaptic terminal. When challenged for 1 min with either 25 m M K⁺ or 300 µ M 4-aminopyridine, CA1 synaptosomes released both glutamate and aspartate in a Ca²⁺-dependent manner. The glutamate/aspartate ratio was ∼5:1 in each case. K⁺-evoked glutamate release was unaffected by ligands active at NMDA or ( RS )-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors. Unlike glutamate release, the release of aspartate was enhanced by NMDA, and this effect was blocked by d -2-amino-5-phosphonovalerate ( d -AP5). Kainate selectively depressed and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) selectively increased the K⁺-evoked release of aspartate. AMPA enhanced aspartate release, like the antagonist CNQX. When applied in the presence of diazoxide, which blocks the desensitization of AMPA receptors, AMPA and kainate both depressed aspartate release. These findings support the view that Schaffer collateral-commissural-ipsilateral associational terminals release aspartate as well as glutamate and that these two release processes are regulated by different autoreceptor mechanisms.     

Post-ischemic activation of caspase-3 in the rat hippocampus: evidence of an axonal and dendritic localisation

The relationship between caspase-3 activation and delayed neuronal death after ischemia was examined. Expression of caspase-3 was evaluated by colorimetric assay, immunoblotting and by immunohistochemistry. Apoptosis was characterised by terminal desoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labelling. Immunohistochemistry showed caspase-3 activation in the whole hippocampus as early as 30 min after ischemia with exclusive localisation in fiber systems, especially in the perforant path and mossy fibers, Schaffer-collaterals, as well as apical and basal dendrites of pyramidal cells. One day post-ischemia, the 18 kDa cleavage product of caspase-3 (p18) was seen in all cell compartments (nucleus, cytosol and dendrites) throughout the entire subfields and the dentate gyrus with high distribution in mossy fibers. Two days post-ischemia, p18 kDa was only seen in the nuclei and cytosol of hippocampal cells without specific regional differences among hippocampal subfields. A significant number of apoptotic cells appeared only in the CA1 pyramidal cells at 2-3 days post-ischemia. Our data provides the first evidence that caspase-3 activation was detectable in the trisynaptic pathway fiber bundles which probably correspond to perforant path, alvear path and collaterals of Schaffer, and that activation of caspase-3 led to execution of apoptotic cell death program in selectively vulnerable areas, but not in the resistant area of the hippocampus.     

Changes in the expression of calbindin D-28k in the gerbil hippocampus following seizure

Previous studies have reported that calbindin D-28k (CB), a calcium-binding protein, containing neurons in the hippocampus play an important role in hippocampal excitability in epilepsy, because CB modulates the free calcium ion during seizure. Hence, in the present study, we investigated changes of CB expression in the hippocampus and its association in the Mongolian gerbil to identify roles of CB in epileptogenesis. CB immunoreactivity in the hippocampus was significantly lower in the pre-seizure group of seizure sensitive (SS) gerbils as compared with those seen in the seizure resistant (SR) gerbils. The distribution of CB immunoreactivity in the hippocampus showed significant difference after seizure on-set in SS gerbils. CB immunoreactivity in the hippocampal CA1, CA2 areas, and subiculum was lowest at 3h after seizure on-set; thereafter, the immunoreactivity became to increase to 12h after seizure on-set. Mossy fibers, Schaffer collaterals and dentate granule cells showed the highest CB immunoreactivity at 3h after seizure on-set; thereafter, the immunoreactivity became to decrease. In the case of the intrinsic and output connections of the hippocampus, a rapid decrease of CB serves an inhibitory function, which regulates the seizure activity and output signals from the hippocampus.     

Maternal infection and fever during late gestation are associated with altered synaptic transmission in the hippocampus of juvenile offspring rats

Prenatal exposure to infection is known to affect brain development and has been linked to increased risk for schizophrenia. The goal of this study was to investigate whether maternal infection and associated fever near term disrupts synaptic transmission in the hippocampus of the offspring. We used LPS to mimic bacterial infection and trigger the maternal inflammatory response in near-term rats. LPS was administered to rats on embryonic days 15 and 16 and hippocampal synaptic transmission was evaluated in the offspring on postnatal days 20-25. Only offspring from rats that showed a fever in response to LPS were tested. Schaffer collateral-evoked field excitatory postsynaptic potentials (fEPSPs) and fiber volleys in CA1 of hippocampal slices appeared smaller in offspring from the LPS group compared with controls, but, when the fEPSPs were normalized to the amplitude of fiber volleys, they were larger in the LPS group. In addition, intrinsic excitability of CA1 pyramidal neurons was heightened, as antidromic field responses in the LPS group were greater than those from control. Short-, but not long-term plasticity was impaired since paired-pulse facilitation of the fEPSP was attenuated in the LPS group, whereas no differences in long-term potentiation were noted. These results suggest that LPS-induced inflammation during pregnancy produces in the offspring a reduction in presynaptic input to CA1 with compensatory enhancements in postsynaptic glutamatergic response and pyramidal cell excitability. Neurodevelopmental disruption triggered by prenatal infection can have profound effects on hippocampal synaptic transmission, likely contributing to the memory and cognitive deficits observed in schizophrenia.     

NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD)

Long-term potentiation and long-term depression (LTP/LTD) can be elicited by activating N-methyl-d-aspartate (NMDA)-type glutamate receptors, typically by the coincident activity of pre- and postsynaptic neurons. The early phases of expression are mediated by a redistribution of AMPA-type glutamate receptors: More receptors are added to potentiate the synapse or receptors are removed to weaken synapses. With time, structural changes become apparent, which in general require the synthesis of new proteins. The investigation of the molecular and cellular mechanisms underlying these forms of synaptic plasticity has received much attention, because NMDA receptor–dependent LTP and LTD may constitute cellular substrates of learning and memory.Long-term synaptic plasticity is a generic term that applies to a long-lasting experience-dependent change in the efficacy of synaptic transmission. Here we will focus on N-methyl-d-aspartate (NMDA) receptor–dependent synaptic potentiation (LTP) and depression (LTD), two forms of activity-dependent long-term changes in synaptic efficacy that have been extensively studied. Because both LTP and LTD are believed to represent cellular correlates of learning and memory, they have attracted considerable interest. In this article we will focus on the molecular and cellular mechanisms associated with LTP and LTD. As for other forms of long-term synaptic plasticity, a characterization of LTP and LTD involves describing the molecular mechanisms that are required to elicit the change (induction), followed by an investigation of the mechanism of expression (hours) and maintenance (days). The best-characterized form of NMDA receptor (NMDAR)-dependent LTP occurs between CA3 and CA1 pyramidal neurons of the hippocampus (Fig. 1). Throughout the chapter we will mostly refer to this specific form of LTP. At these CA3-CA1 Schaffer collateral synapses, the loci of both induction and expression are situated in the postsynaptic neuron.Open in a separate windowFigure 1.NMDAR-dependent LTD and LTP in the hippocampus. (A) Historical drawing by Ramon y Cajal (1909) of the trisynaptic pathway in the hippocampus. LTP and LTD are induced by activation of NMDARs at synapses between CA3 and CA1 pyramidal neurons (blue and red). In contrast, LTP at mossy fiber synapses onto CA3 neurons (green on blue) is NMDAR-independent. (B) This electron microscopy image shows the densely packed neuropil in the CA1 region of the hippocampus and highlights two asymmetric CA3-CA1 synapses. Note the typical “bouton en passant” configuration of synapse 1 and the prominent spine in synapse 2. The postsynaptic densities (PSDs) are visible. Scale bar, 200 nm. (Image kindly provided by Rafael Luján, Universitad de Castilla-La Mancha.) (C) Bidirectional change in CA3-CA1 synaptic efficacy by LTD and LTP in the same synapses monitored by extracellular field recordings in an acute slice preparation of the hippocampus. Note the contrasting induction protocols (Data from C Lüscher, unpubl.).     

Coincident activity of converging pathways enables simultaneous long-term potentiation and long-term depression in hippocampal CA1 network in vivo

Memory is believed to depend on activity-dependent changes in the strength of synapses, e.g. long-term potentiation (LTP) and long-term depression (LTD), which can be determined by the sequence of coincident pre- and postsynaptic activity, respectively. It remains unclear, however, whether and how coincident activity of converging efferent pathways can enable LTP and LTD in the pathways simultaneously. Here, we report that, in pentobarbital-anesthetized rats, stimulation (600 pulses, 5 Hz) to Schaffer preceding to commissural pathway within a 40-ms timing window induced similar magnitudes of LTP in both pathways onto synapses of CA1 neurons, with varied LTP magnitudes after reversal of the stimulation sequence. In contrast, in urethane-anesthetized or freely-moving rats, the stimulation to Schaffer preceding to commissural pathway induced Schaffer LTP and commissural LTD simultaneously within a 40-ms timing window, without affecting synaptic efficacy in the reversed stimulation sequence. Coincident activity of Schaffer pathways confirmed the above findings under pentobarbital and urethane anesthesia. Thus, coincident activity of converging afferent pathways tends to switch the pathways to be LTP only or LTP/LTD depending on the activity states of the hippocampus. This network rule strengthens the view that activity-dependent synaptic plasticity may well contribute to memory process of the hippocampal network with flexibility or stability from one state to another.     

液压打击损伤后海马CA1区神经元兴奋性变化的研究

为考察脑损伤对海马CA1区锥体神经元电活动的影响并研究大黄素对神经元的超兴奋性和突触传递的作用,应用液压打击大鼠脑损伤模型和细胞外记录方法提取诱发的海马CA1区场兴奋性突触后电位(fPSP)和群峰电位(PS),进行相关的数据处理和分析。发现损伤侧比非损伤侧的fPSP斜率明显升高,PS波峰个教显著增加,而PS潜伏期明显减小;在灌流液中施加大黄素,CA1区诱发场电位明显减弱。研究结果表明：颅脑损伤可造成海马CA1区锥体神经元的迟发性过度兴奋;大黄素对神经元的兴奋性有抑制作用,可能对颅脑损伤后的中枢神经系统具有保护功能。     

Conditions required for appearance of a double response to a single-shock stimulation of Schaffer collaterals in hippocampal field CA1 in freely moving rats

Schaffer collateral stimulation with a single current impulse can evoke a double response in hippocampal field CA1 of freely moving rats. The late response appears as a population excitatory postsynaptic potential with a preceding short-term potential (frequently biphasic) only after the early population spike and is time-locked to it. The wave shape and polarity of the late response, its latency with respect to the peak of the early population spike suggest that the excitation wave produced in the CA1 field by the stimulation of Schaffer collaterals passes across the entorhinal cortex and returns to the CA1 directly via the perforant path fibers. In waking rat, the medium-intensity stimulation of Schaffer collaterals (able to evoke in the CA1 an early population spike of sufficiently high amplitude) usually does not result in the appearance of the late response. However, similar stimulation becomes efficient after the tetanization of Schaffer collaterals, under conditions of the long-term potentiation of the early population spike. Moreover, the late response occurrence is facilitated in a rat falling asleep after the development in the CA1 of high-amplitude low-frequency EEG oscillations typical for the slow-wave sleep and in a sleeping rat independently of the EEG pattern.     

Clonidine Suppresses the Induction of Long-Term Potentiation by Inhibiting HCN Channels at the Schaffer Collateral–CA1 Synapse in Anesthetized Adult Rats

Activation of alpha2-adrenoceptors inhibits long-term potentiation and long-term depression in many brain regions. However, effectiveness and mechanism of alpha2-adrenoceptors for synaptic plasticity at the Schaffer collateral–CA1 synapses in rat in vivo is unclear. In the present study, we investigated the effects of alpha2-adrenoceptors agonist clonidine on high-frequency stimulation (HFS)-induced long-term potentiation (LTP) and paired-pulse facilitation (PPF) at the Schaffer collateral–CA1 synapse of rat hippocampus in vivo. Clonidine (0.05, 0.1 mg/kg, ip) inhibited synaptic plasticity in a dose-dependent manner, accompanying with the decreasing of aortic pressure and heart rate (HR) in anesthetized rats. Clonidine (1.25, 2.5 μg/kg, icv, 10 min before HFS) also dose-dependently inhibited synaptic plasticity, which had no remarkable effect on HR and aortic pressure. But, 20 min after HFS, administration of clonidine (2.5 μg/kg) had no effect on LTP. The inhibitory effect of clonidine (2.5 μg/kg) on LTP was completely reversed by yohimbine (18 μg/kg, icv) and ZD7288 (5 μg/kg, icv). Moreover, the inhibition was accompanied by a significant increase of the normalized PPF ratio. Furthermore, clonidine at 1 and 10 μM significantly decreased glutamate (Glu) content in the culture supernatants of hippocampal neurons, and yohimbine at 1 and 10 μM had no effect on Glu release, while it could reverse the inhibition of clonidine (1 and 10 μM) on Glu release. In conclusion, clonidine can suppress the induction of LTP at the Schaffer collateral–CA1 synapse, and the possible mechanism is that activation of presynaptic alpha2-adrenoceptors reduces the Glu release by inhibiting HCN channels.     

Age-related Changes in the Insulin Receptor β in the Gerbil Hippocampus

The insulin receptor has been reported to be associated with memory formation via the hippocampus. In this study, we observed age-related changes in the insulin receptor β immunoreactivity and its protein levels in the hippocampus of gerbils of various ages in order to identify the correlation between the insulin receptor β and aging processes in the hippocampus. Insulin receptor β immunoreactivity was mainly detected in the molecular and polymorphic layers of the dentate gyrus, and in mossy fibers, Schaffer collaterals, alveus and stratum lacunosum-moleculare of the hippocampus proper (CA1-3) of gerbils at postnatal month 1 (PM 1). Insulin receptor β immunoreactivity decreased with age in all of these structures, except for the alveus. Reduction of the insulin receptor β immunoreactivity was prominent in the molecular layer of the dentate gyrus at PM 6 and in the stratum lacunosum-moleculare of the CA1 region at PM 12, while insulin receptor β immunoreactivity was decreased in other regions in the PM 18 groups. In addition, insulin receptor β protein level in the whole hippocampus was slightly increased at PM 3, and it decreased in an age-dependent manner from PM 6 to PM 24. These reductions of the insulin receptor β in the hippocampus may be associated with age-related memory deficits in gerbils.     

Origin of Ischemia-Induced Glutamate Efflux in the CA1 Field of the Gerbil Hippocampus: An In Vivo Brain Microdialysis Study

Abstract: In vivo brain microdialysis experiments were performed in the gerbil to evaluate the origin of accumulation of extracellular glutamate under transient ischemia. Microdialysis probes were positioned in the CA1 field of the hippocampus in which proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals had been induced by 5-min ischemia 10–14 days before the microdialysis experiment; in the white matter of the cerebral cortex, which contained few neurons, few presynaptic terminals, and many astrocytes; or in the histologically normal CA1 field of the hippocampus, and then 5- or 20-min ischemia was induced. When 5-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter of the cerebral cortex, whereas a significant increase in glutamate (15-fold) was observed in the histologically normal CA1 field. When 20-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter during the first 10 min after the onset of 20-min ischemia, but remarkable ischemia-induced increases in glutamate were observed during the last 10 min of 20-min ischemia in both areas. An excessive increase in glutamate (100-fold) was observed during 20-min ischemia in the normal CA1 field of the hippocampus. When a probe was positioned in the CA1 field of the hippocampus in which presynaptic terminals of Schaffer collaterals and commissural fibers had been eliminated by bilateral kainate injections into the lateral ventricles 4–7 days before the microdialysis experiment and then 5-min ischemia was induced, a significant increase in glutamate was observed during the last half of 5-min ischemia. These results suggest that the efflux of glutamate from astrocytes does not contribute to the large ischemia-induced glutamate accumulation in the CA1 field of the hippocampus during 5-min ischemia but contributes to the ischemia-induced increase in glutamate level during ischemia with a longer duration and that ischemia-induced efflux of glutamate in the CA1 field during 5-min ischemia originates mainly from neuronal elements: presynaptic terminals and postsynaptic neurons.     

A focal adhesion-like process underlies induction of long-term potentiation in the Schaffer collateral-CA1 region of the hippocampus

In the series of experiments reported here we provide evidence that a focal adhesion-like process underlies the induction of long-term potentiation (LTP) in the Schaffer Collateral-CA1 projection in the hippocampus. Here we show that an integrin binding peptide (RGD) impairs induction of Schaffer Collateral-CA1 LTP in hippocampal slice preparations in vitro. The heparin-binding peptide that binds heparan sulfate proteoglycan (HSPG) and blocks the formation of focal adhesions also impairs induction of LTP. Either the integrin-binding peptide or heparin-binding peptide reduces LTP partially. However, when the two peptides were administered simultaneously, there was no LTP 1 hour after induction. This indicates that these two molecules might function together and that a focal adhesion-like process might be involved in the induction of LTP. Additionally,we report that the RGD effect on LTP is time dependent and occurs only in the first few minutes following LTP induction, that the binding of the RGD peptide in CA1 stratum radiatum increases after LTP induction and that this increased binding depends on Ca(2+). Using electron microscopy we show that integrins are present in synapses.     

Quantitative estimate of the information relayed by the Schaffer collaterals

Within the theory that describes the hippocampus as a device for the on-line storage of complex memories, the crucial autoassociative operations are ascribed mainly to the recurrent CA3 network. The CA3-to-CA1 connections may still be important, both in completing information retrieval and in re-expanding, with minimal information loss, the highly compressed representation retrieved in CA3. To quantify these effects, I have defined a suitably realistic formal model of the relevant circuitry, and evaluated its performance in the sense of information theory. Analytical estimates, calculated with mean-field, replica and saddle-point techniques, of the amount of information present in the model CA1 output, reveal how such performance depends on different parameters characterising these connections. In particular, nearly all the stored information can be preserved if the model Schaffer collaterals are endowed with an optimal degree of Hebbian plasticity, matching that of the CA3 recurrent collaterals.     

Promotion of Neuronal Plasticity by (−)-Epigallocatechin-3-Gallate

The consumption of (−)-epigallocatechin-3-gallate (EGCG), the major polyphenolic compound found in green tea, has been associated with various neurological benefits including cognitive improvement. The physiological basis for this effect is unknown. In this study, we used synaptic transmission between the CA3 and CA1 regions (Schaffer collateral) of the mouse hippocampus to examine the effects of EGCG on neuronal plasticity. We found that the level of high frequency stimulation-evoked long-term potentiation (LTP) was significantly enhanced when hippocampal slices were pre-incubated with 10 μM EGCG for 1 h prior to the experiment. EGCG incubation also enabled hippocampal slices prepared from Ts65Dn mice, a Down syndrome mouse model deficient in LTP, to express LTP to a level comparable to the normal controls. EGCG treatment did not alter the degree of pair-pulse inhibition; therefore, the enhancement effect of EGCG is unlikely to involve the attenuation of this inhibitory mechanism.     

大鼠海马—小脑皮层—小脑深部核团投射的电生理学和HRP研究

本文用电生理学和HRP示踪法,研究了大鼠海马-小脑皮层投射的空间分布,小脑皮层的海马投射区与其深部核团间的纤维联系。 电生理学的实验结果表明,刺激背侧海马CA_1/CA_3区,均可使小脑皮层第Ⅵ小叶的浦肯野细胞产生顺行多突触的诱发简单锋电位和复杂锋电位反应。提示背侧海马CA_1/CA_3区与小脑皮层之间有经苔状纤维和攀缘纤维的多突触投射。实验证明,大鼠的这一投射的终止区域,集中在小脑皮层第Ⅵ小叶中线外侧0.8—1.4mm的范围内;并且来自CA_1区的投射以对侧性为主,CA_3区的投射以同侧性为主。HRP示踪的实验表明,背侧海马CA_1/CA_3区在小脑皮层第Ⅵ小叶的投射区是小脑纵区组构的间位区,该区皮层与间位核之间存在着交互投射关系。