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K Shibuki

Publications and source records attributed to K Shibuki.

At least 19 recordsLinked to original sources
PubMed2001

Long-lasting memory of sounds combined with reward in rats.

We investigated the effects of sound stimuli combined with reward on the subsequent sound discrimination. Water-deprived rats were exposed to one of two sounds (S+ or S-) in a trial, and licking a spout only during the presentation of S+ was rewarded with water. The percentage of trials in which licking occurred was calculated separately for S+ and S-, and sound discrimination was estimated from the difference in the percentage. S+ and S- were significantly discriminated during an 8 h period. In the second test after 1-2 weeks, sound discrimination for the same S+ and S- was significantly better than that for the S+ of the previous S- and S- of the previous S+. These findings indicate that the memory of the sounds combined with reward in the first test was maintained for 1-2 weeks.

Acoustic Stimulation↗
PubMed2001

Sequence dependence of post-tetanic potentiation after sequential heterosynaptic stimulation in the rat auditory cortex.

1. To investigate the mechanisms for the coding stimulus sequence in the auditory cortex (AC), post-tetanic potentiation (PTP) was recorded after sequentially combined heterosynaptic stimulation was applied in rat AC slices. 2. Brief tetanic stimulation (TS) was applied at two sites on AC slices at intervals of 0.5-10 s. PTP of field potentials was induced by the earlier TS, rather than the later TS. PTP was followed by sequence-dependent long-term potentiation (LTP). 3. Using Ca(2+) imaging in the slices loaded with rhod-2, a Ca(2+) indicator, a sequence-dependent distribution of PTP was found in AC slices. 4. The sequence-dependent PTP in excitatory postsynaptic potentials (EPSPs) was observed in supragranular pyramidal neurons. 5. The sequence dependence of PTP was not significantly affected by 1 microM bicuculline, an antagonist of GABA(A) receptors, or 100 microM 2-hydroxysaclofen, an antagonist of GABA(B) receptors. 6. Depolarization and firing recorded in pyramidal neurons during the later TS were less vigorous than when the slices were incubated in the control medium. However, this suppression of the responses during the later TS was not observed in the presence of 50 microM atropine, an antagonist of muscarinic receptors. 7. PTP was induced by the earlier and later TS in the presence of 50 microM atropine, so that the sequence dependence of PTP was abolished. Pirenzepine (50 microM), an antagonist of muscarinic M1 receptors, but not methoctramine (30 microM), an antagonist of M2 receptors, eliminated the sequence dependence of PTP. 8. These findings suggest that the sequence dependence of PTP in AC might have a role in the temporal processing of auditory information on the scale of seconds.

Animals↗
PubMed2001

Suppression of the induction of long-term depression by carbon monoxide in rat cerebellar slices.

Carbon monoxide (CO) suppresses brain functions at doses lower than that suppressing oxygen (O(2)) supply to the brain, and the cerebellum is one of the sites most susceptible to the neurotoxic effects of CO. We investigated the effects of CO on the induction of cerebellar long-term depression (LTD) in the synapses between parallel fibres (PFs) and Purkinje cells. CO, at concentrations between 8 nM and 5 microM, exhibited almost no effect on synaptic responses in Purkinje cells, O(2) consumption and NO release from PFs in rat cerebellar slices. However, the induction of LTD was significantly suppressed by CO at concentrations between 40 and 200 nM. The suppressive effect of 40 nM CO was antagonized by 10 microM NOR3, an NO donor. In contrast, CO exhibited no clear effect on the induction of LTD at concentrations between 1 and 5 microM. The induction of LTD, suppressed by 10 microM N(G)-nitro-L-arginine, an inhibitor of NO synthase, was not restored by 5 microM CO. CO is not only a neurotoxic substance but also a candidate for an intercellular messenger. delta-Aminolevulinate (30 microM), a substance facilitating endogenous CO production, suppressed the induction of LTD, and the effect of delta-aminolevulinate was antagonized by 10 microM NOR3. These findings suggest that CO may have a suppressive effect on the induction of cerebellar LTD at nanomolar concentrations, probably via its effects on NO/cGMP signalling.

Aminolevulinic Acid↗
PubMed1999

Nitric oxide release from substantia gelatinosa of the rat spinal cord in vitro.

To study characteristics of nitric oxide (NO) release from substantia gelatinosa (SG) in the spinal cord, we measured NO concentration in transverse spinal cord slices of rats using electrochemical NO probes. Electrical stimulation of the dorsomedial white matter adjacent to SG elicited transient current changes in NO probes placed on SG and the amplitude corresponded to a NO concentration of 200-300 pM. This NO release was not affected by the application of antagonists of glutamate or substance P receptors. The NO release in the rats, which were neonatally treated with capsaicin for denervating C-fibers, was significantly smaller than that in control rats. These data suggest that NO is mainly derived from the unmyelinated afferent nerves in the SG of the spinal cord.

Animals↗
PubMed1999

Cerebrospinal fluid nitric oxide metabolites in painful diseases.

To elucidate the involvement of NO in pain transmission in humans, we measured NO metabolites (nitrite/nitrate) in the CSF of patients with painful diseases using an NO analyzer based on the Griess method. The nitrite/nitrate levels in patients with degenerative lumbar disease (DLD), but not those with fracture or appendicitis, were significantly higher than those in an age-matched control group. The duration of pain in the DLD group was much longer than that in the fracture or appendicitis group. The nitrite/nitrate levels in the middle-aged and elderly DLD patients depended on the duration of pain. These data probably suggest that the duration of pain is critical for the elevation in nitrite/nitrate levels.

Adult↗
PubMed1999

Long-lasting enhancement of sound discrimination ability after sound exposure in rats.

Changes in the sound discrimination ability of rats were investigated after sound exposure (SE) in a Skinner box. For estimation of the sound discrimination ability, two different amplitude-modulated (AM) sounds (S+ and S-) were presented to the rats deprived of water for 48 h. Pedal press behavior in response to only S+ was rewarded with water. The percentages of trials in which pedal press behavior occurred in response to S+ or S- were calculated separately, and test performance of the rats was determined from the difference between the percentages. Rats were exposed to AM sounds during SE of 48 h, and the sound discrimination test was carried out. Enhancement of discrimination between S+ and S- was elicited by SE in a stimulus-specific manner. Latent extinction of the pedal press behavior in response to sound stimuli was not clearly found after SE. The enhancement of test performance was detected 1-48 h after the cessation of SE, and was blocked by injection of an antagonist of N-methyl-D-aspartate receptors into the auditory cortex bilaterally, immediately before the initiation of SE. These results suggest that SE elicits enhancement of sound discrimination ability, and the responsible site is in the auditory cortex.

Acoustic Stimulation↗
PubMed1999

Irreversible impairment of inhibitory neurons and nitric oxide release in the neocortex produced by low temperature and hypoxia in vitro.

Brain ischemia causes irreversible hyperexcitability, which may be attributed to irreversible impairment of inhibitory neurons. However, the conditions required for selective and irreversible impairment of inhibitory interneurons in vitro are unknown. In this study, we found that a combination of low temperature and hypoxia produced hyperexcitability in the neocortex. Neocortical tissue blocks isolated from rats were exposed to low temperature (1-3 degrees C) for 45 min and subsequently to room temperature (21-23 degrees C) for 60 min in the non-oxygenated medium. In experimental slices prepared from the processed blocks, hyperexcitability, similar to that elicited by an antagonist of GABA(A) receptors, was observed. Exposure of the neocortical tissue blocks to low temperature alone or room temperature alone did not elicit hyperexcitability. The excitability of pyramidal neurons, excitatory synaptic transmission and inhibitory effects of an agonist of GABA(A) receptors were normal in experimental slices. However, excitation of pyramidal neurons was inhibited after local stimulation of inhibitory neurons in control slices, but not in experimental slices. Nitric oxide (NO) release from cortical interneurons was also markedly reduced in experimental slices. These results indicate that irreversible impairment of neocortical inhibitory neurons was produced by low temperature combined with hypoxia produced in vitro.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1999

Long-term potentiation of Ca2+ signal in the rat auditory cortex.

The Ca2+ signal in supragranular layers of the rat auditory cortex (AC) was studied in slice preparations using rhod-2, a Ca2+ indicator. White matter stimulation elicited an increase in the Ca2+ signal, which was maximal in the image taken 34 ms after stimulation. This peak time was the same as that of the Ca2+ signal in pyramidal neurons injected with rhod-2. The intensity of the Ca2+ signal was proportional to the amplitude of the field potentials in supragranular layers. The Ca2+ signal was inhibited almost completely by 200 microM Ni2+ , but only slightly by 50 microM D-2-amino-5-phosphonovalerate (APV), an NMDA-receptor antagonist. Tetanic stimulation of the white matter or supragranular layers elicited long-term potentiation (LTP) of the Ca2+ signal in AC slices, but the potentiation was not clear in slices of the visual cortex (VC). The induction of LTP of the field potentials in AC slices was blocked by 50 microM APV or 50 microM Ni2+. These results indicate that Ca2+ influx through Ni2+ -sensitive Ca2+ channels in pyramidal neurons is potentiated by tetanic stimulation in parallel with LTP of neural activities and might be important for the induction of LTP in AC slices.

2-Amino-5-phosphonovalerate↗
PubMed1998

Layer-specific NO dependence of long-term potentiation and biased NO release in layer V in the rat auditory cortex.

1. We investigated the role of nitric oxide (NO) in the induction of long-term potentiation (LTP) in slices prepared from the rat auditory cortex. 2. Tetanic stimulation of layer IV elicited LTP of field potentials in layer II-III (LTPII-III) and in layer V (LTPV). The magnitude of LTPII-III measured at 30 min after tetanic stimulation was 171 +/- 9% (n = 15, mean +/- s.e.m.) of the control measured before tetanic stimulation, while that of LTPV was 138 +/- 3% (n = 17). 3. NO synthase (NOS) inhibitors had no apparent effect on LTPII-III, but LTPV was significantly suppressed (P < 0.001). This suppression of LTPV was significantly antagonized by a NO donor (P < 0.001) or a cGMP analogue (P < 0.001). 4. Small non-pyramidal neurones in the auditory cortex were stained with an anti-neuronal NOS antibody. More neurones were stained with the antibody in the deeper cortical layers. 5. We measured neocortical NO release with electrochemical NO probes. Layer IV stimulation elicited significantly more NO release in layer V than in layer II-III (P < 0.001). The amplitude of the increase in NO concentration elicited by stimulation at 20 Hz for 5 s was 380 +/- 14 pM (n = 55) in layer V and 55 +/- 8 pM (n = 5) in layer II-III. 6. NO release in layer V was partially but significantly suppressed by non-NMDA (P < 0.002) or NMDA (P < 0.002) receptor antagonists. Simultaneous application of the antagonists of the two types blocked NO release almost completely. 7. These results clearly indicate the NO dependence of the induction of LTPV, and the greater NO release in the deeper layer of the rat auditory cortex.

Animals↗
PubMed1998

cAMP-dependent long-term potentiation of nitric oxide release from cerebellar parallel fibers in rats.

Nitric Oxide (NO) is released from parallel fibers (PFs) after PF stimulation. NO-cGMP signaling is essential for long-term depression (LTD) in cerebellar PF-Purkinje cell synapses, which also exhibit presynaptic long-term potentiation (LTP) after tetanic PF stimulation. This LTP is dependent on cAMP but not NO-cGMP signaling. In this study, we analyzed long-term changes of NO release from PFs in rat cerebellar slices using electrochemical NO probes. Repetitive PF stimulation at 10 Hz for 2 sec elicited a transient increase in NO concentration (2.2 +/- 0.1 nM; mean +/- SEM; n = 116). This NO release exhibited long-term potentiation (LTPNO) by 36 +/- 3% (n = 15) after tetanic PF stimulation. Induction of LTPNO was not affected by Glu receptor antagonists. NO release from PFs was also potentiated by L-Arg (ARG) (100 microM), forskolin (50 microM), and 8-bromo-cAMP (Br-cAMP) (1 mM) but not by 1,9-dideoxyforskolin (50 microM), a biologically inactive analog of forskolin. The potentiation induced by forskolin was significantly suppressed by H89 (10 microM), a blocker of cAMP-dependent protein kinase. The potentiation induced by forskolin, but not that induced by Arg, interfered with LTPNO. H89 (10 microM) and KT5720 (1 microM), another blocker of cAMP-dependent protein kinase, but not KT5823 (300 nM), a blocker of cGMP-dependent protein kinase, significantly suppressed LTPNO. These data indicate that neural NO release is under activity-dependent control, just as synaptic transmitter release is. LTPNO might play a role in cross talk between presynaptic and postsynaptic plasticity by facilitating NO-cGMP-dependent postsynaptic LTD after induction of cAMP-dependent presynaptic LTP and LTPNO.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

Acute neural damage in the rat neocortex in vitro induced by a combination of anoxia and mechanical stress.

To elucidate the mechanisms of neural damage after brain ischemia, rat neocortical slices were exposed to anoxia at room temperature for 1 h, and other slices were prepared from the neocortical blocks exposed to anoxia at room temperature for 1 h. Field potentials elicited by the stimulation of layer IV were recorded in supragranular layers in these slices. No clear damage was observed electrophysiologically or morphologically in these slices. In contrast, a complete loss of the trans-synaptic field potentials and a decrease in the density of the cells stained with Neutral Red were elicited by injecting an anoxic medium into the neocortical blocks at room temperature for 1 h. In the slice preparations, the injection of the anoxic medium failed to reproduce clear neural damage, while a combination of mechanical stress and anoxia elicited a complete loss of trans-synaptic potentials; this was alleviated by Gd3+ (50 microM) and D(-)-2-amino-5-phosphonovaleric acid (100 microM). These results indicate that a combination of mechanical stress and anoxia produces acute and severe neural damage even at room temperature in vitro. The mechanism of the damage and the relationship between the neural damage in vitro and in vivo are discussed.

Animals↗
PubMed1997

Importance of polysynaptic inputs and horizontal connectivity in the generation of tetanus-induced long-term potentiation in the rat auditory cortex.

Supragranular pyramidal neurons in the adult rat auditory cortex (AC) show marked long-term potentiation (LTP) of population spikes after tetanic white matter stimulation (TS). For determination of whether this marked LTP is specific to AC, LTP in rat AC slices was compared with LTP in slices of the visual cortex (VC). The amplitude of TS-induced LTP in AC was twice that in VC. LTP of EPSPs was also studied with perforated patch or whole-cell recording. Although the amplitude of TS-induced LTP of EPSPs in AC was larger that in VC, no cortical difference was found in LTP elicited by low-frequency stimulation paired with current injection. Neocortical LTP is dependent on the activation of NMDA receptors, and induction of LTP requires postsynaptic depolarization for removal of Mg2+ blockade of NMDA receptors. The postsynaptic depolarization elicited by TS in supragranular pyramidal neurons in AC was significantly larger than that in VC. Cutting of supragranular horizontal connections resulted in a decrease in the depolarization amplitude in AC but an increase in the depolarization amplitude in VC. The cortical difference in TS-induced LTP was diminished in the slices in which horizontal connections in supragranular layers were cut. The estimated density of horizontal axon collaterals of supragranular pyramidal neurons in AC was approximately twice that in VC. These results strongly suggest that the marked polysynaptic and postsynaptic depolarization during TS and the resulting marked LTP in AC are attributed to well developed horizontal axon collaterals of supragranular pyramidal neurons in AC.

2-Amino-5-phosphonovalerate↗
PubMed1997

Dynamic properties of nitric oxide release from parallel fibres in rat cerebellar slices.

1. Nitric oxide (NO) release following repetitive electrical stimulation was studied in the molecular layer of rat cerebellar slices using electrochemical NO probes. 2. In parasagittal slices of the vermis, most Purkinje cells showed climbing fibre responses in response to white matter stimulation without accompanying NO release. 3. In frontal slices, parallel fibre volley potentials and NO release were elicited concurrently by parallel fibre stimulation. 4. The NO release following parallel fibre stimulation was not affected by blockers of non-NMDA, NMDA and metabotropic glutamate receptors. 5. The NO release was reduced significantly (P < 0.001) to 29% of the control level after climbing fibre deafferentation with 3-acetylpyridine treatment. 6. The rate of NO release was roughly proportional to the second or third power of the stimulus frequency, and to the third power of the extracellular Ca2+ concentration. 7. The rate of NO release was not affected by nicardipine (10 microM). It was reduced to 87 +/- 4% (n = 5, mean +/- S.E.M.) of the control level by omega-conotoxin GVIA (0.3 microM), and to 18 +/- 4% (n = 4) by omega-agatoxin IVA (0.3 microM). 8. Tetanic parallel fibre stimulation potentiated NO release by 24 +/- 5% (n = 5). 9. These data indicate that NO is derived mainly from parallel fibres. The relationship between NO release and cerebellar synaptic plasticity is discussed.

Animals↗
PubMed1997

Comparison of long-term potentiation between the auditory and visual cortices.

Long-term potentiation of supragranular field potentials was evoked following tetanic stimulation of the white matter in the auditory cortex of adult rats. LTP corresponded to potentiation in orthodromic firing of supragranular pyramidal neurons. The induction of LTP depended on the activation of NMDA receptors. LTP was larger in the auditory than the visual cortex.

Animals↗
PubMed1996

Long-term potentiation of supragranular pyramidal outputs in the rat auditory cortex.

In supragranular layers of the rat auditory cortex, white matter stimulation produces antidromic and transsynaptic field potentials, of which only the latter shows long-term potentiation (LTP) following tetanic stimulation of the white matter. In this study, we investigated the cells responsible for the LTP. The transsynaptic field potentials, excitatory postsynaptic potentials (EPSPs), and orthodromic spikes were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM), but not by D-2-amino-5-phosphonovalerate (D-AP5, 50 microM). The latency of EPSPs was constant, while that of transsynaptic field potentials and orthodromic spikes was shortened by the increase in stimulus intensity. Appearance of antidromic field potentials and antidromic spikes at strong stimulus intensities were accompanied by reduction in amplitude of transsynaptic field potentials and elimination of orthodromic spikes, respectively. Morphological identification of neurons showing antidromic spikes by intracellular injection of biocytin revealed that most of them were supragranular pyramidal cells. The effects of tetanic stimulation were studied by intracellular recording in seven neurons showing antidromic spikes, and it was found that only two of them showed LTP of EPSP slope. However, in all of the other eight units showing antidromic spikes and recorded extracellularly, LTP was clearly observed in orthodromic firing probability. The LTP induction in the orthodromic firing probability was blocked by D-AP5. These findings indicate that the LTP in field potentials corresponds to LTP in supragranular pyramidal outputs, and the input-output relationship in neural networks of the adult rat auditory cortex is strongly modulated by LTP.

Animals↗
PubMed1996

Deficient cerebellar long-term depression, impaired eyeblink conditioning, and normal motor coordination in GFAP mutant mice.

Mice devoid of glial fibrillary acidic protein (GFAP), an intermediate filament protein specifically expressed in astrocytes, develop normally and do not show any detectable abnormalities in the anatomy of the brain. In the cerebellum, excitatory synaptic transmission from parallel fibers (PFs) or climbing fibers (CFs) to Purkinje cells is unaltered, and these synapses display normal short-term synaptic plasticity to paired stimuli in GFAP mutant mice. In contrast, long-term depression (LTD) at PF-Purkinje cell synapses is clearly deficient. Furthermore, GFAP mutant mice exhibited a significant impairment of eyeblink conditioning without any detectable deficits in motor coordination tasks. These results suggest that GFAP is required for communications between Bergmann glia and Purkinje cells during LTD induction and maintenance. The data support the notion that cerebellar LTD is a cellular mechanism closely associated with eyeblink conditioning, but is not essential for motor coordination tasks tested.

Animals↗
PubMed1995

Impairment of motor coordination, Purkinje cell synapse formation, and cerebellar long-term depression in GluR delta 2 mutant mice.

Of the six glutamate receptor (GluR) channel subunit families identified by molecular cloning, five have been shown to constitute either the AMPA, kainate, or NMDA receptor channel, whereas the function of the delta subunit family remains unknown. The selective localization of the delta 2 subunit of the GluR delta subfamily in cerebellar Purkinje cells prompted us to examine its possible physiological roles by the gene targeting technique. Analyses of the GluR delta 2 mutant mice reveal that the delta 2 subunit plays important roles in motor coordination, formation of parallel fiber-Purkinje cell synapses and climbing fiber-Purkinje cell synapses, and long-term depression of parallel fiber-Purkinje cell synaptic transmission. These results suggest a close relationship between synaptic plasticity and synapse formation in the cerebellum.

Animals↗