Potassium currents in acutely isolated neurons from superficial and deep layers of the juvenile rat entorhinal cortex

Using the whole-cell configuration of the patch-clamp technique, outward K⁺ currents were recorded from acutely isolated stellate cells from superficial layers, and pyramidal cells from deep layers, of the entorhinal cortex of juvenile rats. In both cell types a fast transient and a slowly inactivating outward K⁺ current were obtained. Whereas the fast transient current (I _A) activated at potentials beyond −50 mV, the activation threshold of the slowly inactivating current (I _K) was measured at −40 mV in stellate and pyramidal cells. In stellate cells a half-maximal inactivation was estimated for I _A at −80.4 mV and for I _K at −74.6 mV, and in pyramidal cells at −81.1 mV and −71.8 mV, respectively. I _K of both cell types were reduced by tetraethylammonium (TEA) in a concentration-dependent manner. IC₅₀ values were 0.8 mM TEA for stellate cells and 1.1 mM TEA for pyramidal cells. Superfusion of 4-aminopyridine resulted in a reduction of the amplitudes of I _A and I _K as well as in an acceleration of the inactivation time constants of I _A. Extracellularly applied dendrotoxin did not have any effect on entorhinal cortex K⁺ currents. In summary, kinetic and pharmacological properties of I _A as well as of I _K are rather similar in superficial-layer stellate and deep-layer pyramidal cells acutely isolated from the entorhinal cortex of juvenile rats. Received: 20 September 1995/Received after revision: 19 March 1996/Accepted: 27 March 1996     

Network hyperexcitability within the deep layers of the pilocarpine-treated rat entorhinal cortex

In this study we report that in the presence of normal buffer, epileptiform discharges occur spontaneously (duration = 2.60 ± 0.49 s) or can be induced by electrical stimuli (duration = 2.50 ± 0.62 s) in the entorhinal cortex (EC) of brain slices obtained from pilocarpine-treated rats but not in those from age-matched, nonepileptic control (NEC) animals. These network-driven epileptiform events consist of field oscillatory sequences at frequencies greater than 200 Hz that most often initiate in the lateral EC and propagate to the medial EC with 4–63 ms delays. The NMDA receptor antagonist CPP depresses the rate of occurrence ( P < 0.01) of these spontaneous epileptiform discharges but fails in blocking them. Paradoxically, stimulus-induced epileptiform responses are enhanced in duration during CPP application. However, concomitant application of NMDA and non-NMDA glutamatergic antagonists abolishes spontaneous and stimulus-induced epileptiform events. Intracellular recordings from lateral EC layer V cells indicate a lower frequency of spontaneous hyperpolarizing postsynaptic potentials in pilocarpine-treated tissue than in NEC ( P < 0.002) both under control conditions and with glutamatergic receptor blockade; the reversal potential of pharmacologically isolated GABA_A receptor-mediated inhibitory postsynaptic potentials has similar values in the two types of tissue. Finally, immunohistochemical analysis shows that parvalbumin-positive interneurons are selectively reduced in number in EC deep layers. Collectively, these results indicate that reduced inhibition within the pilocarpine-treated EC layer V may promote network epileptic hyperexcitability.     

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat

Effects of cholinergic agents on synaptic transmission and plasticity were examined in entorhinal cortex and hippocampus. Bath application of carbachol (0.25-0.75 microM) induced transient depression of field potential responses in all cases tested (24/24 in layer III of medial entorhinal cortex slices and 24/24 in CA1 of hippocampal slices; 11.0+/-1.9% and 7.8+/-2.5%, respectively) and long-lasting potentiation in some cases (4/24 in entorhinal cortex and 12/24 in hippocampus; 33.7+/-3.7% and 32.1+/-9.9%, respectively, in successful cases). Carbachol (0.5 microM) induced transient depression, but not long-lasting potentiation, of N-methyl-D-aspartate receptor-mediated responses in entorhinal cortex. At 5 microM, carbachol induced transient depression only (55. 9+/-4.7% in entorhinal cortex and 41.4+/-2.9% in hippocampus), which was blocked by atropine. Paired-pulse facilitation was not altered during carbachol-induced potentiation but enhanced during carbachol-induced depression. These results suggest that the underlying mechanisms of carbachol-induced depression and potentiation are decreased transmitter release and selective enhancement of non-N-methyl-D-aspartate receptor-mediated responses, respectively. Long-term potentiation could be induced in the presence of 10 microM atropine by theta burst stimulation. The magnitude was significantly lower (15.2+/-5.2%, n=9) compared with control (37.2+/-6.1%, n=8) in entorhinal cortex, however.These results demonstrate similar, but not identical, cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus.     

Associative interactions within the superficial layers of the entorhinal cortex of the guinea pig

Associative fiber systems in the entorhinal cortex (EC) have been extensively studied in different mammals with tracing techniques. The largest contingent of intra-EC cortico-cortical fibers runs in the superficial layers and is distributed predominantly within longitudinal cortical bands. We studied the patterns of intrinsic EC connectivity in the in vitro isolated guinea pig brain preparation by performing current-source density analysis of field potential laminar profiles recorded with multi-channel silicon probes. The response pattern evoked by stimulation of the lateral olfactory tract was utilized to identify the lateral (l-EC) and medial (m-EC) entorhinal cortex. Stimulation of the deep layers did not evoke consistent responses. Local stimulation of the superficial layers in different portions of the EC induced an early, possibly direct response restricted to layer II-III in the close proximity to the stimulating electrode, followed by a late potential in the superficial layer I, that propagated at distance with a progressively increasing latency. The monosynaptic nature of the delayed response was verified by applying a pairing test. The results demonstrated that stimulation in the rostral-medial part of the EC generated activity restricted to the rostral pole of the l-EC, stimulation of the m-EC induced an associative activation that propagated rostrocaudally within the m-EC, stimulation of the caudal pole of the m-EC induced an additional response directed laterally, and stimulation of the lateral band of the EC determined a prominent longitudinal propagation of neuronal activity, but also induced associative potentials that propagated medially. The results are in partial agreement with the general picture derived from the anatomical studies performed in different species. Even though the largest associative interactions between superficial layers are restricted within either the m-EC or the l-EC, both rostral and caudal stimuli in the EC region close to the rhinal sulcus induced activity that propagated across the border between l- and m-EC.     

Interactions between callosal,thalamic and associational projections to the visual cortex of the developing rat

Summary The patterns of callosal interconnections between the visual cortices of rats display considerable plasticity in response to various neonatal manipulations. In the present study, many neurones in the principal visual thalamic relay nuclei, the dorsal lateral geniculate nucleus (DLG) and to a lesser extent those in the lateral posterior nucleus (LP) were destroyed by injections of the neurotoxin — kainic acid — on the first day of postnatal life. Four weeks later, as demonstrated with the anterograde and retrograde transport of the enzyme horseradish peroxidase (HRP) injected into the occipital lobe of one hemisphere, callosally projecting neurones and terminals were distributed more widely in the retinotopically organized areas 17, 18a and 18b of the visual cortex ipsilateral to the lesioned visual thalamus than in unoperated control animals of the same age. By contrast, in the visual cortex contralateral to the lesioned visual thalamus the areal distribution of callosally projecting neurones and terminals was similar to that of the controls, that is, largely but not exclusively restricted to the common border of areas 17 and 18a. Both in unoperated and operated animals, cells in lamina V of several cytoarchitectonically defined areas that are not retinotopically organized (area 8 in the frontal lobe, area 29d in the retrosplenial limbic cortex and perirhinal areas 35/13 in the temporal lobe) also project to contralateral visual cortices. In areas 8 and 29d, the total numbers, laminar distributions and densities of labelled callosal cells both ipsilateral and contralateral to the kainate-injected visual thalamus were similar to those in the controls. However, in the temporal lobe, the areal distribution of the labelled callosal neurones was more extensive than that in the controls and labelled cells in areas 35/13 of the cortex contralateral to the kainate-lesioned visual thalamus merged with those in the neighbouring areas 20 and 36. By contrast, the areal distribution of associational neurones in area 18a and in nonretinotopically organized areas projecting to area 17 were very similar in controls and in operated animals (neonatal kainate lesion of the visual thalamus, neonatal section of the corpus callosum or both procedures combined). However, in operated animals, the labelled associational neurones projecting from the supragranular laminae (II/III) of area 18a to area 17 constituted a higher proportion of all cells than did those in the unoperated control animals. Thus, overall the number of associational neurones projecting from area 18a to area 17 was slightly increased by the experimental manipulations performed. The implications of these results concerning the mechanism(s) underlying the developmental changes in the distribution of commissural and associational neurones projecting to the rat's visual cortex are discussed.     

Spike-timing-dependent plasticity of inhibitory synapses in the entorhinal cortex

Actions of inhibitory interneurons organize and modulate many neuronal processes, yet the mechanisms and consequences of plasticity of inhibitory synapses remain poorly understood. We report on spike-timing-dependent plasticity of inhibitory synapses in the entorhinal cortex. After pairing presynaptic stimulations at time t(pre) with evoked postsynaptic spikes at time t(post) under pharmacological blockade of excitation we found, via whole cell recordings, an asymmetrical timing rule for plasticity of the remaining inhibitory responses. Strength of response varied as a function of the time interval Deltat = t(post) - t(pre): for Deltat > 0 inhibitory responses potentiated, peaking at a delay of 10 ms. For Deltat < 0, the synaptic coupling depressed, again with a maximal effect near 10 ms of delay. We also show that changes in synaptic strength depend on changes in intracellular calcium concentrations and demonstrate that the calcium enters the postsynaptic cell through voltage-gated channels. Using network models, we demonstrate how this novel form of plasticity can sculpt network behavior efficiently and with remarkable flexibility.     

Long-term potentiation in visual cortical projections to the medial prefrontal cortex of the rat

In order to investigate neural mechanisms by which the prefrontal cortex adaptively modifies its activities based on past experience, we examined whether or not sensory cortical projections to the medial prefrontal cortex support long-term potentiation (LTP) in rats. Monosynaptic projections from the secondary visual cortex, mediomedial area (V2MM) to the infralimbic cortex were confirmed by orthodromic as well as antidromic activation of single units. High-frequency stimulation (50 Hz, 2 s) induced LTP (approximately 45% increase over the baseline) in the V2MM projection to the infralimbic cortex. LTP induction in this pathway was completely blocked by an injection (i.p.) of CPP, an N-methyl-D-aspartate receptor antagonist. LTP was also induced in the ventral hippocampal projection to the infralimbic cortex by the same high-frequency stimulation. The present results suggest that modification of synaptic weights of afferent sensory cortical projections is one mechanism underlying learning-induced changes in prefrontal cortical neural activities.     

Input-and layer-dependent synaptic plasticity in the rat perirhinal cortex in vitro.

The perirhinal cortex is crucially important in several forms of memory. Whilst it is important to understand the underlying mechanisms of this role in memory, little is known about the synaptic physiology or plasticity of this region of transitional cortex. In this study, we recorded evoked field potentials in superficial layers (approximately layer I) of the perirhinal cortex in vitro. One stimulating electrode was placed on the temporal side and the other on the entorhinal side of the rhinal sulcus in either the superficial or intermediate layers (approximately layers II/III). Paired stimuli resulted in depression of the second response. Paired-pulse depression was maximal at a 200-ms interpulse interval. Low-frequency stimulation resulted in synaptic depression, which returned to baseline within 60 min. The magnitude of both paired-pulse depression and low-frequency stimulation-induced depression was significantly greater at synapses activated from the temporal intermediate pathway than the other three pathways. Long-term potentiation, stable for at least 60 min, was induced by high-frequency stimulation of intermediate but not superficial pathways. Long-lasting depression (depotentiation) was induced by low-frequency stimulation following the induction of long-term potentiation. The induction of both long-term potentiation and depotentiation was N-methyl-D-aspartate receptor dependent. The group I/II metabotropic glutamate receptor antagonist (S)-alpha-methyl-4-carboxyphenylglycine was without effect on either of these forms of plasticity. Thus, both long- and short-lasting forms of synaptic plasticity exist at synapses in the perirhinal cortex, and these may mediate the changes in neuronal responses associated with visual recognition memory.     

Significance of the deep layers of entorhinal cortex for transfer of both perirhinal and amygdala inputs to the hippocampus

In the rat, a number of sensory modalities converge in the perirhinal cortex (PC). The neural pathway from the perirhinal cortex to the entorhinal cortex (EC) is considered one of the main routes into the entorhinal–hippocampal network. Evidence accumulated recently suggests that EC and PC, far from being passive relay stations, actively gate impulse traffic between neocortex and hippocampus. Using slice preparation maintaining the neurocircuit connecting PC, EC, hippocampal formation and amygdala, we investigated the associative function of PC and EC with respect to sensory and motivational stimuli and the influence of the association on the neurocircuit. In horizontal slices located ventrally to the rhinal sulcus, where we stimulated area 35 and the lateral amygdala, both inputs can be independently conveyed to the dentate gyrus. In slightly more dorsal slices where we stimulated area 36 and the lateral amygdala, the coincidence of the two inputs was needed to activate the hippocampus. This need for association of the two inputs was apparently mediated by the deep layer of EC. In all instances activation of the deep layers of EC was sufficient to activate the dentate gyrus, suggesting the relevance of the deep layers in cortico–hippocampal interactions.     

Differential contribution of kainate receptors to excitatory postsynaptic currents in superficial layer neurons of the rat medial entorhinal cortex

Although in situ hybridization studies have revealed the presence of kainate receptor (KAR) mRNA in neurons of the rat medial entorhinal cortex (mEC), the functional presence and roles of these receptors are only beginning to be examined. To address this deficiency, whole cell voltage clamp recordings of locally evoked excitatory postsynaptic currents (EPSCs) were made from mEC layer II and III neurons in combined entorhinal cortex-hippocampal brain slices. Three types of neurons were identified by their electroresponsive membrane properties, locations, and morphologies: stellate-like "Sag" neurons in layer II (S), pyramidal-like "No Sag" neurons in layer III (NS), and "Intermediate Sag" neurons with varied morphologies and locations (IS). Non-NMDA EPSCs in these neurons were composed of two components, and the slow decay component in NS neurons had larger amplitudes and contributed more to the combined EPSC than did those observed in S and IS neurons. This slow component was mediated by KARs and was characterized by its resistance to either 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride (GYKI 52466, 100 microM) or 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[lsqb]f[rsqb]quinoxaline-7-sulfonamide (NBQX, 1 microM), relatively slow decay kinetics, and sensitivity to 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10-50 microM). KAR-mediated EPSCs in pyramidal-like NS neurons contributed significantly more to the combined non-NMDA EPSC than did those from S and IS neurons. Layer III neurons of the mEC are selectively susceptible to degeneration in human temporal lobe epilepsy (TLE) and animal models of TLE such as kainate-induced status epilepticus. Characterizing differences in the complement of postsynaptic receptors expressed in injury prone versus injury resistant mEC neurons represents an important step toward understanding the vulnerability of layer III neurons seen in TLE.     

大鼠睁眼前初级视皮层2/3层锥体神经元突触自身稳态可塑性的变化特征

目的：通过对Wistar大鼠睁眼前初级视皮层2/3层锥体神经元突触AMPA（α-氨基-3-羧基-5-甲基异恶唑-4-丙酸）介导的微小兴奋性突触后电流 (mEPSCs)的测定分析,研究突触自身稳态可塑性在生后早期初级视皮层的作用特点。方法: 采用红外可视膜片钳技术全细胞模式记录生后4-11(d)（P4-11）Wistar大鼠初级视皮层脑片2/3层锥体神经元AMPA介导的mEPSCs,钳制电位-70 mV。人工脑脊液中加入河豚毒素（TTX）、荷包牡丹碱（BMI）及2-氨基-5-磷酸基戊酸（AP-5）分离出AMPA介导的mEPSCs,加入阻断剂6-氰基-7-硝基喹喔啉-2,3二酮 (CNQX）可消除mEPSCs。使用Clampfit 9.0进行数据分析。结果: P4至P11,大鼠初级视皮层2/3层锥体神经元AMPA介导的mEPSCs的波幅呈现上升趋势,频率自P7至P11逐渐增加,上升时间常数及下降时间常数均呈缩短趋势,以下降时间常数变化为著。P4至P7可见“单通道样”电流形态。结论: 在大鼠睁眼前初级视皮层2/3层锥体神经元亦存在突触自身稳态可塑性调节机制,其作用特点不同于睁眼后。     

A projection from the deep layers of the entorhinal area to the hippocampal formation in the rat brain

The methods of retrograde fluorescent tracing and anterograde transport of the lectin Phaseolus vulgaris leucoagglutinin (PHA-L) were used to demonstrate the existence of projections from layers IV and VI of the entorhinal area to the hippocampal formation in the rat brain. These two layers of the medial and lateral entorhinal area innervate the molecular layer of Ammon's horn and the area dentata. In the area dentata the projection from layer IV follows that of the perforant path, while that from layer VI innervates the outer two-thirds of the molecular layer, the subgranular zone and the deep part of the hilus of the area dentata.     

Adrenergic facilitation of GABAergic transmission in rat entorhinal cortex

Whereas the entorhinal cortex (EC) receives noradrenergic innervations from the locus coeruleus of the pons and expresses adrenergic receptors, the function of norepinephrine (NE) in the EC is still elusive. We examined the effects of NE on GABA(A) receptor-mediated synaptic transmission in the superficial layers of the EC. Application of NE dose-dependently increased the frequency and amplitude of spontaneous inhibitory postsynaptic currents (IPSCs) recorded from the principal neurons in layer II/III through activation of alpha(1) adrenergic receptors. NE increased the frequency and not the amplitude of miniature IPSCs (mIPSCs) recorded in the presence of TTX, suggesting that NE increases presynaptic GABA release with no effects on postsynaptic GABA(A) receptors. Application of Ca(2+) channel blockers (Cd(2+) and Ni(2+)), omission of Ca(2+) in the extracellular solution, or replacement of extracellular Na(+) with N-methyl-D-glucamine (NMDG) failed to alter NE-induced increase in mIPSC frequency, suggesting that Ca(2+) influx through voltage-gated Ca(2+) or other cationic channels is not required. Application of BAPTA-AM, thapsigargin, and ryanodine did not change NE-induced increase in mIPSC frequency, suggesting that Ca(2+) release from intracellular stores is not necessary for NE-induced increase in GABA release. Whereas alpha(1) receptors are coupled to G(q/11) resulting in activation of the phospholipase C (PLC) pathway, NE-mediated facilitation of GABAergic transmission was independent of PLC, protein kinase C, and tyrosine kinase activities. Our results suggest that NE-mediated facilitation of GABAergic function contributes to its antiepileptic effects in the EC.     

Lesion-induced plasticity of central neurons: sprouting of single fibres in the rat hippocampus after unilateral entorhinal cortex lesion

In response to a central nervous system trauma surviving neurons reorganize their connections and form new synapses that replace those lost by the lesion. A well established in vivo system for the analysis of this lesion-induced plasticity is the reorganization of the fascia dentata following unilateral entorhinal cortex lesions in rats. After general considerations of neuronal reorganization following a central nervous system trauma, this review focuses on the sprouting of single fibres in the rat hippocampus after entorhinal lesion and the molecular factors which may regulate this process. First, the connectivity of the fascia dentata in control animals is reviewed and previously unknown commissural fibers to the outer molecular layer and entorhinal fibres to the inner molecular layer are characterized. Second, sprouting of commissural and crossed entorhinal fibres after entorhinal cortex lesion is described. Single fibres sprout by forming additional collaterals, axonal extensions, boutons, and tangle-like axon formations. It is pointed out that the sprouting after entorhinal lesion mainly involves unlesioned fibre systems terminating within the layer of fibre degeneration and is therefore layer-specific. Third, molecular changes associated with axonal growth and synapse formation are considered. In this context, the role of adhesion molecules, glial cells, and neurotrophic factors for the sprouting process are discussed. Finally, an involvement of sprouting processes in the formation of neuritic plaques in Alzheimer's disease is reviewed and discussed with regard to the axonal tangle-like formations observed after entorhinal cortex lesion.     

Descending projections from the caudal medulla oblongata to the superficial or deep dorsal horn of the rat spinal cord

The location of neurons in the caudal medulla oblongata that project to the superficial or deep dorsal horn was studied in the rat, by means of retrograde labelling from confined spinal injection sites. The tracer cholera toxin subunit B was injected into laminae I–III (fuve rats) or I–V (three rats) at C_4–7 spinal segments. Neurons projecting to the superficial dorsal horn were located in the dorsomedial part of the dorsal reticular nucleus ipsilaterally, the subnucleus commissuralis of the nucleus tractus solitarius bilaterally, and a region occupying the lateralmost part of the ventrolateral reticular formation between the lateral reticular nucleus and the caudal pole of the spinal trigeminal nucleus, pars caudalis, bilaterally. Neurons projecting to the deep dorsal horn, which were only labelled when laminae I–V were filled by the tracer, occurred in the dorsomedial and ventrolateral parts of the dorsal reticular nucleus and in the ventral reticular nucleus bilaterally. A few cells were located in the above described lateralmost portion of the ventrolateral reticular formation bilaterally and in the ventral portion of the ipsilateral cuneate nucleus. In the light of previous data demonstrating that dorsal horn neurons project to the dorsal reticular nucleus, the ventrolateral reticular formation, and the nucleus tractus solitarius, and that neurons in these three medullary regions are involved in pain inhibition at the spinal level, the descending projections demonstrated here suggest the occurrence of spino-medullary-spinal loops mediating the analgesic actions elicited in each nucleus upon the arrival of nociceptive input from the dorsal horn.     

Cannabinoids modulate synaptic strength and plasticity at glutamatergic synapses of rat prefrontal cortex pyramidal neurons

Cannabinoids receptors have been reported to modulate synaptic transmission in many structures of the CNS, but yet little is known about their role in the prefrontal cortex where type I cannabinoid receptor (CB-1) are expressed. In this study, we tested first the acute effects of selective agonists and antagonist of CB-1 on glutamatergic excitatory postsynaptic currents (EPSCs) in slices of rat prefrontal cortex (PFC). EPSCs were evoked in patch-clamped layer V pyramidal cells by stimulation of layer V afferents. Monosynaptic EPSCs were strongly depressed by bath application (1 microM) of the cannabinoid receptors agonists WIN55212-2 (-50.4 +/- 8.8%) and CP55940 (-42.4 +/- 10.9%). The CB-1 antagonist SR141716A reversed these effects. Unexpectedly, SR141716A alone produced a significant increase of glutamatergic synaptic transmission (+46.9 +/- 11.2%), which could be partly reversed by WIN55212-2. In the presence of strontium in the bath, the frequency but not the amplitude of asynchronous synaptic events evoked in layer V pyramidal cells by stimulating layer V afferents, was markedly decreased (-54.2 +/- 8%), indicating a presynaptic site of action of cannabinoids at these synapses. Tetanic stimulation (100 pulses at 100 Hz, 4 trains) induced in control condition, no changes (n = 7/18), long-term depression (LTD; n = 6/18), or long-term potentiation (LTP; n = 5/18) of monosynaptic EPSCs evoked by stimulation of layer V afferents. When tetanus was applied in the presence of WIN 55,212-2 or SR141716-A (1 microM) in the bath, the proportion of "nonplastic" cells were not significantly changed (n = 7/15 in both cases). For the plastic ones (n = 8 in both cases), WIN 55,212-2 strongly favored LTD (n = 7/8) at the apparent expense of LTP (n = 1/8), whereas the opposite effect was observed with SR141716-A (7/8 LTP; 1/8 LTD). These results demonstrate that cannabinoids influence glutamatergic synaptic transmission and plasticity in the PFC of rodent.     

Dark rearing alters the short-term synaptic plasticity in visual cortex

The strength of all chemical synapses can be rapidly up- or down-regulated by their recent activities to reshape the postsynaptic signal through a mechanism of short-term facilitation or depression. It is also true that sensory experience is essential for maturation of cortical circuits and function. We studied the effect of sensory experience on the short-term plasticity in brain slices of rat visual cortex. Repetitive stimulation was applied in layer II/III and the response of pyramidal neuron in layer V was examined by whole-cell recording. We deprived the visual experience of rats by rearing the animals in dark environment. We found that dark rearing (DR) had no effects on paired-pulse interactions of either excitatory postsynaptic currents (EPSCs) or inhibitory postsynaptic currents (IPSCs). However, DR increased the level of IPSCs steady-state depression at stimulation frequency of 20Hz or more. This result, together with the finding that DR reduced the excitability of neural circuit in visual cortex, suggested a compensatory mechanism, which may be important in enhancing the network excitability at a time when synapses are immature.     

Compatibility of bidirectional synaptic plasticity on hippocampo-prefrontal cortex pathway in rats

The hippocampo-prefrontal cortex pathway reportedly expresses long-term potentiation (LTP) and depression (LTD) in anesthetized rats. We examined whether there were any effects governing the induction of LTD after prior induction of LTP, or vice versa. Induction in sequence of LTP and LTD resulted in significantly stable changes of about 140 and 70% of a common control for 1 h each. The reversed sequence, LTD and LTP, showed a mirror image of about 65 and 135% of control, which were not different from the respective changes in the first sequence (P>0.3 for each). The correlation coefficient between changes was significantly positive in the first sequence and weakly negative in the reverse. These results indicate that this pathway can express compatibility of bidirectional synaptic plasticity while historical changes remain covert.