Brighter reporter genes from multimerized fluorescent proteins.
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Fluorescence↗
Biomedical subjects
Alison L Barth
Publications and source records attributed to Alison L Barth.
Alteration of neuronal firing properties after in vivo experience in a FosGFP transgenic mouse.
Identifying the cells and circuits that underlie perception, behavior, and learning is a central goal of contemporary neuroscience. Although techniques such as lesion analysis, functional magnetic resonance imaging, 2-deoxyglucose studies, and induction of gene expression have been helpful in determining the brain areas responsible for particular functions, these methods are technically limited. Currently, there is no method that allows for the identification and electrophysiological characterization of individual neurons that are associated with a particular function in living tissue. We developed a strain of transgenic mice in which the expression of the green fluorescent protein (GFP) is controlled by the promoter of the activity-dependent gene c-fos. These mice enable an in vivo or ex vivo characterization of the cells and synapses that are activated by particular pharmacological and behavioral manipulations. Cortical and subcortical fosGFP expression could be induced in a regionally restricted manner after specific activation of neuronal ensembles. Using the fosGFP mice to identify discrete cortical areas, we found that neurons in sensory-spared areas rapidly regulate action potential threshold and spike frequency to decrease excitability. This method will enhance our ability to study the way neuronal networks are activated and changed by both experience and pharmacological manipulations. In addition, because activated neurons can be functionally characterized, this tool may enable the development of better pharmaceuticals that directly affect the neurons involved in disease states.
Action Potentials↗
A developmental switch in the signaling cascades for LTP induction.
Long-term potentiation (LTP) is thought to be critically involved not only in learning and memory, but also during the activity-dependent developmental phases of neural circuit formation and refinement. Whether the mechanisms underlying LTP change during this phase of postnatal development, however, is unknown. We report here that, unlike LTP in the more mature CA1 region of the hippocampus, LTP in neonatal rodent hippocampus (<9 postnatal days, <P9) requires cyclic AMP-dependent protein kinase A (PKA) but not Ca(2+)/calmodulin-dependent protein kinase II (CaMKII).
Animals↗
Differential plasticity in neocortical networks.
Understanding the synaptic and molecular basis for learning and memory in the neocortex depends upon a clear understanding of the anatomical and connectional diversity within this structure. To the extent that different types of synapses within the neocortex have distinct electrophysiological and, thus, molecular properties, the types of plasticity that these synapses manifest may also be distinct. If thresholds for plasticity are different for excitatory synapses onto inhibitory neurons than for excitatory synapses onto excitatory neurons, the same pattern of excitatory presynaptic activity will have difference consequences on excitatory and inhibitory networks. Differential plasticity will thus affect the way in which experience can modify sensory maps in the neocortex. Experimental support for this hypothesis is presented, as well as some predictions about the function of different types of neocortical pathways and plasticity.
Animals↗