Biomedical subjects

Stanislaw Glazewski

Publications and source records attributed to Stanislaw Glazewski.

3 recordsLinked to original sources

PubMed2003

The origin of cortical surround receptive fields studied in the barrel cortex.

The neocortex is thought to be organized into functional columns of neurons, each of which processes an element of a larger representation. In the barrel cortex, the thalamic input to the column preferentially terminates in a barrel. To study the extent and nature of functional connections between columns, we measured the degree to which whisker responses are relayed between columns in the barrel cortex. Inactivating a single barrel by iontophoresis of the GABA(A) agonist muscimol abolished the representation of that barrel's whisker in neighboring barrels. Reactivating a single barrel by iontophoresis of the GABA(A) antagonist bicuculline while the rest of the cortex was blocked by muscimol led to single whisker receptive fields. Under the same conditions, septal cells tended to exhibit multiwhisker receptive fields. These studies demonstrate that the surround receptive fields of barrel cells are generated by intracortical transmission and that many septal cells derive a component of their surround receptive field from the thalamus.

Anesthetics↗

PubMed2003

Neocortical long-term potentiation and experience-dependent synaptic plasticity require alpha-calcium/calmodulin-dependent protein kinase II autophosphorylation.

Experience-dependent plasticity can be induced in the barrel cortex by removing all but one whisker, leading to potentiation of the neuronal response to the spared whisker. To determine whether this form of potentiation depends on synaptic plasticity, we studied long-term potentiation (LTP) and sensory-evoked potentials in the barrel cortex of alpha-calcium/calmodulin-dependent protein kinase II (alphaCaMKII)T286A mutant mice. We studied three different forms of LTP induction: theta-burst stimulation, spike pairing, and postsynaptic depolarization paired with low-frequency presynaptic stimulation. None of these protocols produced LTP in alphaCaMKIIT286A mutant mice, although all three were successful in wild-type mice. To study synaptic plasticity in vivo, we measured sensory-evoked potentials in the barrel cortex and found that single-whisker experience selectively potentiated synaptic responses evoked by sensory stimulation of the spared whisker in wild types but not in alphaCaMKIIT286A mice. These results demonstrate that alphaCaMKII autophosphorylation is required for synaptic plasticity in the neocortex, whether induced by a variety of LTP induction paradigms or by manipulation of sensory experience, thereby strengthening the case that the two forms of plasticity are related.

Animals↗

PubMed2002

Is there a thalamic component to experience-dependent cortical plasticity?

Sensory deprivation and injury to the peripheral nervous system both induce plasticity in the somatosensory system of adult animals, but in different places. While injury induces plasticity at several locations within the ascending somatosensory pathways, sensory deprivation appears only to affect the somatosensory cortex. Experiments have been performed to detect experience-dependent plasticity in thalamic receptive fields, thalamic domain sizes and convergence of thalamic receptive fields onto cortical cells. So far, plasticity has not been detected with sensory deprivation paradigms that cause substantial cortical plasticity. Part of the reason for the lack of thalamic plasticity may lie in the synaptic properties of afferent systems to the thalamus. A second factor may lie in the differences in the organization of cortical and thalamic circuits. Many deprivation paradigms induce plasticity by decreasing phasic lateral inhibition. Since lateral inhibition appears to be far weaker in the thalamus than the cortex, sensory deprivation may not cause large enough imbalances in thalamic activity to induce plasticity in the thalamus.

Animals↗