The valuation of malnutrition in the mono-digestion of maize silage by anaerobic batch tests.

Anaerobic digestion is a technology which is used to produce methane from organic solids and energy crops. Especially in recent years, the fermentation of energy crops has become more and more important because of increasing costs for energy and special benefits for renewable energy sources in Germany. Anaerobic bacteria require macro and micro nutrients to grow. Absence of these elements can inhibit the anaerobic process significantly. In particular mono-substrates like maize or certain industrial wastewater often cannot provide all required nutrients. For this reason this research investigates the influence of substrate and trace elements on anaerobic digestion in detail. Different agricultural anaerobic biomasses are analysed with special regard to their trace element content. Based on these results, the influence of three trace elements (iron, cobalt, and nickel) on anaerobic digestion was studied in anaerobic batch tests at different sludge loading rates and for different substrates (maize and acetate). Biogas production was found to be 35% for maize silage and up to 70% higher for acetate with trace element dosage than in the reference reactor.

Energy- and CO2-reduction potentials by anaerobic treatment of wastewater and organic kitchen wastes in consideration of different climatic conditions.

The classical municipal wastewater treatment in Germany consists of an aerobic carbon and nitrogen elimination and mostly an anaerobic sludge treatment. Organic kitchen wastes from separate waste collection as well as yard wastes are converted mostly in composting plants to soil conditioner. With these conventional types of treatment, the energy potential in waste and wastewater is lost due to aerobic material conversion. In this article three scenarios for the treatment of municipal wastewater and waste are compared on the subject of energy efficiency and useable potential: Sc1. the classical wastewater treatment and the composting of the organic waste fraction, Sc2. the anaerobic treatment of wastewater combined with deammonification and the digestion of the organic waste fraction, and Sc3. a mutual anaerobic treatment of wastewater and waste as co-digestion with deammonification. The calculation of energy and CO2-balance considers different climatic conditions. In case of using anaerobic treatment, not only the energy balance will be positive, also the CO2-balance is improved by the substitution of fossil fuels with generated biogas.

Anaerobic treatment of municipal wastewater using the UASB-technology.

The anaerobic treatment of municipal wastewater enables new applications for the reuse of wastewater. The effluent could be used for irrigation as the included nutrients are not affected by the treatment. Much more interesting now are renewable energies and the retrenchment of CO(2) emission. With the anaerobic treatment of municipal wastewater, not only can the CO(2) emission be reduced but "clean" energy supply can be gained by biogas. Most important for the sustainability of this process is the gathering of methane from the liquid effluent of the reactor, because the negative climate-relevant effect from the degassing methane is much higher than the positive effect from saving CO(2) emission. In this study, UASB reactors were used with a flocculent sludge blanket for the biodegradation of the carbon fraction in the wastewater with different temperatures and concentrations. It could be shown that the positive effect is much higher for municipal wastewater with high concentrations in hot climates.

Place learning and hippocampal synaptic plasticity in streptozotocin-induced diabetic rats.

Moderate impairment of learning and memory has been recognized as a complication of diabetes. The present study examined behavioral and electrophysiological measures of cerebral function in streptozotocin (STZ)-induced diabetic rats. Behavioral testing consisted of a spatial learning task in a water maze. Electrophysiological testing consisted of in vitro assessment of hippocampal long-term potentiation (LTP), an activity-dependent form of synaptic plasticity, which is believed to be related to the cellular mechanisms of learning and memory. Two experiments were performed: the first with severely hyperglycemic rats and the second with moderately hyperglycemic rats. Rats were tested in the water maze 11 weeks after induction of diabetes. Next, LTP was measured in vitro in trained animals. Both spatial learning and LTP expression in the CA1 field of the hippocampus were impaired in severely hyperglycemic rats as compared with nondiabetic controls. In contrast, spatial learning and hippocampal LTP were unaffected in moderately hyperglycemic rats. The association of alterations in hippocampal LTP with specific learning impairments has previously been reported in conditions other than diabetes. Our findings suggest that changes in LTP-like forms of synaptic plasticity in the hippocampus, and possibly in other cerebral structures, are involved in learning deficits in STZ-induced diabetes. The beneficial effect of moderate glycemic control on both place learning and hippocampal LTP supports the significance of the relation between these two parameters and indicates that the development of the observed deficits may be related to the level of glycemic control.

Hippocampal synaptic plasticity in streptozotocin-diabetic rats: impairment of long-term potentiation and facilitation of long-term depression.

Streptozotocin-diabetic rats, an animal model for diabetes mellitus, show learning deficits and impaired long-term potentiation in the CA1-field of the hippocampus. The present study aimed to further characterize the effects of streptozotocin-diabetes on N-methyl-D-aspartate receptor-dependent long-term potentiation in the CA1-field, to extend these findings to N-methyl-D-aspartate receptor-dependent and independent long-term potentiation in other regions of the hippocampus and to examine effects on long-term depression. First, the effect of diabetes duration on long-term potentiation in the CA1-field was determined. A progressive deficit was observed after a diabetes duration of six to eight weeks, which reached a maximum after 12 weeks of diabetes and remained stable thereafter. Next, long-term potentiation was examined in the dentate gyrus and in the CA3-field after 12 weeks of diabetes. Both were found to be impaired compared to controls. Finally, long-term depression was examined in the CA1-field of the hippocampus after 12 weeks of diabetes and found to be enhanced in slices from diabetic rats compared to controls. Changes in synaptic plasticity were observed in hippocampal slices from streptozotocin-diabetic rats. Expression of N-methyl-D-aspartate receptor-dependent long-term potentiation was impaired in the CA1-field and dentate gyrus and expression of N-methyl-D-aspartate receptor-independent long-term potentiation was impaired in the CA3-field. In contrast, expression of long-term depression was facilitated in CA1. It is suggested that this combination of changes in plasticity may reflect alterations in intracellular signalling pathways.

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus.

Long-term depression, depotentiation and long-term potentiation of field excitatory postsynaptic potentials in the CA1 field of the hippocampus were studied in slices from two-, 12-, 24- and 36-week-old rats. Long-term potentiation was induced by stimulating afferent fibres for 1 s at 100 Hz. Long-term depression was induced either by stimulating the afferent pathways twice for 15 min at 1 Hz (protocol 1), giving in total 1800 pulses, or by stimulating the fibres at 5 min intervals twice at 1 Hz for 5 min followed by 5 min stimulation at 5 Hz (protocol 2), giving in total 2100 pulses. We found significant long-term depression in slices of all groups stimulated with protocol 1; however, the magnitude of long-term depression in slices from 24- and 36-week-old rats was significantly lower than that in slices from two- and 12-week old rats, although there was no such difference in the magnitude of long-term potentiation between slices. Stimulation protocol 2 induced long-term depression only in slices from two- and 12-week-old rats. Comparison of the dynamic range of transmission plasticity in slices from two- and 36-week-old rats, calculated as the difference between the nearly saturated long-term potentiation and nearly saturated depotentiation, revealed a significantly smaller dynamic range in slices from 36-week-old rats in comparison with slices from two-week-old animals. The decrease in the dynamic range in slices from 36-week-old rats was due to a diminished capacity to depotentiate the nearly saturated long-term potentiation and not due to a decreased long-term potentiation expression in these slices. In contrast to long-term depression, in which the slope of the field excitatory postsynaptic potentials consistently and significantly decreased below the baseline level, the nearly saturated depotentiation did not decrease below the original, pre-long potentiation baseline level. The results demonstrate that increasing age reduces expression of long-term depression and the dynamic range of transmission plasticity.

The C-terminal glycopeptide of propressophysin potentiates excitatory transmission in the rat lateral septum.

Effects of peptides synthesized from the same precursor as vasopressin, i.e. the C-terminal 39-amino acid long glycopeptide and neurophysin II, were investigated for biological activities in electrophysiological experiments in brain slices of the rat lateral septum. These slices contained the glycopeptide as the predominant form and a fragment of it, amino acid sequence 22-39, as a minor form (8% of the glycopeptide 1-39), as shown by high performance liquid chromatography of extracts and by radioimmunoassay. None of the peptides, neurophysin II, the glycopeptide 1-39 and the fragment 22-39, tested in a concentration of 10(-12) M, had measurable effects on the resting membrane potential of the neurons. The glycopeptide and the fragment 22-39, however, increased, in some cells, for tens of minutes the excitatory postsynaptic potentials evoked in these neurons by stimulation of the fimbria fibers. The increase in input resistance, seen in many septal neurons treated with either of the peptides was not correlated with the excitatory postsynaptic potential increase. Neurophysin II affected neither the excitatory postsynaptic potentials nor the input resistance of the neurons. It is concluded that the glycopeptide 1-39 and the fragment 22-39 possess biological activities amongst which the facilitation of excitatory amino acid transmission on lateral septum neurons. Therefore, these peptides derived from the vasopressin precursor may act in concert with vasopressin to establish facilitation of excitatory transmission in the brain.

The impaired long-term potentiation in the CA1 field of the hippocampus of cognitive deficient microencephalic rats is restored by D-serine.

Rat embryos exposed on gestational day 15 to methyl-azoxymethanol acetate develop a microencephaly characterized primarily by a hypoplasia of the neocortex and CA fields of the hippocampus that in adulthood is associated with disturbances in learning. In brain slices prepared from microencephalic rats, we have examined the field excitatory postsynaptic potentials and population spike in the CA1 field of the hippocampus evoked by stimulation of the stratum radiatum. These parameters did not differ from those obtained in slices from control rats. High frequency stimulation of the stratum radiatum afferent fibres, which readily induced long-term potentiation of the field excitatory postsynaptic potentials and population spike in the CA1 field of the hippocampus of control rats, failed to induce long-term potentiation in that of microencephalic rats. High frequency stimulation of the perforant path readily elicited long-term potentiation in the dentate gyrus of both control and microencephalic rats. Picrotoxin had no apparent effect on field excitatory postsynaptic potentials and population spike in the CA1 field of the microencephalic rats, indicating that little GABAergic inhibition was present in slices from these rats. D-2-Amino-phosphonovalerate suppressed the field potentials in slices from microencephalic rats by more than 50%, suggesting that N-methyl-D-aspartate receptors contributed markedly to the synaptic responses evoked by single stimuli. D-Serine, but not picrotoxin, restored long-term potentiation in the CA1 field of the microencephalic rats. The D-serine effect was prevented by pretreating the slices with either 7-chloro-kynurenate or D-2-amino-phosphonovalerate. The failure to induce long-term potentiation, if also found in vivo, may be among the factors related to the learning deficits displayed by these rats.

Effects of vasopressin and related peptides on neurons of the rat lateral septum and ventral hippocampus.

The effects of vasopressin (VP), VP fragments and propressophysin glycopeptide on neuronal activities in the septum-hippocampus complex of rats were studied in vitro and in vivo. The frequency of the hippocampus theta rhythm in Brattleboro rats homozygous for diabetes insipidus was significantly slower than that of heterozygous litter mates and normal rats. Intracerebroventricular micro-injection of des-glycine-amide vasopressin corrected for several hours the frequency deficit of the theta rhythm in the homozygous Brattleboro rats and the centrally administered VP slowed down theta rhythm in normal rats. Microinotophoretically administered VP excited single neurons in the lateral septum of ventral hippocampus, and/or facilitated the responses of these neurons to glutamate and to stimulation of the glutamatergic afferent fibers in the fimbria bundle. The excitatory effects of VP vanished within seconds after termination of the peptide administration, however, the peptide-induced enhancement of glutamate and syntatically induced excitations were sustained for up to 60 min after the peptide administration. In vitro, pM concentrations of VP, VP 4-8 and C-terminus glycopeptide of propresophysin facilitated for 30-60 min the glutamate-mediated EPSPs in neurons of the lateral septum or the ventral hippocampus. The EPSPs increase in the lateral septum neurons was not prevented by pretreatment with antagonist of the V1a type of the vasopressin receptor. The resting membrane potential and input resistance were not affected by the peptides. A low-frequency electrical stimulation in the diagonal Band of Broca or in the Bed nucleus of the stria terminals, sources of the vasopressinergic innervation of the septum, facilitated the negative wave of the filed potentials responses evoked in the lateral septum by stimulating the fimbria bundle fibers in control Long-Evans and Brattleboro rats heterozygous for diabetes insipidus. The field potential increase was sustained for several hours after the stimulation, and it was not occluded by long-term potentiation elicited by high frequency stimulation of the fimbria bundle afferent fibers. Brattleboro rats homozygous for diabetes insipidus failed to show the filed potential increase after the diagonal band stimulation. It is suggested that the long-lasting facilitation of glutamate-mediated excitations might be a physiological action of the propressophysin-derived peptides in the septum-hippocampus complex which, in concert with other forms of synaptic plasticity like the long-term potentiation, facilitates the hippocampus-mediated forms of learning and memory. This action is presumably related to the memory enhancing effect of the propressophysin-derived peptides.

Effect of vasopressin, oxytocin and peptides derived from these hormones on field potential induced in lateral septum of rats by stimulation of the fimbria fornix.

Superfusion of the dorsal surface of the septum with artificial cerebrospinal fluid containing 10(-10) M [Arg8]-vasopressin (VP) significantly increased the negative (N) wave in field potentials (FPs) elicited in the lateral septum (LS) of rats by stimulation of the fimbria-fornix. A similar increase in the FPs negativity was also observed following superfusion of the septum with [pGlu4, Cyt6] VP(4-9), [pGlu4, Cyt6] VP(4-8), [Cyt6] VP (5-9), desglycinamide9-VP and 1-deamino, 8-D-arginine-VP. However, for obtaining the effect with these peptides 10(3-4) times higher concentrations had to be used. Superfusion of the septum with 10(-8) M oxytocin (OX) elicited nearly the same N-wave increase as the 10(-8) M VP septal superfusion. The 10(-10) M concentration of OX as well as 10(-7) M [pGlu4, Cyt6] OX(4-9) and [pGlu4, Cyt6] OX(4-8) had little effect on the FPs negativity. The significance of these findings for the elucidation of the VP function in the LS is discussed.

Two actions of vasopressin on neurons in the rat ventral hippocampus: a microiontophoretic study.

Vasopressin (VP), applied by brief iontophoretic pulses on ventral hippocampus neurons in vivo, excited approximately 30% of the neurons tested. Glutamate (Glu) and acetylcholine (ACh) excited nearly all neurons recorded. A selective antagonist of vasopressin V1 receptors suppressed the VP-induced excitation and, in addition, suppressed the excitations induced by Glu but not those by ACh. The specificity of the action in the brain of this VP antagonist must therefore be doubted. Two excitatory amino acid antagonists, D(-)-2-amino-5-phosphonovaleric acid (2APV) and glutamic acid diethyl ester (GDEE), suppressed the responses to Glu and also those to VP. ACh excitations, tested in the same neurons, were little affected by 2APV and GDEE. The remaining 70% of VH neurons were not excitable with VP. However, the responses of these neurons to Glu but not to Ach, increased markedly both while the peptide was released and for tens of minutes thereafter. The increase in Glu responses induced by VP could not be prevented by the VP or excitatory amino acid receptor antagonists applied before the peptide. The possibility that the excitation and the potentiation of Glu responses caused by VP originated from two different actions of the peptide is discussed.

A long-lasting increase and decrease in synaptic excitability in the rat lateral septum are associated with high and low shuttle box performance, respectively.

In a series of experiments with rats, using evoked field potentials, the influence of massed trial training in 2-way shuttle box avoidance and step-through passive avoidance tasks was studied on the synaptic excitability of the lateral septum (LS) neurons and on the induction of long-term potentiation in the lateral septum in vivo. The majority of rats that attained a high performance level in the shuttle box task exhibited, after the shuttle box training, a long-lasting enhancement of synaptic excitability of lateral septum neurons, whereas most of the rats with low performance in the shuttle box showed a long-lasting depression in the LS synaptic excitability. Both types of excitability changes disappeared within 24 h. Neither the first habituation session in the passive avoidance apparatus nor the subsequent one-trial learning in passive avoidance task had a marked influence on lateral septum synaptic excitability. Both high-performance and low-performance rats exhibited a long-term potentiation (LTP)-like potentiation of synaptic excitability of the lateral septum neurons after high frequency stimulation of the fimbria fibers although the amount of LTP in high performance rats was slightly higher than that in low performance animals.

Long-term potentiation and synaptic protein phosphorylation.

Long-term potentiation (LTP) is a well known experimental model for studying the activity-dependent enhancement of synaptic plasticity, and because of its long duration and its associative properties, it has been proposed as a system to investigate the molecular mechanisms of memory formation. At present, there are several lines of evidence that indicate that pre- and postsynaptic kinases and their specific substrates are involved in molecular mechanisms underlying LTP. Many studies focus on the involvement of protein kinase C (PKC). One way to investigate the role of PKC in long-term potentiation is to determine the degree of phosphorylation of its substrates after in situ phosphorylation in hippocampal slices. Two possible targets are the presynaptic membrane-associated protein B-50 (a.k.a. GAP 43, neuromodulin and F1), which has been implicated in different forms of synaptical plasticity in the brain such as neurite outgrowth, hippocampal LTP and neurotransmitter release, and the postsynaptic protein neurogranin (a.k.a. RC3, BICKS and p17) which function remains to be determined. This review will focus on the protein kinase C activity in pre- and postsynaptic compartment during the early phase of LTP and the possible involvement of its substrates B-50 and neurogranin.

Monoamine-induced responses in lateral septal neurons: influence of iontophoretically applied vasopressin.

We examined the effect of iontophoretically applied noradrenaline (NA), dopamine (DA) and serotonin (5-HT) on the spontaneous activity of lateral septal neurons in rats and subsequently investigated if the observed responses to these monoamines were altered in the presence of arginine8-vasopressin (AVP). NA, DA and 5-HT induced a depression of the spontaneous activity in 70% of the spontaneously active neurons on which they were tested. Of the remaining neurons the majority was not affected by the monoamines. The responding cells differed from the non-responding cells in their localization in those parts of the lateral septum where dense monoamine-containing terminal networks have been visualized and in their significantly lower spontaneous activity. The effect of AVP on monoamine-induced responses was tested in neurons in which the spontaneous activity was not affected by the peptide itself. It appeared that in about 30% of these neurons, monoamine-induced inhibitions were reduced in presence of the peptide whereas in the majority of the neurons responses to the monoamines were not markedly altered by AVP. In contrast to this rather low occurrence of a clear AVP-effect on the monoamine responses, the peptide enhanced excitatory responses to glutamate in more than 75% of neurons tested during the same experiments. It was concluded that under these experimental conditions the effect of AVP on excitatory amino acid neurotransmission is more pronounced than on responses to putative monoaminergic neurotransmitters in the lateral septum.

Arginine-vasopressin enhances the responses of lateral septal neurons in the rat to excitatory amino acids and fimbria-fornix stimuli.

In the present study we investigated the effect of arginine-vasopressin (AVP) on responses induced in lateral septal neurons of the rat by iontophoretically administered excitatory and inhibitory amino acids and by synaptical stimuli delivered through fimbria-fornix (fi-fx) fibers. In the majority of the lateral septal neurons, iontophoretically applied AVP induced a marked increase in the excitatory responses to glutamate, aspartate, quisqualate and N-methyl-D-aspartate. The responses to excitatory amino acids frequently remained elevated several minutes after termination of the peptide administration. Inhibitory responses induced by GABA were not affected by AVP. The responsiveness of lateral septal single units to fi-fx stimuli was enhanced during iontophoretic administration of AVP. The enhanced responsiveness also appeared from experiments in which topically applied AVP induced a prolonged increase in the negative but not the positive wave of field potentials evoked in the lateral by fi-fx stimuli. The possible physiological significance of these findings is discussed.

Vasopressin maintains long-term potentiation in rat lateral septum slices.

In brain slices of normal Wistar and Long-Evans rats, brief high frequency stimulation of the fimbria fibers induced long-term potentiation (LTP) in excitatory transmission between these fimbria fibers and neurons of the lateral septum (LS). Slices prepared from diabetes insipidus (DI) Brattleboro rats, that contained no vasopressin (VP), consistently failed to maintain LTP in this excitatory transmission. Exogenous VP, administered to slices from DI Brattleboro rats shortly prior to the experiment or released from a subcutaneous depot in DI Brattleboro rats for several days prior to decapitation, corrected this failure. The maintenance of LTP in the LS in slices from Wistar and Long-Evans rats was prevented by D(CH2)5-Tyr(Me)-arginine VP, an antagonist for the V1 type of VP receptors. These results indicate an important role of VP in the maintenance of LTP in excitatory transmission in the LS. It is conjectured that the effects of VP on LS neurons are related to the role of the peptide in the maintenance of LTP and that these processes play a role in memory formation.

Effects of changes in glucose concentration on synaptic plasticity in hippocampal slices.

The effects of a low or high concentration of glucose in the perfusion medium on synaptic activity and plasticity were studied in hippocampal slices from rats. Low-glucose medium depressed the field excitatory post-synaptic potentials (fEPSP) significantly, whereas high-glucose medium had little effect on the fEPSP. Tetanization of the afferent fibres elicited significant potentiation (LTP) of synaptic activity irrespective of the glucose concentration in the medium. This may indicate that LTP induction does not depend on optimal neural transmission. Paired-pulse facilitation (PPF) experiments showed that the medium glucose concentration did not significantly influence potentiation of the second response.

N-acetyl-aspartylglutamate: binding sites and excitatory action in the dorsolateral septum of rats.

In this study we examined the distribution of binding sites for [3H]N-acetyl-aspartylglutamate (NAAG) in the rat lateral septal nucleus (LSN) and the effect of iontophoretically applied NAAG on neuronal firing in this area. A high density of [3H]NAAG binding sites was found in the dorsolateral part of the LSN. Binding in the intermediate/ventral part of the LSN and medial septum was less dense. NAAG excited 75% of the dorsal neurons in the LSN, but only 36% of the cells in the intermediate/ventral part. Glutamic diethylester, an amino acid antagonist, depressed responses to NAAG to a similar extent as responses to quisqualate. The antagonist amino phosphonovaleric acid, which suppressed responses to N-methyl-D-aspartate almost completely, reduced NAAG-evoked responses only by 40%. A possible role of NAAG as excitatory transmitter in the LSN is discussed.

Water maze learning and hippocampal synaptic plasticity in streptozotocin-diabetic rats: effects of insulin treatment.

Streptozotocin-diabetic rats express deficits in water maze learning and hippocampal synaptic plasticity. The present study examined whether these deficits could be prevented and/or reversed with insulin treatment. In addition, the water maze learning deficit in diabetic rats was further characterized. Insulin treatment was commenced at the onset of diabetes in a prevention experiment, and 10 weeks after diabetes induction in a reversal experiment. After 10 weeks of treatment, insulin-treated diabetic rats, untreated diabetic rats and non-diabetic controls were tested in a spatial version of the Morris water maze. Next, hippocampal long-term potentiation (LTP) was measured in vitro. To further characterize the effects of diabetes on water maze learning, a separate group of rats was pre-trained in a non-spatial version of the maze, prior to exposure to the spatial version. Both water maze learning and hippocampal LTP were impaired in diabetic rats. Insulin treatment commenced at the onset of diabetes prevented these impairments. In the reversal experiment, insulin treatment failed to reverse established deficits in maze learning and restored LTP only partially. Non-spatial pre-training abolished the performance deficit of diabetic rats in the spatial version of the maze. It is concluded that insulin treatment may prevent but not reverse deficits in water maze learning and LTP in streptozotocin-diabetic rats. The pre-training experiment suggests that the performance deficit of diabetic rats in the spatial version of the water maze is related to difficulties in learning the procedures of the maze rather than to impairments of spatial learning.

Long-lasting enhancement of synaptic excitability of CA1/subiculum neurons of the rat ventral hippocampus by vasopressin and vasopressin(4-8).

Vasopressin (VP) is axonally distributed in many brain structures, including the ventral hippocampus. Picogram quantities of VP injected into the hippocampus improve the passive avoidance response of rats, presumably by enhancing memory processes. Vasopressin is metabolized by the brain tissue into shorter peptides, such as [pGlu4,Cyt6]VP(4-9) and [pGlu4,Cyt6]VP(4-8), which preserve the behavioral activity but lose the peripheral activities of the parent hormone. Using brain slices, we investigated whether VP or VP(4-8) affects excitatory postsynaptic potentials (EPSPs) and/or membrane responses to depolarization in neurons of the CA1/subiculum of the ventral hippocampus. The EPSPs were evoked by stimulating the striatum radiatum of the CA1 field; the membrane responses were elicited by current injections. Exposure of slices for 15 min to 0.1 nM solution of these peptides resulted in an increase in the amplitude and slope of the EPSPs in 21 neurons (67%) tested. No consistent change in either the resting membrane potential or the input resistance of the neurons was observed. The peptide-induced increase in EPSPs reached a maximum 30-45 min after peptide application. In 14 of these neurons (66%), the peptide-induced increase in EPSPs remained throughout the entire 60-120 min washout period. In the remaining 7 neurons (33%), the initial increase in EPSPs amplitude was followed by a gradual decline to the pre-administration level. The increase in EPSP amplitude was often, but not always, associated with a decrease in the threshold and increase in the number of action potentials in response to depolarizing current injection. Suppression of GABAA receptor-mediated inhibition and N-methyl-D-aspartate (NMDA) receptor-mediated excitation did not prevent the effects of VP and VP(4-8) on the EPSP amplitude or the threshold for action potentials. The results demonstrate that 0.1 nM concentrations of these neuropeptides can elicit a long-lasting enhancement of the excitability of CA1/subiculum neurons of the ventral hippocampus to excitatory, glutamatergic synaptic input. This novel action of VP and its metabolite in the ventral hippocampus may be the physiological action, mediating the memory-enhancing effect of these peptides.