Transmission In Rat Hippocampus Research Articles

Upregulation of the Endogenous Peptide Antisecretory Factor Enhances Hippocampal Long-term Potentiation and Promotes Learning in Wistar Rats

Antisecretory Factor (AF) is an endogenous peptide known for its powerful antisecretory and anti-inflammatory properties. We have previously shown that AF also acts as a neuromodulator of GABAergic synaptic transmission in rat hippocampus in a way that results in disinhibition of CA1 pyramidal neurons. Disinhibition is expected to facilitate the induction of long-term potentiation (LTP), and LTP is known to play a crucial role in learning and memory acquisition. In the present study we investigated the effect of AF on LTP in CA3-CA1 synapses in rat hippocampus. In addition, endogenous AF plasma activity was upregulated by feeding the rats with specially processed cereals (SPC) and spatial learning and memory was studied in the Morris Water Maze (MWM). We found that LTP was significantly enhanced in the presence of AF, both when added exogenously in vitro as well as when upregulated endogenously by SPC-feeding. In the presence of the GABAA-receptor antagonist picrotoxin (PTX) there was however no significant enhancement of LTP. Moreover, rats fed with SPC demonstrated enhanced spatial learning and short-term memory, compared with control animals. These results show that the disinhibition of GABAergic transmission in the hippocampus by the endogenous peptide AF enhances LTP as well as spatial learning and memory.

Vasopressin facilitates GABAergic transmission in rat hippocampus via activation of V1A receptors

Whereas vasopressin has been shown to enhance memory possibly by increasing long-term potentiation and direct excitation of the pyramidal neurons in the hippocampus, the effects of vasopressin on GABAergic transmission in the hippocampus remain to be determined. Here we examined the effects of vasopressin on GABAergic transmission onto CA1 pyramidal neurons and our results demonstrate that bath application of [Arg8]-vasopressin (AVP) dose-dependently increased the frequency of spontaneous IPSCs (sIPSCs) recorded from CA1 pyramidal neurons via activation of V1A receptors. Immunohistological staining and western blot further confirmed that both CA1 pyramidal neurons and interneurons expressed V1A receptors. Bath application of AVP altered neither the frequency nor the amplitude of miniature IPSCs in the presence of tetradotoxin and failed to change significantly the amplitude of evoked IPSCs recorded from CA1 pyramidal neurons. AVP increased the firing frequency of action potentials by depolarizing the GABAergic interneurons in the stratum radiatum of CA1 region. AVP-mediated depolarization of interneurons was mediated by inhibition of a background K+ conductance which was insensitive to extracellular tetraethylammonium, Cs+, 4-aminopyridine, tertiapin-Q and Ba2+. AVP-induced depolarization of interneurons was dependent on Gαq/11 but independent of phospholipase C, intracellular Ca2+ release and protein kinase C. The inhibitory effects of AVP-mediated modulation of GABA release onto CA1 pyramidal neurons were overwhelmed by its strong excitation of CA1 pyramidal neurons in physiological condition but revealed when its direct excitation of the pyramidal neurons was blocked suggesting that AVP-mediated modulation of GABAergic transmission fine-tunes the excitability of CA1 pyramidal neurons.

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.

Crystal structure of songorine chloride trihydrate, [C22H32NO3]Cl · 3H2O

C22H38ClNO6, trigonal, R3 (no. 146), a = 28.293(2) A, c = 7.4204(7) A, V = 5144.3 A, Z = 9, Rgt(F) = 0.051, wRref(F ) = 0.137, T = 296 K. Source of material Songorine, a C20-diterpenoid alkaloid is isolated from the chloroform extract of the roots ofAconitum szechenyianumGay, wetted by 10%ammoniumhydroxide solution before. The purified compound is dissolved in a 1% hydrochloric acid solution at first. Then the solution is adjusted to pH 6.5 with a 10% NaOH solution. Colorless single crystals were obtained at room temperature for days by slowly volatilizing the solvent. Experimental details Water H atoms were located in a difference Fourier map and refined with restrained O—H bond lengths (0.85(1) A) and fixed isotropic displacement parameters (0.08A). OtherH atomswere placed at calculated positions and refined using a riding model with O—H distances restrained to 0.82 A, C—H distances restrained to 0.93 A and N—H distance restrained to 0.91 A. Discussion Songorine belongs to the class of C20-diterpenoid alkaloids, a large group of biologically active compounds of naturally occurrence. As a diterpenoid alkaloid, songorine has been found to enhance both the orthodromic population spike and field excitatory postsynaptic potential (EPSP) in CA1 region of hippocampal slices [1]. Recently, it was indicated that songorine can enhance the excitatory synaptic transmission in rat hippocampus, and was proved that songorine is a novel non-competitive antagonist at the GABAA receptor in rat brain [2]. In the title crystal structure, there are one songorine cation, one chloride ion and 3 crystal water molecules (figure top). The bond length of C12—O2 is 1.202 A, and the angles of O2−C12−C11, O2−C12−C13 and C11−C12−C13 are 121.8(4)°, 122.8(4)° and 115.4(3)°, respectively, which indicates that the C12 and O2 are sp hybridized, and C11, C12, C13 and O2 atoms are in a plane. The bond length of C17—C16 is 1.322(6)A. The angles of C13− C16−C15, C17−C16−C15 and C17−C16−C13 are 108.0(3)°, 126.2(4)° and 125.5(4)°, respectively, which show an exomethylene attached to C16. The songorine cations are interlinked by hydrogen bonds (figure bottom). Intra-molecular hydrogen bonds O6W−H6WA···Cl1 and O5W−H5WA···Cl1 link the Cl−, crystal water O5W and O6W together. The hydrogen bonds C2−H2A···O4W, O1− H1···O4W, N1−H1N···O4W fix the crystal water O4W to songorine. The intermolecular hydrogen bonds O6W− H6WB···O5W (symmetric code: x,y,z−1) and C21−H21A···O1, C19−H19B···O1, C15−H15···O2 (symmetric code: x,y,z+1), link the songorinemolecules along [001]. The hydrogen bondsO5W− Z. Kristallogr. NCS 223 (2008) 111-113 / DOI 10.1524/ncrs.2008.0047 111 © by Oldenbourg Wissenschaftsverlag, Munchen

Suppression of glucocorticoid secretion enhances cholinergic transmission in rat hippocampus

We previously demonstrated that suppression of glucocorticoid secretion by adrenalectomy (ADX) impaired prefrontal cortex-sensitive working memory, but not reference memory. Since the cholinergic system in the hippocampus is also involved in these memories, we examined the effects of glucocorticoid suppression on cholinergic transmission in the rat hippocampus. A microdialysis study revealed that ADX did not affect the basal acetylcholine release, but enhanced the KCl-evoked response. This enhanced response was reversed by the corticosterone replacement treatment. The extracellular choline concentrations increased under both basal and KCl-stimulated conditions in the ADX rats, and these increases were also reversed by the corticosterone replacement. These results indicate that suppression of glucocorticoid secretion enhances cholinergic transmission in the hippocampus in response to stimuli. It is possible that this enhanced cholinergic transmission may not contribute to the ADX-induced working memory impairment, but it may be involved in maintenance of reference memory.

Glycine-Gated Chloride Channels Depress Synaptic Transmission in Rat Hippocampus

An inhibitory role for strychnine-sensitive glycine-gated chloride channels (GlyRs) in mature hippocampus is beginning to be appreciated. We have reported previously that CA1 pyramidal cells and GABAergic interneurons recorded in 3- to 4-wk-old rat hippocampal slices express functional GlyRs, dispelling previous misconceptions that GlyR expression ceases in early development. However, the effect of GlyR activation on cell excitability and synaptic circuits in hippocampus has not been fully explored. Using whole cell current-clamp recordings, we show that activation of strychnine-sensitive GlyRs through exogenous glycine application causes a significant decrease in input resistance and prevents somatically generated action potentials in both CA1 pyramidal cells and interneurons. Furthermore, GlyR activation depresses the synaptic network by reducing suprathreshold excitatory postsynaptic potentials (EPSPs) to subthreshold events in both cell types. Blockade of postsynaptic GlyRs with the chloride channel blocker 4, 4'-diisothiocyanatostilbene-2-2'-disulfonic acid (DIDS) or altering the chloride ion driving force in recorded cells attenuates the synaptic depression, strongly indicating that a postsynaptic mechanism is responsible. Increasing the local glycine concentration by blocking reuptake causes a strychnine-sensitive synaptic depression in interneuron recordings, suggesting that alterations in extracellular glycine will impact excitability in hippocampal circuits. Finally, using immunohistochemical methods, we show that glycine and the glycine transporter GlyT2 are co-localized selectively in GABAergic interneurons, indicating that interneurons contain both inhibitory neurotransmitters. Thus we report a novel mechanism whereby activation of postsynaptic GlyRs can function to depress activity in the synaptic network in hippocampus. Moreover, the co-localization of glycine and GABA in hippocampal interneurons, similar to spinal cord, brain stem, and cerebellum, suggests that this property is likely to be a general characteristic of inhibitory interneurons throughout the CNS.

Systemic hypoxia and the depression of synaptic transmission in rat hippocampus after carotid artery occlusion.

The relationship between step reductions in inspired oxygen and the amplitude of evoked field excitatory postsynaptic potentials (fEPSPs) recorded from hippocampal CA1 neurons was examined in anaesthetized rats with a unilateral common carotid artery occlusion. The amplitudes of fEPSPs recorded from the hippocampus ipsilateral to the occlusion were significantly more depressed with hypoxia than were the fEPSPs recorded from the contralateral hippocampus. The adenosine A1-selective antagonist, 8-cyclopentyl-1,3-dimethylxanthine (8-CPT), blunted the hypoxic depression of the fEPSP. Tissue partial pressure of oxygen (Ptiss,O2) was measured in the ipsilateral and contralateral hippocampus using glass Clark-style microelectrodes. Ptiss,O2 fell to similar levels as a function of inspired oxygen in the ipsilateral and contralateral hippocampus, and in the ipsilateral hippocampus after administration of 8-CPT. Hippocampal blood flow (HBF) was measured using laser Doppler flowmetry. A decline in HBF was associated with systemic hypoxia in both hippocampi. HBF, as a function of inspired oxygen, fell significantly more in the ipsilateral than in the contralateral hippocampus. We conclude that endogenous adenosine acting at the neuronal A1 receptor plays a major role in the depression of synaptic transmission during hypoxic ischaemia. The greater susceptibility of the fEPSP in the ipsilateral hippocampus to systemic hypoxia cannot be explained entirely by differences in Ptiss,O2 or HBF between the two hemispheres.

Songorine, a diterpenoid alkaloid of the genus Aconitum, is a novel GABA A receptor antagonist in rat brain

Songorine, a diterpenoid alkaloid isolated from the genus Aconitum, was recently found to enhance the excitatory synaptic transmission in rat hippocampus. The mechanism underlying the effects was examined in the present study. The alkaloid at 0.1–300 μM inhibited the specific binding of [ 3H]muscimol to Triton-treated synaptic membranes of rat brain in a concentration-dependent manner ( IC 50=7.06 μM; 95% confidence limits: 3.28–10.84 μM). Scatchard analysis and Lineweaver–Burk double reciprocal plot of [ 3H]muscimol saturation binding data indicate a non-competitive inhibition of the alkaloid on the γ-aminobutyric acid A (GABA A) receptor. In acutely dissociated rat hippocampal neurons the alkaloid did not elicit current response, but markedly inhibited the GABA-induced inward current ( IC 50=19.6 μM). The results suggest that songorine is a novel non-competitive antagonist at the GABA A receptor in rat brain.

Gabapentin inhibits presynaptic Ca 2+ influx and synaptic transmission in rat hippocampus and neocortex

Gabapentin is a widely used drug with anticonvulsant, antinociceptive and anxiolytic properties. Although it has been previously shown that Gabapentin binds with high affinity to the α 2δ subunit of voltage-operated Ca 2+ channels (VOCC), little is known about the functional consequences of this interaction. Here, we investigated the effect of Gabapentin on VOCCs and synaptic transmission in rat hippocampus and neocortex using whole-cell patch clamp and confocal imaging techniques. Gabapentin (100–300 μM) did not affect the peak amplitude or voltage-dependency of VOCC currents recorded from either dissociated or in situ neocortical and hippocampal pyramidal cells. In contrast, Gabapentin inhibited K +-evoked increases in [Ca 2+] in a subset of synaptosomes isolated from rat hippocampus and neocortex in a dose-dependent manner, with an apparent half-maximal inhibitory effect at ∼100 nM. In hippocampal slices, Gabapentin (300 μM) inhibited the amplitude of evoked excitatory- and inhibitory postsynaptic currents recorded from CA1 pyramidal cells by 30–40%. Taken together, the results suggest that Gabapentin selectively inhibits Ca 2+ influx by inhibiting VOCCs in a subset of excitatory and inhibitory presynaptic terminals, thereby attenuating synaptic transmission.

Effect of chronic stress on cholinergic transmission in rat hippocampus

We previously demonstrated that chronic stress impaired prefrontal cortex-sensitive working memory, but not reference memory. Since the hippocampal cholinergic system is also involved in these memories, we examined the effects of chronic stress on cholinergic transmission in the rat hippocampus. A microdialysis study revealed that the stress did not affect the basal acetylcholine release, but enhanced the KCl-evoked response. These results suggest that cholinergic transmission in the chronically stressed hippocampus does not contribute to working memory impairment, but it may be involved in maintenance of reference memory.

Adenosine induces initial hypoxic-ischemic depression of synaptic transmission in the rat hippocampus in vivo.

The present study was designed to investigate the role of adenosine in the hypoxic depression of synaptic transmission in rat hippocampus. An in vivo model of hypoxic synaptic depression was developed in which the common carotid artery was occluded on one side in the urethane-anesthetized rat. Inspired oxygen levels were controlled through a tracheal cannula. Rats were placed in a stereotaxic apparatus for stimulation and recording of bilateral hippocampal field excitatory postsynaptic potentials. The percent inspired oxygen could be reduced to levels that produced a reversible and repeatable depression of evoked synaptic transmission restricted to the hippocampus ipsilateral to the occlusion. Further reduction in the level of inspired oxygen depressed synaptic transmission recorded from both hippocampi. The adenosine nonselective antagonist caffeine and the A(1) selective antagonist 8-cyclopentyltheophylline prevented the initial depression in synaptic transmission. We conclude that the initial depression of synaptic transmission observed in the rat hippocampus in vivo is due to endogenous adenosine acting at neuronal adenosine A(1) receptors.

Characterisation of ATP-induced facilitation of transmission in rat hippocampus

Superfusion of rat hippocampal slices with ATP induces a form of facilitation that has been poorly characterised. The present study has confirmed that at low concentrations of ATP (10 μM or less), an initial depression of evoked potential size is followed by a rebound facilitation which is not reproduced by αβ-methyleneATP, βγ-methyleneATP, or the dinucleotide P1,P6-diadenosine hexaphosphate. The post-ATP facilitation could be prevented by the adenosine A 1 receptor antagonists 8-phenyltheophylline or 1,3-dipropyl-8-cyclopentyltheophylline (50 nM), or superfusion of adenosine deaminase. The adenosine A 2A receptor antagonist 8-(chlorostyryl)-caffeine did not affect the inhibition but prevented the post-ATP facilitation. The NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid prevented the establishment of post-ATP facilitation. The post-ATP facilitation was also blocked by suramin at a concentration (50 μM) that does not block glutamate receptors. Suramin prevented the induction but not the maintenance phase of the post-ATP facilitation. The repeated induction of post-ATP facilitation by bursts of electrical stimulation designed to saturate the normal mechanisms of long-term potentiation prevented the induction of post-ATP facilitation. However, repeated applications of ATP to achieve saturation of its receptor did not prevent the subsequent induction of electrically evoked long-term potentiation. It is concluded that ATP can induce a form of synaptic facilitation which resembles only partially that induced by electrical stimulation and which may require the simultaneous activation of P1 and P2 receptors.

Effects of the neuropeptide Y Y 2 receptor antagonist BIIE0246 on presynaptic inhibition by neuropeptide Y in rat hippocampal slices

We previously reported that ( S)- N 2-[[1-[2-[4-[( R, S)-5,11-dihydro-6(6 h)-oxodibenz[ b, e]azepin-11-yl]-1-piperazinyl]-2-oxoethyl]cylopentyl]acetyl]- N-[2-[1,2-dihydro-3,5(4 H)-dioxo-1,2-diphenyl-3 H-1,2,4-triazol-4-yl]ethyl]argininamid, BIIE0246, is a potent and highly selective neuropeptide Y Y 2 receptor antagonist. Neuropeptide Y Y 2 receptors have been proposed to mediate the inhibition by neuropeptide Y of excitatory synaptic transmission in rat hippocampus. Therefore, we investigated the effects of BIIE0246 on the electrophysiological properties of neuropeptide Y in rat hippocampal slices and determined the affinity of this novel antagonist for rat hippocampal neuropeptide Y Y 2 receptors. BIIE0246 displayed an affinity of IC 50=4.0±1.6 ( n=4) for neuropeptide Y receptor binding sites labelled by 125I-neuropeptide Y in rat hippocampal membranes. At a concentration of 1 μM, BIIE0246 completely antagonized the inhibitory effects of 300 nM neuropeptide Y on synaptic transmission in rat hippocampal slices. This is the first study showing that a selective neuropeptide Y Y 2 receptor antagonist is able to block neuropeptide Y mediated effects in the hippocampus and unambiguously characterizes the presynaptic receptor in the rat hippocampus as the neuropeptide Y Y 2 receptor.

Mu opioids enhance mossy fiber synaptic transmission indirectly by reducing GABA B receptor activation

The cellular mechanisms underlying mu opioid facilitation of mossy fiber (MF) long-term potentiation (LTP) and synaptic transmission were investigated in the rat hippocampal slice. Naloxone (10 μM) significantly inhibited the induction of mossy fiber LTP, an effect attributed by Derrick and Martinez [B.E. Derrick, J.L.J. Martinez, Opioid receptor activation is one factor underlying the frequency dependence of mossy fiber LTP induction, J. Neurosci. 14 (1994) 4359–4367] to antagonism of endogenous opioid peptide action. We found that the inhibitory effects of naloxone were not blocked by bicuculline, suggesting that endogenous opioids did not enhance mossy fiber LTP by depressing GABA A inhibition. [ d-Ala2, NMePhe4, Glyol5] enkephalin, DAMGO (300 nM), a mu opioid agonist, mimicked the action of endogenous opioids, enhancing both mossy fiber LTP induction and paired-pulse facilitation. DAMGO potentiation of the paired-pulse facilitation of mossy fiber response was also insensitive to bicuculline but was blocked by the mu selective antagonist CTOP. Further analysis of the cellular mechanism showed that the depletion of internal Ca 2+ stores by thapsigargin (1 μM), or inhibition of protein kinases by application of staurosporine (1 μM) did not block the DAMGO facilitation of mossy fiber–CA3 synaptic transmission. However, application of phaclofen (100 μM GABA B receptor antagonist or SCH 50911, a more potent GABA B antagonist significantly inhibited the DAMGO effect (49±15%; 51±19% inhibition, P<0.05). The data indicate that the DAMGO effect on the mossy fiber pathway is partially mediated by a reduction in GABA activation of GABA B receptors. These findings further suggest that endogenous opioid peptides activate mu opioid receptors to facilitate mossy fiber LTP and synaptic transmission in rat hippocampus partially by GABA B receptor-mediated disinhibitory mechanism.

Hydroxylamine blocks adenosine A 1 receptor-mediated inhibition of synaptic transmission in rat hippocampus

The nitric oxide donor hydroxylamine (NH 2OH) induced a transient depression of the evoked synaptic potential recorded in the rat hippocampal CA1 region. This depression was abolished with an adenosine A 1 antagonist, 8-cyclopentyltheophylline. In addition, hydroxylamine reversed adenosine A 1 receptor-mediated inhibition of the evoked population spike, the fEPSP and the intracellularly recorded EPSP. The inhibitory modulation of adenosine A 1 receptor activation by hydroxylamine suggests the presence of a potent endogenous regulatory site.

β-Amyloid produces a delayed NMDA receptor- dependent reduction in synaptic transmission in rat hippocampus

The delayed effect of in vivo injection of beta-amyloid on glutamatergic synaptic transmission was investigated in the rat hippocampus. The amplitude of field excitatory postsynaptic potentials recorded in the CA1 region of awake rats was reduced 24 h after the injection of beta-amyloid (1-40) (0.4 or 3.5 nmol i.c.v.). The effect lasted for at least 5 days and was prevented by treatment with the N-methyl-D-aspartate (NMDA) receptor antagonist CPP (7 mg kg-1 x 2, i.p.). Similar results were obtained ex vivo in the dentate gyrus. There was no change in the ability to induce long-term potentiation. These results provide direct evidence that beta-amyloid produced a delayed reduction in the function of glutamatergic synapses, probably as a result of an initial over-activation of the NMDA receptor-mediated component of transmission.

Beta-Amyloid selectively augments NMDA receptor-mediated synaptic transmission in rat hippocampus.

The effect of beta-amyloid on alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic excitatory postsynaptic currents measured with whole-cell voltage-clamp techniques, was investigated in the rat dentate gyrus in vitro. Application of beta-amyloid (1-40) by extracellular perfusion (200 nM) or intracellularly via the recording pipette (100 nM) resulted in a gradual enhancement of the NMDA receptor-mediated synaptic currents which did not reverse on washout. Basal AMPA receptor-mediated transmission, resting membrane potential or input resistance of the granule cells did not change. These results provide direct evidence that beta-amyloid selectively interacts with the potentially neurotoxic NMDA receptor via a postsynaptic site. It is proposed that this action may help explain the synaptic changes seen in Alzheimer's disease.

Philanthotoxin inhibits Ca 2+ currents in rat hippocampal CA1 neurons

The wasp venom philanthotoxin-4.3.3 (PhTX-4.3.3) is an antagonist of glutamate transmission in the insect as well as in the mammalian brain. It was recently shown that PhTX-4.3.3 inhibits the N- methyl- D-asparttate (NMDA) transmission in rat hippocampus. In this study we show that dideaza-philanthotoxin-12 (dideaza-PhTX-12), an analogue of PhTX-4.3.3, is a potent antagonist of voltage-dependent Ca 2+ currents in rat hippocampal CA1 neurons. At a concentration of 10 μM it reduces the Ca 2+ current to 40%. Two voltage-dependent potassium currents, the A current and the delayed rectifier, were hardly affected calcium influx via voltage dependent as well as NMDA mediaded calcium channels and thus reduce excitability in the hippocampus.

Adenosine-dependent enhancement by methylxanthines of excitatory synaptic transmission in hippocampus of rats.

Whole-cell patch-clamp was used to investigate synaptic transmission in hippocampal slices. Excitatory post-synaptic currents (EPSCs) were facilitated by low (less than or equal to 1 microM) adenosine (Ado) concentrations, while high concentrations had well-known inhibitory effects on the EPSC. When added on the background of preapplied Ado, methylxanthines caused a large potentiation of EPSCs. At saturation, the enhanced EPSC could exceed the control almost by an order of magnitude. Pertussis toxin strongly impaired the ability of Ado to block EPSCs but did not augment the facilitatory effect. The two components of the EPSC mediated by N-methyl-D-aspartate (NMDA) and non-NMDA receptors were facilitated simultaneously and in equal proportions.

Acidic fibroblast growth factor modulates synaptic transmission in rat hippocampus

Acidic fibroblast growth factor modulates synaptic transmission in rat hippocampus