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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 GABAA 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 PD 98059. 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.
EN
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 ranking 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.
EN
The influence of compounds interacting with cholinergic systems on field potentials evoked in layer II/III horizontal connections was investigated in rat motor cortex in vitro. The cholinesterase inchibitor eserine (10 mM) decreased field responses by 20?2%. This inhibito effect could be prevented by preincubation with atropine (10 mM) Application of 5 mM carbachol resulted in reduction of the responses by 30?1% These reductions were reversible, repeatable and independent of stimulus intensity; they could be blocked by the M1 muscarinic receptor antagonist pirenzepine (3 mM) but not by the M2 ,muscarinic receptor antagonist gallamine (10 mM). During carbachol application, paired-pulse facilitation (40 ms interpulse interval) was increased. The results indicate that endogenous acetylcholine may modulate excitatory synaptic transmission in horizontal connections of rat motor cortex, most likely by acting upon M1 receptors located presynaptically on glutamatergic terminals, and may contribute both to information processing and synaptic plasticity within the motor cortex
EN
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.
EN
Certain antidepressant medications exert effects on the serotonergic (5-HT) syste but their machanisms 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.
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