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PubMed2001

Development of synaptic responses and plasticity at the SC-CA1 and MF-CA3 synapses in rat hippocampus.

1. The development of synaptic transmission and indicators of short- and long-term plasticity was studied by recording from areas CA1 and CA3 upon activation of monosynaptic excitatory inputs in rat hippocampal brain slices obtained from Wistar rats of different ages. 2. Although population field excitatory postsynaptic potentials (fEPSPS) are small in animals at postnatal day 10 (P10), both areas already exhibited short-term [posttetanic potentiation (PTP) and paired pulse potentiation (PPF)] and long-term [long-term potentiation (LTP)] plastic responses. 3. The amplitudes of the fEPSP and LTP increased with age in both regions, but peaked at P30 in CA3 while they were still increasing at the oldest age studied (P60) in CA1. In CA3, but not CA1, LTP at P60 was less than at P30. 4. PTP did not show clear alterations with age in either region. PPF decreased with age in CA1 but not CA3.

Animals↗

PubMed2005

Repetition of mGluR-dependent LTD causes slowly developing persistent reduction in synaptic strength accompanied by synapse elimination.

Synaptic plasticity, the cellular basis of memory, operates in a bidirectional manner. LTP (long-term potentiation) is followed by structural changes that may lead to the formation of new synapses. However, little is known whether LTD (long-term depression) is followed by morphological changes. Here we show that the repetitive induction of metabotropic glutamate receptor (mGluR)-dependent LTD in stable cultures of rat hippocampal slices led to a slowly developing persistent (ranging over weeks) reduction in synaptic strength that was accompanied by the loss of synaptic structures. LTD was induced pharmacologically 1-3 times at 24-h intervals by applying aseptically ACPD (1-aminocyclopentane-1,3-dicarboxylic acid), an agonist of group I/II mGluR, and APV (2-amino-5-phosphonovalerate), an antagonist of the NMDA (N-methyl-D-aspartate) receptor. One ACPD/APV application induced LTD that lasted less than 24 h. After three LTD inductions, however, a gradual attenuation of the fEPSP (field excitatory postsynaptic potential) amplitude and a decrease in the number of pre- and postsynaptic structures were observed. The blockade of LTD by an mGluR antagonist or a protein phosphatase 2B inhibitor abolished the development of the synaptic attenuation. In contrast to our previous finding that the repetitive LTP induction triggered a slowly developing persistent synaptic enhancement, the incremental and decremental forms of synaptic plasticity appeared to occur symmetrically not only on the minutes-hours time order but also on the days-weeks time order.

Animals↗

PubMed2002

Augmentation by zinc of NMDA receptor-mediated synaptic responses in CA1 of rat hippocampal slices: mediation by Src family tyrosine kinases.

Normal neuronal activity results in the release of zinc from the synaptic vesicles of glutamatergic terminals and subsequent entry into postsynaptic neurons. Although the exact physiological role of zinc translocation is currently unknown, it is very likely that intracellular zinc exerts long-term modulatory effects upon synaptic transmission since zinc affects various molecules involved in signaling pathways. In this study we used rat hippocampal slices to examine the effect of zinc on glutamatergic synaptic transmission in the Schaffer collateral-CA1 synapses. Following a 10-min exposure to 0.3-1 mM zinc, the magnitude of NMDA receptor-mediated field excitatory postsynaptic potentials (fEPSP) gradually increased over the subsequent 30-40 min. In contrast, the magnitude of AMPA/kainate receptor-mediated fEPSPs remained unchanged. The selective potentiation of NMDA receptor-mediated fEPSPs by zinc was unlikely to be a presynaptic event, since the degree of paired-pulse facilitation was unaltered. Interestingly, the specific Src family tyrosine kinase inhibitor PP2 completely blocked zinc-induced potentiation of NMDA receptor-mediated fEPSP while the inactive analog PP3 had no effect, thereby suggesting the involvement of Src family tyrosine kinases. Furthermore, zinc exposure increased levels of total and tyrosine-phosphorylated forms of NR2A and NR2B in a PP2-dependent manner in both hippocampal slices and cell cultures. In addition, zinc treatment of hippocampal cultures increased the levels of tyrosine phosphorylation at the two positive regulatory sites of Src family tyrosine kinases. Our results demonstrate that zinc increases NMDA receptor function via Src family tyrosine kinase-mediated increases of NR2A and 2B tyrosine phosphorylation. We speculate that intense release of endogenous synaptic zinc may potentiate NMDA receptor-mediated transmission in zinc-containing glutamatergic pathways by a similar mechanism.

2-Amino-5-phosphonovalerate↗

PubMedDate not supplied

Role of GABA(B) receptor in the regulation of excitatory synaptic transmission in trigeminal motoneurons.

The aim of the present study was to determine if excitatory synaptic transmission onto trigeminal motoneurons is subject to a presynaptic modulation by gamma-aminobutyric acid (GABA) via GABA(B) receptor in this system. Whole cell recordings were made from trigeminal motoneurons in longitudinal brain stem slices taken from 8-day-old rats. Monosynaptic excitatory postsynaptic potential (EPSP) activity was evoked by placing bipolar stainless steel electrodes dorsal-caudal to the trigeminal motor nucleus. Bath application of the GABA(B) receptor agonist, baclofen, produced a marked reduction in the mean amplitude and variance of evoked EPSPs and also increased the portion of transmission failures. It also produced a decrease in the frequency, but not in the mean amplitude, of spontaneous miniature EPSPs. Bath application of GABA(B) receptor antagonists 6-hydroxy-saclofen and CGP35348 increased both the amplitude and frequency of miniature EPSP activity. Taken together the above results suggest that the excitatory synaptic inputs onto trigeminal motoneurons are controlled by tonic presynaptic modulation by GABA(B) receptor.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1992

An intracellular study of perineal and hindlimb afferent inputs onto sphincter motoneurons in the decerebrate cat.

The external urethral sphincter (EUS) and external anal sphincter (EAS) are striated muscles that function to maintain urinary and fecal continence respectively. This study examines the short-latency synaptic input from a variety of cutaneous perineal and muscle/cutaneous hindlimb afferents to the motoneurons innervating these muscles. Intracellular recordings from antidromically identified EUS and EAS motoneurons provided records of the postsynaptic potentials (PSPs) produced by electrical stimulation of peripheral afferents in decerebrate or chloralose anesthetized cats. Excitatory postsynaptic potentials (EPSPs) were produced in most EUS and EAS motoneurons by stimulation of ipsilateral and contralateral sensory pudendal (SPud) and superficial perineal (SPeri) cutaneous nerves. The shortest central latencies in the study (1.5 ms) suggest that there are disynaptic excitatory, in addition to tri- and oligosynaptic, connections within these reflex pathways. EPSPs mixed with longer latency inhibitory potentials (E/I PSPs) were observed in both motoneuron populations, but were found more frequently in EAS motoneurons. These E/I PSPs were evoked more often from contralateral afferents than from ipsilateral afferents. Cutaneous nerves innervating the hindlimb had weaker if any synaptic effects on sphincter motoneurons. Stimulation of ipsilateral hindlimb muscle nerves rarely produced PSPs in EUS motoneurons and had weak synaptic actions on EAS motoneurons. In 2 of 22 animals (both decerebrate), large inhibitory potentials predominated over early small EPSPs suggesting that inhibitory pathways from these afferents to sphincter motoneurons can be released under certain circumstances. The relation between the segmental afferents to EUS and EAS motoneurons and the neural circuitry influencing them during micturition and defecation are discussed.

Afferent Pathways↗

PubMed1999

The effects of chronic lead exposure on long-term depression in area CA1 and dentate gyrus of rat hippocampus in vitro.

Long-term potentiation (LTP) and long-term depression (LTD), two forms of synaptic plasticity, are believed to underlie the mechanisms of learning and memory. Previous studies have demonstrated that low-level lead exposure can impair the induction and maintenance of LTP in vivo and in vitro. The present study was carried out to investigate whether the low-level lead exposure affected the induction and maintenance of LTD. Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams drinking 0.2% lead acetate solution. Field excitatory postsynaptic potentials (EPSPs) were recorded in hippocampal slices in adult rats (50-65 days) to study the alterations of LTD in area CA1 and dentate gyrus (DG) of hippocampus following chronic lead exposure. The input-output (I/O) curves before conditioning in both areas showed no evident alterations in basic synaptic transmission between the control and lead exposure groups. In area CA1, the mean amplitude of EPSP slope in control rats (61+/-11%, n=15) decreased significantly greater than that in lead-exposed rats (78+/-8%, n=8, P<0.05) following low frequency stimulation (LFS, 1 Hz, 15 min), which lasted at least 45 min. In area DG, with application of the same LFS, the LTD was induced in control rats (72+/-22%, n=8), while the LFS failed to induce LTD in lead-exposed rats (100+/-26%, n=8). These results showed that chronic lead exposure affected the induction of LTD in both area CA1 and DG. The effect of lead on synaptic plasticity in area CA1 was also investigated. The alteration of the amplitude of LTP in hippocampal slices caused by lead was reexamined in order to compare with that on LTD (control: 189+/-23, n=5; lead-exposed: 122+/-12, n=10). The result demonstrated that low-level lead exposure could reduce the range of synaptic plasticity, which might underlie the dysfunction of learning and memory caused by chronic lead exposure.

Animals↗

PubMed2000

Altered synaptic transmission in the hippocampus of the castrated male mouse is reversed by testosterone replacement.

PURPOSE: To determine the effect of castration on hippocampal function, we have investigated synaptic transmission in the castrated male mouse in vivo. We also examined whether administering testosterone can reverse the changes. MATERIALS AND METHODS: Male 12 weeks-old C57BL/6J mice were divided into three experimental groups; sham-castration (Control), the castration group (Cast), and the castration plus testosterone propionate group (Cast+TP). Field excitatory postsynaptic potentials (fEPSP) were evoked in the CA1 area of the hippocampus by stimulating the commissural fibers of the contralateral hippocampus. Field EPSPs were evoked in the granular cells of the dentate gyrus (DG) by stimulating the ipsilateral perforant path fibers. RESULTS: Laminar analysis of the fEPSPs in the hippocampal CA1 pyramidal cell layer did not differ significantly between the three experimental groups. However, paired pulse facilitation (PPF) of the fEPSP with short inter-stimulus intervals (30 to 100 msec) was significantly suppressed in Cast group. This suppression was reversed by testosterone injection (Cast+TP). Longterm potentiation (LTP) in the CA1 pyramidal neurons by high frequency stimulation (HFS) did not differ significantly between the three experimental groups, whereas potentiation evoked by primed burst stimulation (PBS) was much weaker in the Cast group compared with the Control group. Testosterone injection restored the PBS-induced potentiation to the control level. Synaptic transmission between perforant pathway and the granule cells in the dentate gyrus (DG) did not differ significantly among the three experimental groups. CONCLUSIONS: Suppression of PPF and impairment of the potentiation by PBS in CA1 hippocampal neurons was observed in castrated male mice and these changes were reversed by testosterone injection. These findings suggest that altered synaptic transmission in the castrated male mouse is caused by disturbance of inhibitory neuronal networks that are influenced by testosterone.

Animals↗

PubMed1999

Prior short-term synaptic disinhibition facilitates long-term potentiation and suppresses long-term depression at CA1 hippocampal synapses.

Long-term potentiation (LTP) and long-term depression (LTD) are two main forms of activity-dependent synaptic plasticity that have been extensively studied as the putative mechanisms underlying learning and memory. Current studies have demonstrated that prior synaptic activity can influence the subsequent induction of LTP and LTD at Schaffer collateral-CA1 synapses. Here, we show that prior short-term synaptic disinhibition induced by type A gamma-aminobutyric acid (GABA) receptor antagonist picrotoxin exhibited a facilitation of LTP induction and an inhibition of LTD induction. This effect lasted between 10 and 30 min after washout of picrotoxin and was specifically inhibited by the L-type voltage-operated Ca2+ channel (VOCC) blocker nimodipine, but not by the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphopentanoic acid (D-APV). Moreover, this picrotoxin-induced priming effect was mimicked by forskolin, an activator of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA), and was blocked by the adenylyl cyclase inhibitor 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22536) and the PKA inhibitor Rp-adenosine 3',5'-cyclic monophosphothioate (Rp-cAMPS). It was also found that following picrotoxin application, CA1 neurons have a higher probability of synchronous discharge in response to a population of excitatory postsynaptic potential (EPSP) of fixed slope (EPSP/spike potentiation). However, picrotoxin treatment did not significantly affect paired-pulse facilitation (PPF). These findings suggest that a brief of GABAergic disinhibition can act as a priming stimulus for the subsequent induction of LTP and LTD at Schaffer collateral-CA1 synapses. The increase in Ca2+ influx through L-type VOCCs in turn triggering a cAMP/PKA signalling pathway is a possible molecular mechanism underlying this priming effect.

Adenine↗

PubMed2004

Overexpression of calbindin D(28k) in dentate gyrus granule cells alters mossy fiber presynaptic function and impairs hippocampal-dependent memory.

Calcium is a key signaling ion for induction of synaptic plasticity processes that are believed to influence cognition. Mechanisms regulating activity-induced increases in neuronal calcium and related synaptic modifications are not fully understood. Moreover, involvement of specific synapses in discrete aspects of spatial learning remains to be elucidated. We used herpes simplex amplicons to overexpress calbindin D(28k) (CaBP) selectively in dentate gyrus (DG) granule cells. We then examined the effects on hippocampal network activity by recording evoked synaptic responses in vivo and in vitro and analyzing hippocampal-dependent behavior. Relative to Lac-Z- and sham-infected controls, CaBP overexpression increased mossy fiber (MF-CA3) excitatory postsynaptic potentials and reduced paired-pulse facilitation (PPF), suggesting an increase in presynaptic strength. Additionally, CaBP overexpression reduced long-term potentiation (LTP), caused a frequency-dependent inhibition of post-tetanic potentiation (PTP), and impaired spatial navigation. Thus, increasing CaBP levels selectively in the DG disrupts MF-CA3 presynaptic function and impairs spatial cognition. The results demonstrate the power of gene delivery in the study of the neural substrates of learning and memory and suggest that mossy fiber synaptic plasticity is critical for long-term spatial memory.

Animals↗

PubMed1999

Priming-induced shift in synaptic plasticity in the rat hippocampus.

The activity history of a given neuron has been suggested to influence its future responses to synaptic input in one prominent model of experience-dependent synaptic plasticity proposed by Bienenstock, Cooper, and Munro (BCM theory). Because plasticity of synaptic plasticity (i.e., metaplasticity) is similar in concept to aspects of the BCM proposal, we have tested the possibility that a form of metaplasticity induced by a priming stimulation protocol might exhibit BCM-like characteristics. CA1 field excitatory postsynaptic potentials (EPSPs) obtained from rat hippocampal slices were used to monitor synaptic responses before and after conditioning stimuli (3-100 Hz) of the Schaffer collateral inputs. A substantial rightward shift (>5-fold) in the frequency threshold between long-term depression (LTD) and long-term potentiation (LTP) was observed <1 h after priming. This change in the LTD/P crossover point occurred at both primed and unprimed synaptic pathways. These results provide new support for the existence of a rapid, heterosynaptic, experience-dependent mechanism that is capable of modifying the synaptic plasticity phenomena that are commonly proposed to be important for developmental and learning/memory processes in the brain.

2-Amino-5-phosphonovalerate↗

PubMed1997

Nociceptin-like immunoreactivity in the rat dorsal horn and inhibition of substantia gelatinosa neurons.

Nociceptin, also referred to as orphanin FQ, is believed to be the endogenous ligand for the ORL1. Nociceptin, when injected intracerebroventricularly to mice, produced hyperalgesia in behavioral tests. Recent studies have demonstrated the presence of ORL1 transcript in the spinal cord, and ORL1-like immunoreactivity has been localized to nerve fibers and somata throughout the spinal cord. Here, we report the localization of nociceptin-like immunoreactivity to fiber-like elements of the superficial layers of the rat dorsal horn by immunohistochemical techniques. Whole-cell recordings from substantia gelatinosa neurons in transverse lumbar spinal cord slices of 22-26-day-old rats showed that exogenous nociceptin at low concentrations (100-300 nM) depressed excitatory postsynaptic potentials evoked by stimulation of dorsal rootlets without causing an appreciable change of resting membrane potentials and glutamate-evoked depolarizations. At a concentration of 1 microM, nociceptin hyperpolarized substantia gelatinosa neurons and suppressed spike discharges. The hyperpolarizing and synaptic depressant action of nociceptin was not reversed by the known opioid receptor antagonist naloxone (1 microM). Our result provides evidence that nociceptin-like peptide is concentrated in nerve fibers of the rat dorsal horn and that it may serve as an inhibitory transmitter within the substantia gelatinosa.

Animals↗

PubMed1983

The action of aminopyridine on the electromotor synapse of Torpedo marmorata.

An investigation of the action of 4-aminopyridine (4-AP) on Torpedo electromotor synapses was performed using the microelectrode technique. 4-AP in concentrations of 1--10 micrometers increased the peak amplitude (p) and half-decay time (t 1/2) of the intracellularly recorded excitatory postsynaptic potentials (EEP), independent of alterations in miniature EPPs or membrane potential. 4-AP also increased the amplitude and time constant of decay (tau) of the excitatory postsynaptic current (EPC). Analysis of the results supports potentiated transmitter release and accumulation of the transmitter in the synaptic cleft as the mechanism by which 4-AP produces its effect.

Aminopyridines↗

PubMed2006

AM251, a selective antagonist of the CB1 receptor, inhibits the induction of long-term potentiation and induces retrograde amnesia in rats.

Long-term potentiation (LTP) has a long history as putative mechanism of memory formation, specially in the hippocampus, a structure essential for memory formation. Endocannabinoids are one of the endogenous systems that modulate this plasticity event: the activation of hippocampal CB1 receptors may inhibit local GABA release. Here, we have studied both (1) the role of the selective CB1 antagonist AM251 upon LTP induction in a hippocampal slice preparation, and (2) the effect of its intrahippocampal administration in the step-down inhibitory avoidance (IA) and the open field habituation tasks (OF). Standard extracellular electrophysiology techniques were used to record field excitatory postsynaptic potentials from the dendritic region of CA1 neurons in response to a high frequency stimulation of Schaffer's collaterals; a micropipette ejected 0.2 microM of AM251 (in DMSO/PBS) 2 min before the stimulus: LTP was induced and lasted more than 30 min in the control, but not in the AM251-treated group. Immediately after training, either in IA (footshock, 0.5 mA) or OF, animals received a bilateral infusion of 0.55 or 5.5 ng/side of AM251 or its vehicle in the CA1 region, and test was performed 24 h later. AM251 has caused a significative decrease in the test step-down latency when compared to the control group, but no differences were detected in the OF task, including the number of crossings, i.e., there were no motor effects. The LTP supression could be caused by AM251 acting over GABAergic interneurons that modulate the LTP-bearing glutamatergic neurons. Endocanabinoids would then be the natural dis-inhibitors of local plasticity in the dorsal hippocampus, and the amnestic action of AM251 would be due to a disruption of this endogenous modulatory system.

Amnesia, Retrograde↗

PubMed2004

Effects of mannitol on ischemia-induced degeneration in rat hippocampus.

Although mannitol has been used as an osmotherapeutic drug on brain injury, the clinical efficiency of the drug are still controversial. In the present study, we examined the effects of mannitol on the edema in a hippocampal slice due to brief ischemia. To evaluate the effects, we employed an image analysis system that consists of an infrared-differential interference contrast (IR-DIC) microscope, an infrared CCD camera, and a computer with custom-made software. By this system, severity of the edema can be quantified as the coefficient of variation (CV) of digitalized slice images. The dose-dependent improvement on the deteriorated hippocampal slices could be obtained by administration of mannitol (10, 50, and 100 mM) after 10-min ischemia. However, field excitatory postsynaptic potentials (fEPSP) in CA1 stratum radiatum, which disappeared during 10-min ischemia, were never recovered by mannitol after more than 20-min treatment. fEPSP were blocked by the effective dose of mannitol for morphological recovery, but the effects found to be reversible. Although we failed to find positive rescuing effects of mannitol on the synaptic activities after ischemia, the protective effects of the drug on ischemic edema may rescue the secondary damages around the infarct area.

Animals↗

PubMed1999

Duodenal neurons provide nicotinic fast synaptic input to sphincter of Oddi neurons in guinea pig.

We have investigated the existence of neural connections between the duodenum and the sphincter of Oddi (SO). Stimulation of duodenal myenteric fiber bundles elicited synaptic responses in SO neurons, which included nicotinic fast excitatory postsynaptic potentials (EPSPs), slow EPSPs, and alpha(2)-adrenoreceptor-mediated inhibitory postsynaptic potentials. After 48 h in organ culture, when extrinsic fibers had diminished, only the fast EPSPs persisted. Duodenal mucosal stimulation also elicited nicotinic fast EPSPs in SO neurons. There was no association between the SO neurons that received duodenal input and their chemical coding. A reciprocal projection also exists from the SO to the duodenum. In acute and cultured preparations, duodenal myenteric stimulation caused antidromic responses in 20% of SO neurons. Furthermore, 45.6 +/- 10.5 neurons in SO ganglia were retrogradely labeled from dye application sites in the duodenum. It is proposed that bidirectional neural communication occurs between the duodenum and the SO and that duodenal neurons provide excitatory fast synaptic input to SO neurons through a reflex that can be activated at the duodenal mucosa.

Afferent Pathways↗

PubMedDate not supplied

Inhibition as binding controller at the single neuron level.

Natural stimulus for a neuron is a sum of large number of unitary excitatory postsynaptic potentials (EPSP) slightly dispersed in time. We analyze, based on numerical solution of the Hodgkin and Huxley equations, how does the triggering ability of the compound stimulus depend on the relative timing of the EPSPs it comprises. The dependences found suggest that a neuron stimulated from many synaptic inputs can be treated as performing elementary binding function and that inhibition serves as a controller of that kind of binding. The transient process characterized by EPSP operates in this context as a short-term memory mechanism inherent to a single neuron.

Algorithms↗

PubMed1999

The modulation of excitatory synaptic transmission by adenosine in area CA1 of the rat hippocampus is temperature dependent.

We tested the possibility that extracellular adenosine concentration varies with tissue temperature by measuring the tonic adenosinergic inhibition of excitatory synaptic transmission at different temperatures in the in vitro rat hippocampus. Application of the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) enhanced population excitatory postsynaptic potentials (EPSPs) by antagonizing tonic adenosinergic inhibition; this effect was greatest at 25 degrees C, and was progressively reduced at 35 and 37.5 degrees C. These results demonstrate that tonic adenosinergic inhibition is inversely related to temperature. In a second experiment, an exogenous A1 agonist, N6-cyclohexyladenosine (CHA), was applied to slices to inhibit evoked EPSPs. CHA inhibition of EPSPs was greater at 35 than at 25 degrees C, demonstrating that the reduced adenosinergic inhibition at higher temperatures is not a result of reduced A1 receptor function.

Adenosine↗

PubMed2006

Behavioral and electrophysiological studies of chronic oral administration of L-type calcium channel blocker verapamil on learning and memory in rats.

It has been shown that L-type voltage dependent calcium channels (VDCCs) have important role in learning and memory. In vivo and in vitro electrophysiological recordings of hippocampal neurons have demonstrated their involvement in long-term potentiation (LTP), which considers being one possible cellular mechanism underlying learning and memory. The long-term effect of VDCCs of hippocampal dentate gyrus (DG) so far on synaptic plasticity has not received much attention. In this study, the effect of chronic (60 days) oral administration of L-type calcium channel blocker verapamil on learning and memory and synaptic plasticity of hippocampal dentate gyrus in rats has been investigated. L-type calcium channel antagonist, verapamil chronically and orally at different doses (10, 20 and 50 mg/kg) was used to investigate learning and memory by passive avoidance learning. LTP in perforant-DG synapses was assessed (by either 200 or 400 Hz tetanization) in order to investigate long-term effect of verapamil on synaptic plasticity. In this case, field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude were measured. Our behavioral study has shown that chronic oral treatment of verapamil has no effect on learning whereas verapamil (50 mg/kg) decreased memory retrieval. Verapamil (20 and 50 mg/kg) inhibited EPSP-LTP induction at 400 Hz but not at 200 Hz tetanization. Furthermore, only verapamil (50mg/kg) decreased PS-LTP with respect to control group. These data suggest that 400 Hz LTP is required for activation of L-type VDCCs and it seems that verapamil is more effective on L-type calcium channels of DG dendrites than their soma.

Administration, Oral↗