PubMed · 10966609
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C G Galizia, R Menzel. 2000. Probing the olfactory code.. https://doi.org/10.1038/78741
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Zebra finches first form demonstrable memories of specific songs between 25 and 35 days of age--several days after fledging from the nest. What accounts for the late onset of specific song memory formation? Here we investigated physiological development of the caudomedial neostriatum (NCM), part of the avian analogue of auditory cortex and a probable component of the system involved in song perception. Two types of physiological responses were characterized: electrophysiological (single-unit spike rate) and genomic (induction of the immediate early gene zenk, also known as zif-268, egr-1, ngfi-a, krox-24). We found that by day 20, zebra finches already have robust electrophysiological responses in NCM to song stimulation. Spike activity was greater in response to conspecific songs compared to heterospecific songs, white noise, or tones, and approximately 10% of the units showed selective responses to forward versus reversed songs. In contrast, at this age the zenk gene is expressed at a constitutively high level and undergoes no further induction in response to song presentation. At day 30, electrophysiological responses remained similar, but the zenk gene began to shift from a constitutive to an inducible pattern of expression. These results are consistent with a general role for NCM in the representation of song auditory patterns, and with a role for zenk gene expression in governing the efficiency of specific song memory storage at different ages.
Epileptic discharges propagate through apparently normal circuits, although it is still unclear how this recruitment takes place. To understand the role of different classes of neurons in neocortical epilepsy, we have developed a novel imaging assay that detects which neurons participate in epileptiform discharges. Using calcium imaging of neuronal populations during bicuculline-induced spontaneous epileptiform events in slices from juvenile mouse somatosensory cortex, we find that fast calcium transients correlate with epileptiform field potentials and intracellular depolarizing shifts and can be used as an optical signature that a given neuron has participated in an epileptiform event. Our results demonstrate a novel method to characterize epileptiform events with single-cell resolution. In addition, our data are consistent with an important role for layer 5 in generating neocortical seizures and indicate that subgroups of neurons are particularly prone to epileptiform recruitment.
In adrenal chromaffin cells, a rise in cytosolic calcium concentration ([Ca(2+)]i) is a key event in the triggering of catecholamine exocytosis after splanchnic nerve activation. Action potential- or nicotine-induced [Ca(2+)]i transients are well described in individual chromaffin cells, but whether they remain spatially confined to the stimulated cell or propagate to adjacent cells is not yet known. To address this issue, the spatiotemporal organization of electrical and associated Ca(2+) events between chromaffin cells was investigated using the patch-clamp technique and real-time confocal imaging in rat acute adrenal slices. Spontaneous or electrically evoked action potential-driven [Ca(2+)]i transients were simultaneously detected in neighboring cells. This was likely attributable to gap junction-mediated electrotonic communication, as shown by (1) the bidirectional reflection of voltage changes monitored between cell pairs, (2) Lucifer yellow (LY) diffusion between cells exhibiting spontaneous synchronized [Ca(2+)]i transients, and (3) the reduction of LY diffusion using the uncoupling agent carbenoxolone. Furthermore, transcripts encoding two connexins (Cx36 and Cx43) were found in single chromaffin cells. This gap junctional coupling was activated after a synaptic-like application of nicotine that mediated synchronous multicellular [Ca(2+)]i increases. In addition, nicotinic stimulation of a single cell triggered catecholamine release in coupled cells, as shown by amperometric detection of secretory events. Functional coupling between chromaffin cells in situ may represent an efficient complement to synaptic transmission to amplify catecholamine release after synaptic stimulation of a single excited chromaffin cell.