The effect of microiontophoretically applied vasopressin and oxytocin on single neurones in the septum and dorsal hippocampus of the rat

When arginine8-vasopressin (AVP) or oxytocin (OXT) were applied microiontophoretically to neurones in the lateral septal complex and dorsal hippocampus of rats, more than 50% of the neurones responded with excitation. The remaining neurones were not affected by AVP or OXT. Both the AVP- and OXT-induced responses displayed a short latency in onset and offset. Medial septal neurones were almost never excited by AVP or OXT. In more than 50% of the lateral septal and hippocampal neurones, the responses to glutamate were enhanced during the iontophoretic release of AVP or OXT. The possible role of both peptides as neurotransmitters in the structures examined is discussed

Arginine8-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 arginine8-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--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 septum by fi-fx stimuli. The possible physiological significance of these findings is discussed

Amino acid neurotransmission between fimbria-fornix fibers and neurons in the lateral septum of the rat: A microiontophoretic study

We investigated the nature of the excitatory amino acid and the type of amino acid receptor involved in the projection of fimbria-fornix (fi-fx) fibers on neurons in the lateral septal complex (LSC) of the rat. It appeared that neurons which were strongly orthodromically activated (SOA) by stimulation of fi-fx fibers were excited by glutamate (GLU) and aspartate (ASP) at much lower ejecting currents than neurons which were only weakly orthodromically excited. In addition, GLU was a stronger agent than ASP, particularly in SOA septal cells. Two amino acid antagonists tested, glutamic acid diethylester (GDEE) and 2-amino-5-phosphonovaleric acid (2-APV), selectively antagonized responses to the amino acid agonists quisqualate (QUIS) and N-methyl--aspartate (NMDA), respectively. They also depressed GLU- and ASP-induced responses, although in that case the antagonists frequently had to be expelled with currents higher than those needed to block QUIS- and NMDA-evoked excitations. Furthermore, GDEE frequently antagonized GLU-induced responses better than ASP-evoked excitations, whereas 2-APV often blocked responses to ASP more effectively than those to GLU. It was observed that GDEE, ejected with currents that blocked responses to QUIS reversibly, decreased the number of synaptic responses induced in SOA cells by fi-fx stimuli. Synaptically induced excitation in these neurons was consistently unaffected by 2-APV, even when the antagonist was expelled with high currents. According to these results, LSC neurons, in particular the SOA neurons, are more readily activated by GLU than by ASP. Monosynaptic excitations elicited in SOA septal cells by fi-fx stimuli appear to be predominantly if not exclusively mediated by QUIS receptors. There are indications that GLU-induced responses in the LSC neurons are presumably mediated by the QUIS receptors. From these data it may be inferred that GLU rather than ASP is the transmitter involved in the projection of fi-fx fibers on LSC neurons

Amino acid neurotransmission between fimbria-fornix fibers and neurons in the lateral septum of the rat: A microiontophoretic study

We investigated the nature of the excitatory amino acid and the type of amino acid receptor involved in the projection of fimbria-fornix (fi-fx) fibers on neurons in the lateral septal complex (LSC) of the rat. It appeared that neurons which were strongly orthodromically activated (SOA) by stimulation of fi-fx fibers were excited by glutamate (GLU) and aspartate (ASP) at much lower ejecting currents than neurons which were only weakly orthodromically excited. In addition, GLU was a stronger agent than ASP, particularly in SOA septal cells. Two amino acid antagonists tested, glutamic acid diethylester (GDEE) and 2-amino-5-phosphonovaleric acid (2-APV), selectively antagonized responses to the amino acid agonists quisqualate (QUIS) and N-methyl--aspartate (NMDA), respectively. They also depressed GLU- and ASP-induced responses, although in that case the antagonists frequently had to be expelled with currents higher than those needed to block QUIS- and NMDA-evoked excitations. Furthermore, GDEE frequently antagonized GLU-induced responses better than ASP-evoked excitations, whereas 2-APV often blocked responses to ASP more effectively than those to GLU. It was observed that GDEE, ejected with currents that blocked responses to QUIS reversibly, decreased the number of synaptic responses induced in SOA cells by fi-fx stimuli. Synaptically induced excitation in these neurons was consistently unaffected by 2-APV, even when the antagonist was expelled with high currents. According to these results, LSC neurons, in particular the SOA neurons, are more readily activated by GLU than by ASP. Monosynaptic excitations elicited in SOA septal cells by fi-fx stimuli appear to be predominantly if not exclusively mediated by QUIS receptors. There are indications that GLU-induced responses in the LSC neurons are presumably mediated by the QUIS receptors. From these data it may be inferred that GLU rather than ASP is the transmitter involved in the projection of fi-fx fibers on LSC neurons

Electroencephalographic changes in the lateral septum complex following systemic administration of DES-TYR1 -[alpha]-endorphin, Des-Tyr1-[gamma]-endorphin and haloperidol in rats

The influence of systemically administered Des-Tyr1-α-endorphin (DTαE), Des-Tyr1-γ-endorphin (DTγE) and haloperidol on electroencephalographic (EEG) activity of the lateral septum complex (LSC) and the frontal cortex was studied in male rats. DTαE (2 μg) significantly increased whereas DTγE (10 μg) significantly decreased the amounts of activity in the 5 Hz band. In addition, DTαE promoted production of 15 - 20 Hz activity, while DTγE decreased the amount of 20 - 30 Hz activity. EEG activity exhibited a marked variability which persisted throughout the recording session following administration of the peptides. Haloperidol markedly decreased the proportion of 10 - 15 Hz activity. The alterations in EEG of the frontal cortex were similar to those in LSC but less pronounced. The differences in the time course and frequency bands affected suggest that the effects of peptides and haloperidol on EEG activity of LSC are not mediated by the same mechanisms

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--aspartate receptor-dependent long-term potentiation in the CA1-field, to extend these findings to N-methyl--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--aspartate receptor-dependent long-term potentiation was impaired in the CA1-field and dentate gyrus and expression of N-methyl--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

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