Effects of melatonin on synaptic transmission and long-term potentiation in two areas of mouse hippocampus

We have examined the effects of melatonin on synaptic transmission and long-term potentiation (LTP) in the Schaffer Collateral-CA1 and the mossy fiber-CA3 pathways in mouse hippocampus brain slices. Melatonin (0.1-1 mM) application had different actions on both the field excitatory postsynaptic potentials (fEPSPS) and LTP in the CA1 as compared to the CA3. In CA1, 0.1 mM melatonin blocked LTP, while 1 mM melatonin also depressed the fEPSP. In CA3, neither 0.1 nor 1 mM melatonin altered the fEPSP, whereas both concentrations only slightly reduced LTP. These results demonstrate that melatonin significantly alters synaptic transmission and LTP in the CA1 but has only modest actions in CA3.     

Long-lasting increase in protein kinase C activity in the hippocampus of amygdala-kindled rat

Previous studies have demonstrated that membrane-associated protein kinase C (PKC) activities in the right and left hippocampus of rats kindled from the left hippocampus increased significantly at 4 weeks [9] and 4 months [22] after the last seizure compared with those in matched control rats. In this study, we investigated the effect of kindling from the left amygdala on PKC activities in the amygdala/pyriform cortex and hippocampus at long seizure-free intervals (4 and 16 weeks) from the last amygdala-kindled seizure. Membrane-associated PKC activity of the kindled group increased significantly only in the left hippocampus compared with the left side control (the left hippocampus of rats subjected to a sham operation) at 4 weeks (by 34%, P < 0.03) and 16 weeks (by 24%, P < 0.05) after the last seizure. There was no significant alteration in the membrane-associated PKC activity of the kindled group in the right hippocampus or amygdala/pyriform cortex in any seizure-free interval after the last amygdala seizure. Cytosolic PKC activity did not differ between the kindled and control groups in any brain region examined in any seizure-free interval. At 16 weeks after the last seizure, the PKC activity in the P₁ fraction of the kindled group increased significantly only in the left hippocampus (by 49%, P < 0.005), but not in the right hippocampus. Neither PKC activity in the P₂ fraction nor that in the cytosolic fraction was altered in the kindled group after this seizure-free interval. The prolonged increase in activity of the membrane-associated PKC and that in the P₁ fraction in the hippocampus induced by amygdala-kindling may contribute to long-lasting seizure susceptibility induced by kindling.     

Acute effects of lithium on synaptic transmission in rat hippocampus studied in vitro

Acute effects of lithium on synaptic transmissions in the CA1 neurones of rat hippocampus were examined. Perfusion of 2-10 mM lithium chloride (LiCl) produced a dose-dependent increase in the amplitude of field EPSPs, whereas change in the population spikes was variable. The increasing ratio of second field EPSP, which was examined by paired-pulse stimulation, was reduced about 10% by 5 mM LiCl. Intracellularly recorded EPSPs and IPSPs were facilitated by 10 mM LiCl, and the soma membrane was depolarized about 3.2 mV. Intracellular calcium concentration was measured in single hippocampal neurones using fura-2. Although calcium concentration at rest was approximately 30 nM and was increased to an average of 220 nM by 10(-5) M glutamate, 10 mM LiCl had no influence on it. The effects of Li on calcium-dependent processes were not manifested in this study. Variable changes of population spikes may be dependent on the balance between the excitatory and inhibitory postsynaptic potentials during lithium application.     

Ontogeny of synaptic transmission in the rat hippocampus

Electrophysiological characteristics of the hippocampal slices of juvenile (14-27 days) or young (36-40 days) Wistar rats have been compared. In the juvenile rats measurements were taken daily, from postnatal day (PN) 14 to PN27. Input-output curves were used to quantify the ontogeny of excitatory processes. The dynamic of population spike (PS) maturation was not even during the investigated postnatal period. After day 19 transient decrease of PS amplitude was observed until day 22. There were also some differences between the shape of input-output curves from the slices of rats of different ages. In general, PS was saturated at lower intensities in younger animals. The slices from 19-day-old rats did not display saturated input-output curve with 2-20 V stimuli intensities. But input-output curves on PN20-22 were rather similar to that obtained before PN19. The periods of gradual increase and subsequent decrease of PS amplitudes during early ontogeny correlate with the appearance of certain forms of behaviour. This fact suggests that hippocampal PS amplitude depression may be relevant functionally.     

Docosahexaenoic acid inhibits synaptic transmission and epileptiform activity in the rat hippocampus

Docosahexaenoic acid (DHA) has been suggested to be required for neuronal development and synaptic plasticity. However, in view of the fact that DHA facilitates NMDA responses and blocks K(+) channels, it might predispose the neurons to epileptiform bursting. By using extracellular recording of population spikes in the CA1 region of rat hippocampal slices, we tested this possibility by examining the effect of DHA on the epileptiform activity induced by bicuculline or in Mg(2+)-free medium. When stimuli were delivered to the Schaffer collateral/commissural pathway every 20 or 30 sec, DHA had no significant effect on the epileptiform activity. However, when the frequency of stimulation was increased to 0.2 Hz, DHA attenuated the amplitude of the bursting activity induced by bicuculline to 57.5+/- 10.8% and those induced by Mg(2+)-free ACSF to 65.8+/-13.9% of control. DHA reduced the slope of field excitatory postsynaptic potential (fEPSP) to 77.1+/-7.4% of baseline, without significant effect on the ratio of paired-pulse facilitation (PPF). By intracellular recording of neurons in the stratum pyramidale of rat hippocampal slices, we found that DHA markedly inhibited the repetitive firing of action potentials elicited by depolarizing current pulses but did not affect the initial action potential. Thus, DHA may attenuate epileptic activity mainly through the frequency-dependent blockade of Na(+) channels.     

Taurine uptake activity in the rat retina: protein kinase C-independent inhibition by chelerythrine

Taurine, a regulatory amino acid of various biochemical processes in the retina, requires an efficient uptake system to maintain the high physiological concentration of taurine in the retina. Taurine uptake was characterized in both whole retinal preparations and in isolated rod outer segments (ROS) in terms of uptake kinetics and possible protein kinase C (PKC)-dependent regulation. Two uptake systems, a high- and a low-affinity system, were found in whole retinal preparations while only the high-affinity system was found in the isolated ROS. All the uptake systems characterized were inhibited by guanidinoethane sulfonate (GES), a well-known competitive inhibitor of taurine uptake. Stimulation and inhibition of PKC activity with phorbol myristate acetate and with staurosporine, respectively, produced no significant effect on taurine uptake. On the other hand, chelerythrine (CHT), a documented potent PKC inhibitor, was found to cause significant inhibition of the two taurine uptake systems, presumably through a PKC-independent mechanism. The data demonstrate that CHT may be a useful tool in studying taurine uptake in the retina and specifically in the ROS.     

Cholesterol depletion inhibits synaptic transmission and synaptic plasticity in rat hippocampus

Several neurodegenerative disorders are associated with impaired cholesterol homeostasis in the nervous system where cholesterol is known to play a role in modulating synaptic activity and stabilizing membrane microdomains. In the present report, we investigated the effects of methyl-β-cyclodextrin-induced cholesterol depletion on synaptic transmission and on the expression of 1) paired-pulse facilitation (PPF); 2) paired-pulse inhibition (PPI) and 3) long-term potentiation (LTP) in the CA1 hippocampal region. Results demonstrated that cyclodextrin strongly reduced synaptic transmission and blocked the expression of LTP, but did not affect PPF and PPI. The role of glutamatergic and GABAergic receptors in these cholesterol depletion-mediated effects was evaluated pharmacologically. Data indicate that, in cholesterol depleted neurons, modulation of synaptic transmission and synaptic plasticity phenomena are sustained by AMPA-, kainate-and NMDA-receptors but not by GABA-receptors. The involvement of AMPA-and kainate-receptors was confirmed by fluorimetric analysis of intracellular calcium concentrations in hippocampal cell cultures. These data suggest that modulation of receptor activity by manipulation of membrane lipids is a possible therapeutic strategy in neurodegenerative disease.     

Inhibition of excitatory synaptic transmission by trans-resveratrol in rat hippocampus

The red wine polyphenol trans-resveratrol has been found to exert potent protective actions in a variety of cerebral ischemia models. The neuroprotection by trans-resveratrol thus far is mainly attributed to its intrinsic antioxidant properties. In the present study, the effects of the red wine polyphenol on excitatory synaptic transmission were investigated in the CA1 region of rat hippocampal slices. Perfusion with trans-resveratrol (10-100 microM) caused a concentration-dependent inhibition on the filed excitatory postsynaptic potentials (the field EPSPs) without detectable effect on the presynaptic volleys. The inhibition had a slow onset and was reversible. Trans-resveratrol (30 microM) did not change the ratios of paired-pulse facilitation of the field EPSPs tested at intervals of 20, 40 and 80 ms, nor did it alter the membrane properties of postsynaptic CA1 pyramidal neurons. However, trans-resveratrol (30 microM) significantly suppressed glutamate-induced currents in postsynaptic CA1 pyramidal neurons. In dissociated hippocampal neurons, the IC(50) value of trans-resveratrol in inhibition of glutamate-induced currents was 53.3+/-9.4 microM. Kainite and NMDA receptors were more sensitive to the red wine polyphenol than AMPA receptors. The present study for the first time demonstrates that trans-resveratrol inhibits the postsynaptic glutamate receptors, which probably works in concert with its antioxidant action for ameliorating the brain ischemic injury. The findings also support the future use of trans-resveratrol in the treatment of various neurodegenerative disorders.     

Depolarization-dependent actions of dihydropyridines on synaptic transmission in the in vitro rat hippocampus

Field potential and intracellular recordings were obtained in the in vitro hippocampal slice to study the effects on synaptic transmission of dihydropyridine (DHP) derivatives. Nimodipine or nifedipine by itself had little effect upon the postsynaptic response as determined by field potential analysis. However, facilitation became evident when DHP application was coupled with manipulations which induced a moderate degree of membrane depolarization. In accordance with the hydrophobic nature of these compounds, extensive washing in normal Krebs' solution failed to reverse the facilitation indicating that the DHP effects outlasted the induced depolarization. Nifedipine is photolabile and its actions were reversed when intense light was applied to the slice. Application of the DHP Bay K 8644, resulted in a similar depolarization-dependent increase in neuronal excitability which, upon washout and exposure to light, was at first attenuated and then reversed, resulting in a long-lasting depression of the EPSP that was sensitive to caffeine. This depressant action of Bay K 8644 appeared to be mediated at a site presynaptic to the pyramidal cell because the postsynaptic component of the field potential response to pulsed applications of glutamate was not altered. Intracellular recording from CA1 neurons supports a presynaptic locus for the depressant actions of Bay K 8644; spike threshold for synaptically evoked responses was greatly increased while spike threshold to direct depolarization of the soma was unchanged. These results indicate that DHPs can exert effects on synaptic transmission in hippocampal brain slice under conditions of moderate membrane depolarization.     

A presynaptic role for protein kinase C in hippocampal mossy fiber synaptic transmission.

It has been suggested that the maintenance of long-term potentiation (LTP) in the hippocampal mossy fiber (MF) synapse involves a presynaptic mechanism that does not require the activation of protein kinase C (PKC), since this enzyme appears to be absent in the MF presynaptic terminals. In the present study the authors evaluated this proposal by directly comparing the metabolic properties of hippocampal MF synaptosomes and a conventional P2B synaptosomal preparation prepared from the same hippocampal tissue. Protein kinase C-dependent histone phosphotranferase activity was found to be comparable in MF and P2B synaptosomes. Western blot analysis was performed using antisera prepared against four of the PKC isoforms, and the results demonstrate that the alpha, beta, and gamma PKC isoforms are present in relatively equivalent amounts in these two subcellular fractions. However, the cytosolic fraction derived from the hippocampal MF synaptosomes appeared to contain a greater amount of the PKC-epsilon isoform when compared to the P2B synaptosomal preparation. Four distinct endogenous substrates present in the MF synaptosomes are shown to be phosphorylated in response to PKC activation. A functional role for PKC in the hippocampal MF nerve endings seems to be indicated by the finding that 4 beta-phorbol 12,13-dibutyrate (PDBu) and 4 beta-phorbol 12,13-diacetate produce a dose-dependent potentiation of the K(+)-evoked release of endogenous glutamate and dynorphin B, while the inactive 4-alpha-phorbol was without effect. The PDBu-induced enhancement of transmitter release was blocked by the PKC inhibitor, staurosporine. In addition, PDBu significantly facilitated the rise in cytosolic free calcium that immediately followed depolarization of the MF synaptosomal membrane. It is concluded that hippocampal MF presynaptic terminals possess a variety of PKC isoforms and that their activation may have an important facilitory influence on MF synaptic transmission and plasticity.     

GABAB受体对大鼠海马CA1区锥体细胞突触传递的作用

目的研究激活GABA_B受体对大鼠海马CA1区锥体细胞突触传递的影响。方法对成年大鼠海马脑片CA1区锥体细胞采用“盲法”全细胞电压钳记录,分别检测和分析巴氯芬(10μmol/L)对自发性的兴奋性突触后电流(EPSCs)和抑制性突触后电流(IPSCs)的影响。结果巴氯芬可显著降低符氨酸能EPSCs和γ-氨基丁酸能IPSCs的频率(P＜0．01),各自达58%±7%(n=17)和42%±10%(n=15),而对它们的幅度无显著性影响。结论巴氯芬对海马CA1区锥体细胞EPSCs和IPSCs的抑制作用属于突触前抑制,推测GABA_B受体所介导的这种抑制作用对CA1区神经元兴奋性的传出具有抑制作用,从而对癫痫的产生有控制作用。     

Differential effect of carbamazepine and oxcarbazepine on excitatory synaptic transmission in rat hippocampus

In this study, we have compared the effects of two structurally related compounds carbamazepine (CBZ) and oxcarbazepine (OXC), both in current use for the treatment of epilepsy and bipolar disorder, on fast excitatory transmission in rat hippocampal slices. Using electrophysiological recordings, we have investigated the effects of CBZ and OXC on repetitive action potential discharge of CA1 pyramidal neurons demonstrating that both compounds produced firing inhibition with similar IC(50) values. Moreover, we show that bath applied CBZ (0.01-1 mM) exerted a concentration-dependent decrease in the amplitude of the field excitatory postsynaptic potentials with an IC(50) of approximately 194.3 microM. When OXC was used at the same concentrations, the concentration-response curve was shifted to the right (IC(50) of approximately 711.07 microM). In addition, we demonstrated that CBZ and OXC reduced, to a different extent, both evoked excitatory postsynaptic currents and NMDA-, AMPA-, and KA-mediated inward currents, CBZ being more potent than OXC. These data highlight distinct presynaptic and postsynaptic sites of action for both compounds and suggest that CBZ, by markedly depressing postsynaptic ionotropic glutamate receptors-mediated responses, may produce more severe cognitive and memory impairment. Thus, we assume that relatively high doses of OXC could be better tolerated than therapeutically equivalent doses of CBZ, justifying the preferential use of OXC as first-line treatment in the therapy of neurological and psychiatric disorders, particularly when compared with CBZ.     

Orphanin FQ inhibits synaptic transmission and long-term potentiation in rat hippocampus

It is known that opioid peptides acting on opioid receptors can modulate hippocampal synaptic functions. Although a novel member of the opioid receptor family, ORL₁ receptors, that displays high-sequence homology with classical opioid receptors is abundant in the hippocampus, little is known regarding its role in synaptic function. The present study was designed to investigate whether activation of the ORL₁ receptor by its natural ligand, orphanin FQ, could modulate synaptic transmission and synaptic plasticity in the hippocampus. The actions of orphanin FQ in the CA1 and dentate gyrus were examined by field potential recordings in response to stimulation of Schaffer collaterals and perforant path, respectively. Our results showed that orphanin FQ, but not the inactive analog des-Phe¹-orphanin FQ, reduced both the slope of the excitatory postsynaptic potentials and population spike amplitude. The inhibitory effect of orphanin FQ is dose dependent and probably involves a presynaptic mechanism, as suggested by the significantly increased paired-pulse facilitation evoked in the presence of orphanin FQ. In addition, orphanin FQ was found to inhibit the induction of long-term potentiation at the Schaffer collateral-CA1 synapse. These results demonstrate that orphanin FQ can function as an inhibitory modulator regulating synaptic transmission and synaptic plasticity in the hippocampus, suggesting that activation of ORL₁ receptors may play an important role in synaptic plasticity involved in learning and memory. Hippocampus 7:88–94, 1997. © 1997 Wiley-Liss, Inc.     

Sympathetic sprouting reverses decreases in membrane-associated activity of protein kinase C following septohippocampal denervation of the rat hippocampus

Hippocampal sympathetic ingrowth (HSI), a form of neuronal plasticity, is induced by medial septal lesions and consists of the sprouting of peripheral sympathetic fibers, arising from the superior cervical ganglion, into the dentate gyrus and CA₃ region of the hippocampus. HSI has been previously shown to alter learned and spontaneous behaviors, phosphatidyl inositide hydrolysis, and the antagonist binding kinetics of both muscarinic cholinergic receptors and phorbol ester receptors. We now report that sympathetic sprouting reverses decreases in membrane-associated activity of protein kinase C (PKC) following septohippocampal denervation of the rat hippocampus. Further, no changes were found in α, β or γ PKC isoenzymes among experimental groups, suggesting that the group A PKC isoforms do not mediate the observed changes in activity and phorbol ester binding.     

Protein kinase C inhibitors enhance the 5-HT2A receptor-mediated excitatory effects of serotonin on interneurons in rat piriform cortex

Previously it has been shown that excitatory effects of 5-hydroxytryptamine (5-HT) upon interneurons in the rat piriform cortex are mediated by 5-HT_2A receptors. This receptor is linked to phosphoinositide turnover, and one consequence of stimulating this receptor is the activation of protein kinase C (PKC). In the present study, the effect of PKC inhibitors on the 5-HT excitation of piriform cortical interneurons was examined by extracellular recording in a rat brain slice preparation. Bath application of the selective PKC inhibitors, bisindolylmalemide and chelerythrine, and the nonselective protein kinase inhibitor, H-7, all enhanced the excitatory effects of 5-HT. Two other nonselective protein kinase inhibitors, H-8 and HA 1004, which are 2.5-fold and 6.7- fold less potent than H-7 at inhibiting PKC, produced a slight or no enhancement, respectively, of the excitatory effect of 5-HT. Bisindolylmalemide, chelerythrine, and H-7 did not enhance the excitatory effects of norepinephrine or carbachol on the same interneurons. The PKC activator phorboll2,13-diacetate (PDA) decreased the excitatory effect of 5-HT this decrease was rapidly reversed by H-7. As inhibitors of PKC selectively enhanced rather than blocked the excitation by 5-HT mediated by 5-HT_2A receptors, we conclude that activation of PKC does not mediate the excitation by 5-HT of piriform cortical interneurons. Instead, we propose that PKC may have a negative feedback role in modulating the excitation by 5-HT of piriform cortical interneurons. © 1995 Wiley-Liss, Inc.     

Action of phencyclidine on synaptic transmission in the hippocampus

A neurophysiological investigation of the effects of phencyclidine (PCP) and ketamine on synaptic transmission was carried out at the level of two excitatory connections of the hippocampal formation: the interhippocampal projections from contralateral CA3 (cCA3) to CA1 and the entorhino-dentate pathway.In urethane-anesthetized rats PCP i.v. produced a moderate depression of the population EPSP elicited in the stratum radiatum of CA1 by cCA3 stimulations (16–40%) and a large decrease (up to 97%) of the amplitude of the corresponding population spike recorded at the level of the CA1 pyramidal cell bodies (ED₅₀:1.83 mg/kg).Single-unit analysis of CA1 pyramidal cell activation triggered by cCA3 stimulations indicated that i.v. PCP did not decrease the amplitude of individual action potentials suggesting that the decrease in the size of the population spike was due to a decrease in the number of CA1 pyramidal cells activated by the stimulus. Moreover, PCP administered i.v. in the same dose range (0.6-4.0 mg/kg) reduced the maintained activity of CA1 pyramidal cells and their excitation by iontophoretically applied glutamate or ACh.Similar effects on both field potentials and single-unit activity in the CA1 area were also observed following the administration of larger i.v. doses of ketamine (ED₅₀: 7.2 mg/kg), but the effects of the latter drug were of considerably shorter duration than those of PCP.     

Action of tachykinins in the rat hippocampus: modulation of inhibitory synaptic transmission

Substance P and other neuropeptides of the tachykinin family can powerfully excite CA1 hippocampal interneurons present in the CA1 region. In the present work we show that, by exciting hippocampal interneurons, tachykinins can indirectly inhibit pyramidal neurons. We found that tachykinins caused a decrease in the inhibitory synaptic current interval and an increase in the inhibitory synaptic current amplitude in almost all pyramidal neurons tested. This effect was tetrodotoxin sensitive. Tachykinins did not alter the frequency or amplitude of miniature inhibitory synaptic currents and were without effect on evoked inhibitory synaptic currents. Thus, these neuropeptides acted at the somatodendritic membrane of GABAergic interneurons, rather than at their axon terminals. The effect of substance P on spontaneous inhibitory synaptic currents could be mimicked by a selective agonist of NK1 receptors, but not by selective agonists of NK2 and NK3 receptors. It was suppressed by an NK1 receptor antagonist. In CA1 interneurons located in stratum radiatum, substance P generated a sustained tetrodotoxin-insensitive inward current or induced membrane depolarization and action potential firing. This direct excitatory action was mediated by NK1 receptors. Current-voltage relationships indicate that the net tachykinin-evoked current reversed in polarity at or near the K+ equilibrium potential, suggesting that a suppression of a resting K+ conductance was involved. By increasing the excitability of CA1 GABAergic interneurons, tachykinins can powerfully facilitate the inhibitory synaptic input to pyramidal neurons. This indirect inhibition could play a role in regulating short-term and/or long-term synaptic plasticity, promoting neuronal circuit synchronization or, in some physiopathological situations, influencing epileptogenesis.     

The endosomal protein NEEP21 regulates AMPA receptor-mediated synaptic transmission and plasticity in the hippocampus

The neuron-enriched endosomal protein 21 (NEEP21) has recently been implicated in the regulation of AMPA receptor (AMPAR) trafficking and proposed to participate in the control of synaptic strength. We tested here this possibility at CA3-CA1 synapses in hippocampal slice cultures using antisense-mediated down-regulation of NEEP21 expression or transfection of a fragment of the cytosolic domain of NEEP21. We found that NEEP21 suppression or expression of the dominant-negative fragment reduced spontaneous and evoked AMPAR-mediated synaptic currents without affecting presynaptic properties. The effect specifically resulted from a reduction of currents mediated by AMPA as opposed to NMDA receptors. Blockade of endocytosis, using a peptide interfering with dynamin, revealed a progressive increase of AMPAR responses due to receptor accumulation in control cells, but not following NEEP21 suppression or expression of the fragment. Also, the enhanced receptor cycling induced by bath application of NMDA resulted in a depression that was enhanced following interference with NEEP21 function. Finally, LTP induction, which involves expression of new synaptic receptors, was abolished in NEEP21-depleted cells or cells expressing the dominant-negative fragment. Together, we conclude that NEEP21 contributes to the regulation of synaptic transmission and plasticity in slice cultures by affecting the recycling and targeting of AMPA receptors to the synapse.     

Lack of central effects of peripherally administered adenosine A(1) agonists on synaptic transmission in the rat hippocampus

Peripheral administration of adenosine A(1) receptor selective agonists is generally thought to protect the hippocampus against ischemic damage via central actions. We examined the effects of two peripherally administered A(1) agonists, cyclohexyladenosine (CHA) and adenosine amine congener (ADAC), on synaptic transmission in the hippocampus and on indices of cardiovascular function. We conclude that the permeability of these agonists is not sufficient to result in concentrations necessary to activate central adenosine A(1) receptors within the hippocampus.     

Electron microscopic localization of gamma- and beta II-subspecies of protein kinase C in rat hippocampus

The subcellular distributions of the gamma- and beta II-subspecies of protein kinase C (gamma- and beta II-PKC) were studied in the rat hippocampus by light and electron microscopic immunocytochemistry. Both subspecies were abundant in the hippocampus with distinct subcellular distributions. The immunoreactivity of gamma-PKC was observed throughout the Ammon's horn, while intense beta II-PKC immunoreactivity was observed predominantly in the CA1 region. gamma-PKC was distributed diffusely through the cytoplasm of pyramidal cells from the perikarya to the dendritic spines. In contrast, beta II-PKC was concentrated around the Golgi complex and present diffusely in distal dendrites, except for the dendritic spines. Neither PKC subspecies could be detected in the presynaptic terminal. The postsynaptic localization of gamma- and beta II-PKC in CA1 suggests that both PKC subspecies may correlate to long-term potentiation in the CA1 region contributing to the postsynaptic side. gamma-PKC may have a specific function not only in CA1 but also in the mossy fiber-CA3 pathway at the postsynaptic side. beta II-PKC may have another function concerning the Golgi complex in CA1.