Biomedical subjects

K G Reymann

Publications and source records attributed to K G Reymann.

117 records · Page 7Linked to original sources

PubMed1985

Effects of beta-casomorphin on dentate hippocampal field potentials in freely moving rats.

Intracerebroventricular administration of 166 nmoles of the exogenic opioid beta-casomorphin (5) produced a potent and reversible depression of the compound action potential evoked in dentate granule cells by stimulation of the medial perforant path, whereas the extracellularly recorded excitatory postsynaptic potential is left unchanged. This in vivo effect of beta-casomorphin was obviously different from those observed previously in the CA 1 region in hippocampal slice experiments. The results suggest that more than one opioid mechanism determines the granule cell excitability. Some of the possible mechanisms involved in the effects of beta-casomorphins in the hippocampus are briefly discussed.

Animals↗

PubMed1983

Footshock-induced modification of a monosynaptic evoked potential in the hippocampus.

Parameters of dentate gyrus field potentials evoked by stimulation of the perforant path were studied in freely moving rats before and after repeated footshock application. An increase of population-EPSP steepness and a shortening of population spike latency was demonstrated immediately after the footshocks. These results indicate control for variables in behavior should be included in studies of monosynaptic potentials.

Animals↗

PubMed1982

Monosynaptic activation of the hippocampus as a conditioned stimulus: behavioral effects.

The aim of the present study with rats was to show that electrical stimulation of a monosynaptic pathway, whose high plastic potency is well-known, can serve as a conditioned stimulus (CS) in a learning paradigm. Using chronic rats, stimulation of the perforant pathway, which activates the entorhinal cortex input to the dentate gyrus of the hippocampus, was used as the CS in a footshock motivated two-way avoidance task (shuttle box). Among the different stimulation parameters tested, only trains of at least 15 Hz were shown to be effective as a CS, whereas the application of single impulses with a frequency of 1,7 Hz did not result in the establishment of conditioned behavior. Using the 15 Hz-paradigm, in "good learners," the development of reliable conditioned responses started at the end of the first training session (40 trials) and become fairly stable during a further training session, given on the following day. The application of stimulation trains with 100 Hz as a CS led to the development of a high rate of conditioned responses, however, there was also a high level of intertrial reactions. Considering the critical importance of the frequency parameters of the perforant pathway stimulation for the development of conditioned behavior the possible involvement of hippocampal long-term potentiation in behavioral plasticity is discussed. Additionally, it is concluded that this new learning paradigm offers the advantage of concurrent analysis of plastic processes both at the behavioral level and at the level of the synaptic population.

Animals↗

PubMedDate not supplied

Effects of deprolorphin, a casomorphin analog, on hippocampal CA1 field potentials in vitro.

The effects of infusion of low concentrations of the synthetic opioid peptide D-Pro4-beta-casomorphin-5(deprolorphin) on electrical field responses in the in vitro hippocampal slice preparation of mice were investigated. Deprolorphin (0.01-10 microM) causes a large enhancement of the population spike (PS) and appearance of additional spikes of CA1 pyramidal cells to Schaffer-commissural stimulation, which were partially antagonized by the opiate receptor antagonist naloxone. It is likely that this analgesic peptide in the hippocampus acts through mu-receptors and neuronal mechanisms already described for morphine and enkephalin analogs.

Animals↗

PubMedDate not supplied

Neuronal transmission of hippocampal CA1 neurones is modulated by corticotropin-like intermediate lobe peptide [CLIP; ACTH(18-39)].

The study was conducted to test whether CLIP [ACTH(18-39)] influences the neuronal transmission and the induction of long-term potentiation (LTP) in the hippocampus. The population spike was recorded in the hippocampal CA1 region of freely moving rats before and after intracerebroventricular (ICV) administration of CLIP in comparison to ACTH and saline (controls). After infusion of CLIP, the population spike amplitude (PSA) rose to about 200% of baseline values. After reaching this level, it was impossible to induce a further increase of PSA by tetanization. However, if the stimulus intensity was reduced to a new baseline level, electrically induced LTP could be observed. There were no significant changes after infusion of ACTH. Our results indicate that the ICV administration of CLIP leads to an enhancement of excitability in the hippocampal CA1 region, which might be independent of LTP.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Group 1 metabotropic glutamate receptors contribute to slow-onset potentiation in the rat CA1 region in vivo.

It has been demonstrated in the CA1 region of the hippocampus in vitro, and in the dentate gyrus and CA1 region in vivo, that application of the metabotropic glutamate receptor (mGluR) agonist, 1S, 3R-amino cyclopentane 2,3-dicarboxylic acid triggers a slow-onset potentiation of synaptic transmission in the hippocampus. This study examined the involvement of group 1 and 2 mGluRs in this phenomenon in the CA1 region of freely moving rats. Drugs were applied via the lateral cerebral ventricle, and measurements were obtained from the CA1 region via permanently implanted electrodes. The group 1 mGluR agonists, 3,5-dihydroxyphenylglycine (DHPG, 20-100 nmol/5 microl) and trans-azetidine-2,4-dicarboxylic acid (ADA, 100 nmol-1 micromol/5 microl) induced a dose-dependent potentiation of basal synaptic transmission. The mGluR antagonist R,S-alpha-methyl-carboxyphenylglycine (MCPG, 1 micromol), and the group 1 mGluR antagonist, S-4-carboxyphenylglycine (4CPG, 100 nmol) completely inhibited the effects of both DHPG and ADA. The group 2 mGluR agonist, (S)-4-carboxy-3-hydroxy phenylglycine (4C3H-PG, 50-200 nmol/5 microl) induced a dose-dependent decrease of basal synaptic transmission. These results suggest that in the CA1 region in vivo, slow-onset potentiation may be mediated by group 1 mGluRs.

Animals↗

PubMedDate not supplied

Metabotropic glutamate receptors in spatial and nonspatial learning in rats studied by means of agonist and antagonist application.

We examined the effects of both the metabotropic glutamate receptor (mGluR) antagonist MCPG and the agonist tADA in two behavioral paradigms in rats: (1) brightness discrimination and (2) spatial alternation. Compounds were applied intracerebroventricularly at different times, either 30 min prior to training or immediately after training, and rats were tested for retention 24 hr later in the same paradigms. Both MCPG and tADA caused amnesia in the spatial alternation test, when applied pretraining, but no effect was obtained in the brightness discrimination paradigm. Drug-induced amnesia was shown not to be attributable to state-dependent effects of MCPG or tADA. Moreover, the memory inhibiting effect of MCPG was dose dependent, with a low dose (20 mM/5 ml) having no effect on learning and memory and a 10 times higher concentration (200 mM/5 ml) causing complete amnesia. Application of both saline and MCPG immediately post-training prevented memory formation, which may be attributable to an interference by the injection procedure with the process of memory formation. The mGluR agonist tADA, however, facilitated memory formation in the spatial alternation task, when injected immediately after training. Post-training application of the compounds had no effect on retention in the brightness discrimination task. On the basis of these data we conclude that (1) mGluRs are of particular importance for spatial learning and play no role in visual discrimination; (2) both the block and the activation of mGluRs inhibit spatial learning, suggesting that saturated activation prevents further modulation of mGluRs, which may be required during learning or memory formation; and (3) mGluR agonist tADA may be memory facilitating when applied after training, thus enhancing the establishment of the memory trace.

Animals↗

PubMedDate not supplied

A specific role for group I mGluRs in hippocampal LTP and hippocampus-dependent spatial learning.

Metabotropic glutamate receptors (mGluRs) have been implicated in long-term potentiation and in learning and memory formation. In this study, we tested the effects of group I mGluR inhibition on synaptic plasticity and learning of rats at different levels of organization (1) in the hippocampal slice preparation; (2) in freely moving animals implanted with chronic hippocampal electrodes; and (3) in different spatial learning paradigms. To allow a direct comparison of the effects obtained the same doses were used in all paradigms. Bath-application of the selective group I mGluR antagonist (S)4-carboxyphenylglycine (4-CPG) impaired a decremental long-term potentiation (LTP) induced by a weak tetanization paradigm, but failed to affect a robust LTP generated by strong tetanization. In contrast, 4-CPG impaired a robust LTP in freely moving animals if applied 30 min before tetanization. The same dose of 4-CPG only impeded spatial learning mildly in the eight-arm radial maze and had no effect on a simple configuration of the Y-maze spatial alternation task. In the more difficult configuration of this task, however, 4-CPG caused complete amnesia. The lack of state-dependent 4-CPG actions and the absence of any 4-CPG effects in the open-field test classify the obtained retention deficit as a selective impairment of memory storage. Our results indicate a specific role of group I mGluRs in certain types of synaptic plasticity and of spatial learning.

Animals↗

PubMedDate not supplied

[Long-term potentiation and unit evoked responses in the cingulate cortex of freely moving rats].

Long-term potentiation (LTP) of synaptic efficacy is considered to be the most probable physiological mechanism of long-term memory. However, lack of understanding of cellular and subcellular mechanisms of LTP induction in freely behaving animals does not correspond to the importance of the problem. It was tested whether the characteristics of potentiation in the cingulate cortex after tetanization of the subiculocingulate tract (SCT) meet the criteria of true LTP (that passes all known stages in its development and lasts for more than a day in freely-behaving animals). Additionally, characteristics of spike responses to SCT stimulation and the effects of application of different glutamate receptor blockers were studied. Without application of GABA receptor blockers, the LTP lasted for more than 24 hours. Application of NMDA glutamate receptor blockers significantly inhibited field potentials evoke by testing stimulation. Short-latency spike responses to SCT stimulation were recorded with low probability that increased with stimulation intensity. The obtained data reveal the possibility to compare the involvement of cingulate neurons in acquisition of adaptive behavior and changes in their spike responses during the LTP development in freely-moving rats.

2-Amino-5-phosphonovalerate↗