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Grzegorz Hess

Publications and source records attributed to Grzegorz Hess.

13 recordsLinked to original sources

Imipramine treatment ameliorates corticosterone-induced alterations in the effects of 5-HT1A and 5-HT4 receptor activation in the CA1 area of rat hippocampus.

This study tested whether imipramine reverses adaptive modifications in the function of hippocampal 5-HT1A and 5-HT4 receptors induced by repetitive administration of corticosterone. Rats received corticosterone for 1 or 3 weeks or imipramine for 2 weeks. The fourth experimental group was treated with corticosterone for 3 weeks and additionally with imipramine, beginning on the eighth day of corticosterone administration. Hippocampal slices were prepared 48 h after the last drug administration. 5-HT1A and 5-HT4 receptor-mediated effects on CA1 population spike amplitude were measured. While repeated corticosterone attenuated the inhibitory effect of 5-HT1A receptor activation by 8-OH-DPAT and enhanced the excitatory effect of 5-HT4 receptor activation by zacopride, imipramine treatment of naïve rats resulted in opposite changes. In the corticosterone plus imipramine group, the effect of 8-OH-DPAT and zacopride were not different from control, indicating that corticosterone-induced adaptive changes in the reactivity of 5-HT1A and 5-HT4 receptors were reversed by imipramine treatment.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Repeated administration of citalopram and imipramine alters the responsiveness of rat hippocampal circuitry to the activation of 5-HT7 receptors.

The effects of a selective serotonin reuptake inhibitor, citalopram, and a tricyclic antidepressant drug, imipramine, administered repetitively for 14 days, were investigated ex vivo in rat hippocampal slices. Spontaneous epileptiform bursts were recorded from the CA3 area in nominally Mg(2+)-free incubation conditions. 5-carboxamidotryptamine (5-CT) dose-dependently increased bursting frequency in the presence of N-[2-[4-(2-methoxyphenyl)-1 piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide (WAY 100635). This effect could be dose-dependently blocked by (2R)-1-[(3-Hydroxyphenyl)sulfonyl]-2-[2-(4-methyl-1-piperidinyl)ethyl]pyrrolidine hydrochloride (SB 269970), thus implicating the involvement of 5-HT(7) receptors. Repeated treatment with citalopram or imipramine resulted in an attenuation of the excitatory effects of the activation of hippocampal 5-HT(7) receptor.

Analysis of Variance↗

Effects of sensory learning on intracortical synaptic transmission in the barrel cortex of mice.

Pairing tactile stimulation of a row of whiskers with a tail shock results in an expansion of the functional representation of the stimulated whiskers within the primary somatosensory cortex of mice. Using the same paradigm, the present study examined field potentials evoked in ex vivo slices of the barrel cortex. The amplitude of responses, evoked by single and repetitive stimuli in layer IV-layer II/III pathway contained within the barrel column corresponding to the whisker stimulated during training, was unchanged. In contrast, in a transcolumnar pathway from the "trained" barrel to layer II/III of the neighboring, "untrained" column, the amplitude of responses was reduced and responses to trains of stimuli applied at 40 Hz, but not at lower frequencies, depressed faster. These data are suggestive of a selective weakening of excitatory transmission and/or enhancement of inhibitory transmission in transcolumnar pathways, which accompany associative learning-induced cortical plasticity.

Afferent Pathways↗

Chemically-induced long-term potentiation in rat motor cortex involves activation of extracellular signal-regulated kinase cascade.

The involvement of the extracellular signal-regulated kinase 1/2 (ERK1/2) cascade in long-lasting potentiation of synaptic transmission, induced by tetraethylammonium (TEA) or by elevated extracellular calcium concentration, was investigated in layer V horizontal connections within motor cortex in rat brain slices. Brief application of TEA (25 mM) resulted in a long-lasting potentiation of field potentials by 54+/-12%. A transient exposure of slices to elevated extracellular calcium (5 mM) induced long-lasting potentiation of responses reaching 30+/-8%. The induction of both forms of potentiation was prevented by the exposure of slices to inhibitors of the upstream activator of ERK 1/2, MEK (ERK kinase), U0126 (20 microM) and PD 98059 (50 microM). PhosphoERK2 immunoreactivity was transiently increased above baseline levels 15 min after termination of the exposure of slices to either TEA or elevated calcium concentration. Both forms of potentiation were partially occluded by Sp-adenosine 3',5'-cyclic monophosphorothioate triethylammonium salt (Sp-cAMPS; 100 microM), an activator of cAMP-dependent protein kinase (PKA), and they were blocked after preincubation with Rp-adenosine 3',5'-cyclic monophosphorothioate triethylammonium salt (Rp-cAMPS; 100 microM), a specific inhibitor of PKA activation by cAMP. It has previously been shown that TEA-induced potentiation represents a N-methyl-d-aspartate (NMDA) receptor-independent form of persistent synaptic enhancement, and, on the contrary, calcium-induced potentiation depends on NMDA receptors. Thus, the activation of PKA and the ERK1/2 cascade are required for two forms of chemically induced long-lasting increases of synaptic efficacy in slices of rat motor cortex.

Animals↗

Synaptic plasticity of local connections in rat motor cortex.

This paper reviews studies that investigated mechanisms of the induction of long-term synaptic efficacy increase in local horizontal connections in slices of adult rat motor cortex. Long-term potentiation (LTP) could be induced by electrical stimulation of afferents using theta burst stimulation (TBS) conditionally, when synaptic inhibition was transiently blocked by focal application of GABA(A) receptor antagonist. Robust, long-lasting enhancement of synaptic transmission in horizontal connections was induced by brief application of the potassium channel blocker, tetraethylammonium (TEA, 25 mM), to the incubation medium. This TEA-LTP could be blocked by nifedipine, a voltage-dependent calcium channel blocker. A transient exposure of slices to elevated extracellular calcium (5 mM) resulted in a long-lasting enhancement of responses, termed Ca-LTP, which could be blocked by the antagonist of NMDA receptors, APV. The induction of both TEA-LTP and Ca-LTP, could be prevented by inhibitors of the extracellular signal regulated kinase (ERK) cascade U0126 and PD98059. A transient activation of the ERK, 15 min after application of TEA or elevated [Ca2+], was demonstrated using immunofluorescence. Both forms of plasticity could also be prevented by the inhibitor of cAMP-dependent protein kinases (PKA), Rp-cAMPS. These studies indicate the involvement of the ERK and PKA signaling mechanisms in synaptic plasticity of the motor cortex in vitro. Since LTP in horizontal connections of the motor cortex has previously been shown to be related to the acquisition of a motor skill, it is suggested that the ERK and PKA signaling pathways may be involved in motor learning.

Animals↗

5-HT7 receptors increase the excitability of rat hippocampal CA1 pyramidal neurons.

In the CA1 area of rat hippocampal slices, a combined application of 5-CT, a potent 5-HT(1A) and 5-HT(7) receptor agonist, and WAY 100635, a selective 5-HT(1A) receptor antagonist, resulted in a reversible increase of the CA1 extracellular population spike amplitude. In whole-cell recording from identified pyramidal neurons, the effects of 5-CT applied in the presence of WAY 100635 involved a reduction of the slow afterhyperpolarization (sAHP) and the frequency adaptation of action potential firing, which could be blocked by a specific 5-HT(7) receptor antagonist SB 269970. The results indicate that the activation of 5-HT(7) receptors increases the excitability of hippocampal CA1 pyramidal cells.

Action Potentials↗

Adaptive changes in the reactivity of 5-HT1A and 5-HT2 receptors induced in rat frontal cortex by repeated imipramine and citalopram.

Using extracellular ex vivo recording we studied changes in the reactivity of rat frontal cortical neurons to the 5-HT(1A), 5-HT(2) and 5-HT(4) receptor agonists (+/-)-2-dipropyloamino-8-hydroxy-1,2,3,4-tetrahydronaphtalene hydrobromide (8-OH-DPAT), (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) and zacopride, respectively, induced by a repeated treatment with imipramine or citalopram. Rats were treated with imipramine or citalopram for 14 days (10 mg/kg p.o.) twice daily. Frontal cortical slices were prepared 2 days after the last drug administration. Spontaneous epileptiform discharges were induced in slices by perfusion with a medium devoid of Mg(2+) ions and with added picrotoxin (30 microM). While the application of 2 microM 8-OH-DPAT resulted in a reversible decrease of the discharge frequency, in the presence of DOI (1 microM) or zacopride (5 microM), the discharge frequency was increased. Both repeated imipramine and citalopram enhanced the effect of the activation of 5-HT(1A) receptor and attenuated the effect related to 5-HT(2) receptor activation, while the effect of the activation of 5-HT(4) receptor remained unchanged. Moreover, imipramine, but not citalopram, induced a reduction of epileptiform discharge frequency and an increase of the time of occurrence of epileptiform activity. These data indicate that antidepressants enhance the 5-HT-mediated inhibition in neuronal circuitry of the frontal cortex.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Comparison of the effects of 5-HT1A and 5-HT4 receptor activation on field potentials and epileptiform activity in rat hippocampus.

The effects of serotonin (5-HT) as well as 5-HT(1A) and 5-HT(4) receptor agonists, (+/-)-2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydronaphthalene hydrobromide (8-OH-DPAT) and zacopride, respectively, on population spikes evoked by electrical stimulation and on spontaneous epileptiform activity were investigated in CA1 area of hippocampal slices. Spontaneous epileptiform activity was recorded from slice in a nominally Mg(2+)-free medium. While 5-HT application resulted in a decrease of population spikes evoked in standard incubation conditions, in accordance with earlier studies, it exerted two opposite effects on epileptiform activity. The early inhibitory effect was mimicked by 8-OH-DPAT while the later, excitatory, by zacopride. The application of 8-OH-DPAT decreased, and that of zacopride increased, the amplitude of population spikes. A comparison of the dose-dependence of the excitatory and inhibitory effects of serotonergic agonists on the amplitude of the population spike and on the frequency of epileptiform discharges indicated that the latter is a more sensitive measure of the activation of 5-HT(1A) and 5-HT(4) receptors than the former. Thus, spontaneous epileptiform activity recorded in a nominally Mg(2+)-free slice medium represents a convenient model for investigation of hippocampal neuronal reactivity to the activation of various 5-HT receptor subtypes.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Calcium-induced long-term potentiation in horizontal connections of rat motor cortex.

A transient (10 min) exposure of brain slices of young adult rats to elevated extracellular calcium (5 mM) resulted in a long-lasting potentiation of field potentials evoked in layer II/III and layer V horizontal connections of the primary motor cortex. This form of synaptic plasticity was blocked by D,L-2-amino-5-phosphonovalerate (APV, 100 micro M), an antagonist of NMDA receptors.

Age Factors↗

Differential effects of repeated imipramine on hippocampal responsiveness to adenosine and serotonin.

Imipramine-induced enhancement of the inhibitory action of 5-HT(lA) receptor activation in hippocampal pyramidal neurons has been attributed to alterations in the transduction mechanism that involves G protein-dependent opening of K(+) channels. Postsynaptic 5-HT(lA) and adenosine Al receptors may share that transduction pathway. We investigated the influence of repeated imipramine administration on 5-HT(lA) and adenosine A1 receptor-mediated effects in rat hippocampal slices. Repeated imipramine selectively enhanced the postsynaptic effects of 5-HT(1A) receptor activation, including hyperpolarization and reduction of input resistance of neurons and reduction of the population spike amplitude. In contrast, after imipramine treatment only the presynaptic effect of adenosine receptor agonists, a decrease of the field excitatory postsynaptic potential, was enhanced. The data demonstrate that alterations in the presumed common transduction mechanism that was postulated for the 5-HT(lA) and adenosine A1 receptor-mediated activation of K(+) channels are not involved in the effect of repeated imipramine administration.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Long-term depression and long-term potentiation in horizontal connections of the barrel cortex.

Synaptic plasticity of horizontally orientated connections between barrels, in the barrel cortex of adult mice, was studied in slice preparations cut across rows of barrels. Field potentials were evoked in the middle of one barrel column (in layer IV or V) and recorded in the neighbouring barrel (in layer IV and V). In layer IV, long-term depression (LTD) by 26.5 +/- 5% was first induced by a low-frequency stimulation (2 Hz) applied for 10 min. After 30 min, theta-burst stimulation was delivered to previously depressed connections, resulting in long-term potentiation (LTP) by 28.8 +/- 11.8%. When theta-burst stimulation was delivered without an earlier low-frequency stimulation, no LTP was induced. Similar results were obtained in layer V connections (LTD: 40.6 +/- 12.5%; LTP: 26.9 +/- 12.5%). In layer IV, the application of 100 micro m d,l-2-amino-5-phosphonovaleric acid (APV), an antagonist of NMDA receptors, blocked the induction of both LTD and LTP. These experiments show that a potential for synaptic plasticity is retained in granular and infragranular layers of adult mice.

Animals↗

[Use of models for spontaneous paroxysmal activity in studies of adaptive changes in serotonin receptors].

Certain antidepressant medications exert effects on the serotonergic (5-HT) system but their mechanisms are still not well understood. Using extracellular ex vivo recording of spontaneous, epileptiform activity of neurons we determined changes in the reactivity of cortical and hippocampal slices to agonists of main subtypes 5-HT receptors, induced by repeated administration of the antidepressants. Repeated treatment with antidepressants enhances the 5-HT-mediated inhibition in both frontal cortex and hippocampal regions. Drugs administration induce opposite adaptive changes within 5-HT2 and 5-HT1A receptors in frontal cortex as well as in 5-HT1A and 5-HT4 receptors in the hippocampus. These effects may contribute to therapeutic effects of antidepressants administration.

Adaptation, Physiological↗

[Synaptic plasticity in the motor cortex].

Horizontally-oriented intracortical connections have been proposed to serve as a substrate for plastic reorganizations of adult motor cortex. N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) of synaptic efficacy is a candidate mechanism of these reorganizations in mammalian species ranging from rats to humans. The acquisition of a motor skill is accompanied by increased strength of synaptic connections within adult rat primary motor cortex, most likely due to LTP-like mechanisms.

Animals↗