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P Balaban

Publications and source records attributed to P Balaban.

9 recordsLinked to original sources
PubMed2001

Decrease of effectivity of "competing" synaptic input requires protein synthesis.

We describe that tetanus-induced long-term increase of the response amplitude in one input to an identified neuron is accompanied by a decrease of synaptic responses in another, non-tetanized input. Induction of the decrease of responses in non-tetanized inputs was prevented by bath application of protein synthesis blockers (anisomycin or cycloheximide). The decrease of responses also did not occur in experiments when tetanization was substituted by short-term serotonin applications or extracellular stimulation of serotonergic cells known to potentiate investigated synaptic inputs. The results suggest that the heterosynaptically evoked decrease of synaptic response amplitude may be due to involvement of postsynaptic protein synthesis-dependent mechanisms.

Action Potentials↗
PubMed2000

Retrograde signalling with nitric oxide at neocortical synapses.

Long-term changes of synaptic transmission in slices of rat visual cortex were induced by intracellular tetanization: bursts of short depolarizing pulses applied through the intracellular electrode without concomitant presynaptic stimulation. Long-term synaptic changes after this purely postsynaptic induction were associated with alterations of release indices, thus providing a case for retrograde signalling at neocortical synapses. Both long-term potentiation and long-term depression were accompanied by presynaptic changes, indicating that retrograde signalling can achieve both up- and down-regulation of transmitter release. The direction and the magnitude of the amplitude changes induced by a prolonged intracellular tetanization depended on the initial properties of the input. The inputs with initially high paired-pulse facilitation (PPF) ratio, indicative of low release probability, were most often potentiated. The inputs with initially low PPF ratio, indicative of high release probability, were usually depressed or did not change. Thus, prolonged postsynaptic activity can lead to normalization of the weights of nonactivated synapses. The dependence of polarity of synaptic modifications on initial PPF disappeared when plastic changes were induced with a shorter intracellular tetanization, or when the NO signalling pathway was interrupted by inhibition of NO synthase activity or by application of NO scavengers. This indicates that the NO-dependent retrograde signalling system has a relatively high activation threshold. Long-term synaptic modifications, induced by a weak postsynaptic challenge or under blockade of NO signalling, were nevertheless associated with presynaptic changes. This suggests the existence of another retrograde signalling system, additional to the high threshold, NO-dependent system. Therefore, our data provide a clear case for retrograde signalling at neocortical synapses and indicate that multiple retrograde signalling systems, part of which are NO-dependent, are involved.

Animals↗
PubMed1999

NMDA receptor blockade prevents LTD, but not LTP induction by intracellular tetanization.

Intracellular tetanization, the activation of a postsynaptic cell without concomitant presynaptic stimulation, was applied to layer II/III pyramidal cells in slices of rat visual cortex. In standard extracellular medium, intracellular tetanization led to LTP (21 of 43 inputs) or LTD (14 of 43 inputs), the direction of the amplitude change depending on initial paired-pulse facilitation (PPF) ratio: inputs with high initial PPF ratio were usually potentiated, and inputs with initially low PPF were most often depressed or did not change. When applied during blockade of NMDA receptors (50 microM APV), intracellular tetanization failed to induce LTD, but was still capable of inducing LTP (14 of 26 inputs). Although LTP could occur in inputs with both, low and high initial PPF ratio, the correlation between the amplitude change and initial PPF ratio remained: potentiation was stronger in inputs with initially higher PPF. These data suggest that intracellular tetanization activated simultaneously NMDA receptor-dependent LTD mechanisms and NMDA receptor-independent LTP mechanisms, the final change of synaptic gain depending on their balance.

2-Amino-5-phosphonovalerate↗
PubMed1999

Interaction between intracellular tetanization and pairing-induced long-term synaptic plasticity in the rat visual cortex.

Long-term changes in synaptic transmission in slices of rat visual cortex were induced either by pairing the excitatory postsynaptic potentials with postsynaptic depolarization or by intracellular tetanization without synaptic stimulation. Changes in the excitatory postsynaptic potential amplitude induced by any of the protocols applied in isolation persisted for longer than 1 h. Pairing-induced long-term potentiation was input specific. We studied the interaction between intracellular tetanization and pairing-induced plasticity by applying the two protocols one after the other at 10-min intervals. The pairing procedure applied after intracellular tetanization did not lead to any further potentiation, but to a depotentiation of the potentiated inputs. A second pairing protocol applied 10 min later led to further depotentiation, while previously unaffected inputs became weakly depressed. If intracellular tetanization was applied after the pairing procedure, the synaptic responses did not change immediately, but a slow return of the excitatory postsynaptic potential amplitude to the control level could be observed. Therefore, intracellular tetanization is not capable of inducing further potentiation after pairing, and pairing cannot further potentiate the inputs which have already been potentiated by intracellular tetanization. The maintenance of long-term potentiation induced by any of the protocols was impaired by successive application of another procedure. These results suggest a similarity of the mechanisms of synaptic changes induced by the two protocols and demonstrate that the direction of synaptic gain change depends on the history of the synapse.

Action Potentials↗
PubMed1997

Dependence of synaptic facilitation postsynaptically induced in snail neurones on season and serotonin level.

The problem of stability of long-lasting synaptic facilitation postsynaptically induced by intracellular current pulses without concomitant presynaptic activation was addressed. A short (15-20 min) phase of synaptic facilitation induced by intracellular tetanization in identified snail neurones was stable and present in all experiments, while a long-term phase (lasting > or = 50 min) was observed only some experiments. Data analysis revealed dependence of the long-term phase on season. Dependence of the long-term phase of facilitation on serotonin concentration in hemolymph, which is known to change with season, was shown using the selective neurotoxin 5,7-dihydroxytriptamine. Dependence of habituation rate in the same synaptic connection on season and serotonin level was shown.

Animals↗
PubMed1993

Long-term sensitization and environmental conditioning in terrestrial snails.

The hypothesis that a long-term increase of behavioural responses in snails (over a period of days) might be due to environmental conditioning was examined. Training consisted of delivering electric shocks non-contingently with test stimuli twice per day for 5 days to freely moving snails on a ball floating in water. After training, a significant difference in amplitude of a withdrawal reaction to tactile test stimulation appeared between shocked and control snails. Responses were significantly facilitated in shocked animals for up to 12 days after training, but only if the animals were tested in the environment used for training. Testing of the same groups of animals crawling freely on the glass lid of a tank in which they lived between experimental sessions revealed no difference in responses to the same stimuli between shocked and control snails. Injection of the neurotoxin 5,7-dihydroxytryptamine, which selectively impairs serotonergic cells, eliminated the differences between shocked and control animals. Changing the pH of the water in which the ball floated, by addition of citric acid, led to a significant selective increase of responsiveness in snails sensitized in this environment relative to the responsiveness of the same snails with normal water in the tank. The results suggest that the long-term sensitization of withdrawal reactions observed is at least in part a manifestation of an associative process, namely environmental conditioning.

5,7-Dihydroxytryptamine↗
PubMed1993

Serotonergic input on identified command neurons in Helix.

In Helix, serotonin evokes long-lasting alteration of activity of withdrawal triggering neurons. Cell bodies of these neurones are surrounded by a dense network of serotonin-containing fibres without any synaptic membrane specializations, which confirm the suggestion on the non-synaptic, modulatory action of serotonin on the withdrawal command elements.

Animals↗
PubMed1992

He-Ne laser irradiation of single identified neurons.

Silent (LPa2 and LPa3) and spontaneously active (V3, V5, V17) neurons of subesophageal ganglia of Helix pomatia were irradiated via a 125-mm fiber probe with a 10-mW He-Ne laser (lambda = 632.8 nm), and the rate of membrane depolarization, duration of latent period, and probability of spike activity were measured as the functions of light intensity. It was found that silent neurons can not be activated by He-Ne laser irradiation. When the spontaneously active neurons generating spikes every 7-10 min were irradiated in between their spontaneous spikes, the depolarization of membrane and generation of action potentials occurred as a function of light intensity, I. The probability of spike generation increased until the intensity reached 1 W/cm2, and when I = 4 W/cm2 was equal to 1. The depolarization of the membrane had a threshold at I = 0.1 W/cm2, then increased with increasing the intensity, and reached a plateau at I = 0.7 W/cm2 (depolarization rate 0.18 mV/s). Duration of the latent period decreased from 28 s to 17 s when the intensity was increased from 0.05 to 0.3 W/cm2. Further increase of the light intensity, from 0.3 to 1.5 W/cm2, caused a less pronounced change in the duration of the latent period (e.g., latent period equal to 11 s at I = 1.5 W/cm2).

Action Potentials↗