Publications by authors named "E A Debski"

Nicotine exposure alters activity-dependent synaptic plasticity processes. Effects on learning and memory outcomes, and the synaptic changes that underlie them, are well-documented. Parallels in hippocampal and visual system pharmacology suggest that nicotine has the potential to alter activity-dependent structural organization in visual areas.

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The precise mapping of one surface onto another is fundamental to visual system organization and depends upon adequate stimulation of postsynaptic targets to stabilize correctly placed synapses. As exogenous nicotine alters neuronal activity, we investigated whether it would affect the visual map created by retinal ganglion cell terminals in the frog optic tectum. Chronic exposure of the tectum to nicotine decreased the retinal area from which cells project to a given tectal site.

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The reticular formation contributes serotonin to many brain regions, including the optic tectum. We examined the organization and development of its serotonergic neurons in the leopard frog. Serotonin-immunoreactive (5-HT-ir) cells in adult frogs were organized into 10 distinct populations that were identified on the basis of their location and cellular morphology.

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Both nicotinic and muscarinic cholinergic receptors are present in the optic tectum. To begin to understand how the activation of these receptors affects visual activity patterns, we have determined the types of physiological responses induced by their activation. Using tectal brain slices from the leopard frog, we found that application of nicotine (100 microM) evoked long-lasting responses in 60% of patch-clamped tectal cells.

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Cholinergic input to the optic tectum is necessary for visual map maintenance. To understand why, we examined the effects of activation of the different cholinergic receptor subtypes in tectal brain slices and determined whether the retinotectal map was affected by manipulations of their activity in vivo. Both alpha-bungarotoxin sensitive and insensitive nicotinic receptor agonists increased spontaneous postsynaptic currents (sPSCs) in a subpopulation of patch-clamped tectal cells; application of subtype selective receptor antagonists reduced nicotine-induced increases in sPSCs.

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