Short-term cerebral ischemia causes the dysfunction of interneurons and more excitation of pyramidal neurons in rats

Wang, Jin Hui

doi:10.1016/s0361-9230(03)00026-1

Cited by 98 publications

(105 citation statements)

References 22 publications

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“…Electrophysiological studies for acute slices showed that oxygen deprivation causes an immediate reduction of GABAergic synaptic transmission (42,43). At the same time, the expression of functional GABA A receptors is reduced (44,45), synaptic glutamate release becomes elevated (46,47), and NMDA receptor activity is enhanced (45,48). Taken together, these effects lead to hyperexcitability and may facilitate propagation of residual sensory responses to sites away from damaged maps (36).…”

Section: Relationship Between Rapid and Delayed Changes To Sensory Mapsmentioning

confidence: 99%

“…Taken together, these effects lead to hyperexcitability and may facilitate propagation of residual sensory responses to sites away from damaged maps (36). Excitation-inhibition balance could also change as a result of a loss of surround inhibition (1,47,49,50), which leads to enhanced out-of-territory responses. These altered electrophysiological properties could induce potentiation of excitatory inputs in the peri-infarct cortex within the first hour after stroke (16) and form an environment suitable for later rewiring (3,4,36,37,51) that correlates with functional reorganization (1,49,50,52).…”

Section: Relationship Between Rapid and Delayed Changes To Sensory Mapsmentioning

confidence: 99%

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Imaging rapid redistribution of sensory-evoked depolarization through existing cortical pathways after targeted stroke in mice

Sigler

Mohajerani²,

Murphy³

2009

Proc. Natl. Acad. Sci. U.S.A.

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Evidence suggests that recovery from stroke damage results from the production of new synaptic pathways within surviving brain regions over weeks. To address whether brain function might redistribute more rapidly through preexisting pathways, we examined patterns of sensory-evoked depolarization in mouse somatosensory cortex within hours after targeted stroke to a subset of the forelimb sensory map. Brain activity was mapped with voltage-sensitive dye imaging allowing millisecond time resolution over 9 mm 2 of brain. Before targeted stroke, we report rapid activation of the forelimb area within 10 ms of contralateral forelimb stimulation and more delayed activation of related areas of cortex such as the hindlimb sensory and motor cortices. After stroke to a subset of the forelimb somatosensory cortex map, function was lost in ischemic areas within the forelimb map center, but maintained in regions 200 -500 m from blood flow deficits indicating the size of a perfused, but nonfunctional, penumbra. In many cases, stroke led to only partial loss of the forelimb map, indicating that a subset of a somatosensory domain can function on its own. Within the forelimb map spared by stroke, forelimbstimulated responses became delayed in kinetics, and their center of activity shifted into adjacent hindlimb and posterior-lateral sensory areas. We conclude that the focus of forelimb-specific somatosensory cortex activity can be rapidly redistributed after ischemic damage. Given that redistribution occurs within an hour, the effect is likely to involve surviving accessory pathways and could potentially contribute to rapid behavioral compensation or direct future circuit rewiring.brain plasticity ͉ focal ischemia ͉ in vivo imaging ͉ recovery of cortical function ͉ somatosensory cortex representation T he majority of those suffering a stroke will survive the initial insult, but will experience some form of sensory, motor, or cognitive impairment. Many will experience some restitution of function over the ensuing weeks to months after stroke. Evidence suggests that circuit changes within adjacent surviving regions of the brain may be critically involved in this recovery process (1-4). The extent of circuit reorganization in peri-infarct cortex correlates with recovery of cortical function lost after stroke (5, 6). Mechanisms suggested for mediating cortical reorganization involve the formation of novel circuits, the unmasking of existing, but latent, synaptic connections, and modulation of synaptic efficacy in active connections (7,8). Although redistribution of circuit function is obviously the final outcome, in the first hours to days after stroke a competing process termed ''diaschisis'' may lead to reversible suppression of function in regions adjacent to and physiologically connected to the infarct (9, 10). We postulate that the distribution of residual function hours after stroke and its relation to local blood flow is a critical determinant of what circuits are available for future activity dependent plasticity over days to ...

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Section: Relationship Between Rapid and Delayed Changes To Sensory Mapsmentioning

confidence: 99%

Section: Relationship Between Rapid and Delayed Changes To Sensory Mapsmentioning

confidence: 99%

Imaging rapid redistribution of sensory-evoked depolarization through existing cortical pathways after targeted stroke in mice

Sigler

Mohajerani²,

Murphy³

2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Slices were cut with a vibratome in modified and oxygenated (95% O 2 /5% CO 2 ) artificial cerebrospinal fluid (124 mM NaCl, 3 mM KCl, 1.2 mM NaH 2 PO 4 , 26 mM NaHCO 3 , 0.5 mM CaCl 2 , 5 mM MgSO 4 , 10 mM dextrose and 5 mM HEPES, pH 7.35) at 4°C, and then were held in normal oxygenated ACSF (124 mM NaCl, 3 mM KCl, 1.2 mM NaH 2 PO 4 , 26 mM NaHCO 3 , 2.4 mM CaCl 2 , 1.3 mM MgSO 4 , 10 mM dextrose and 5 mM HEPES, pH 7.35) at 24°C for 1-2 hours before experiments. A slice was transferred to the submersion chamber (Warner RC-26G) that was perfused with normal ACSF at 31°C for the whole-cell recordings (Wang, 2003). The procedures were approved by IACUC in Beijing.…”

Section: Brain Slicesmentioning

confidence: 99%

“…Principal neurons have a pyramidal-like soma and apical dendrite, and interneurons are round with multipolar processes under DIC optics (Nikon FN-600). Pyramidal neurons and interneurons show different properties in response to hyperand depolarization pulses (Wang and Kelly, 2001;Wang, 2003).…”

Section: Neuron Selectionmentioning

confidence: 99%

Gain and fidelity of transmission patterns at cortical excitatory unitary synapses improve spike encoding

Wang

Wei

Chen

et al. 2008

Journal of Cell Science

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Neuronal spike encoding and synaptic transmission in the brain need be precise and reliable for well-organized behavior and cognition. Little is known about how a unitary synapse reliably transmits presynaptic sequential spikes and how multiple unitary synapses precisely drive their postsynaptic neurons to encode spikes. To address these questions, we investigated the dynamics of glutamatergic unitary synapses as well as their role in driving the encoding of cortical fast-spiking neurons. Synaptic transmission patterns randomly fluctuate among facilitation, depression and parallel over time. The postsynaptic calmodulin-signaling pathway enhances initial responses and converts this fluctuation to a synaptic depression. We integrated current pulses mathematically based on synaptic plasticity and found that they improve spike capacity and timing precision by shortening the spike refractory period at postsynaptic neurons. Our results indicate that the gain and fidelity of synaptic patterns enable reliable transmission of presynaptic signals by the synapse and precise encoding of spikes by postsynaptic neurons. These reproducible neural codes may be involved in controlling well-organized behavior.

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“…Slices were cut with a vibratome in modified and oxygenated (95% O 2 , 5% CO 2 ) artificial cerebrospinal fluid (ACSF) (124 mM NaCl, 3 mM KCl, 1.2 mM NaH 2 PO 4 , 26 mM NaHCO 3 , 0.5 mM CaCl 2 , 5 mM MgSO 4 , 10 mM dextrose and 5 mM HEPES, pH 7.35) at 4°C, and then were held in the normally oxygenated ACSF (124 mM NaCl, 3 mM KCl, 1.2 mM NaH 2 PO 4 , 26 mM NaHCO 3 , 2.4 mM CaCl 2 , 1.3 mM MgSO 4 , 10 mM dextrose and 5 mM HEPES, pH 7.35) 24°C for 1-2 hours. One slice was transferred into a submersion chamber (Warner RC-26G) and perfused using normally oxygenated ACSF at 31°C for electrophysiological recording (Wang, 2003). Chemicals were from Sigma.…”

Section: Brain Slicesmentioning

confidence: 99%

Homeostasis established by coordination of subcellular compartment plasticity improves spike encoding

Chen

Wang

2008

Journal of Cell Science

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Homeostasis in cells maintains their survival and functions. The plasticity at neurons and synapses may destabilize their signal encoding. The rapid recovery of cellular homeostasis is needed to secure the precise and reliable encoding of neural signals necessary for well-organized behaviors. We report a homeostatic process that is rapidly established through Ca2+-induced coordination of functional plasticity among subcellular compartments. An elevation of cytoplasmic Ca2+ levels raises the threshold potentials and refractory periods of somatic spikes, and strengthens the signal transmission at glutamatergic and GABAergic synapses, in which synaptic potentiation shortens refractory periods and lowers threshold potentials. Ca2+ signals also induce an inverse change of membrane excitability at the soma versus the axon. The integrative effect of Ca2+-induced plasticity among the subcellular compartments is homeostatic in nature, because it stabilizes neuronal activities and improves spike timing precision. Our study of neuronal homeostasis that is fulfilled by rapidly coordinating subcellular compartments to improve neuronal encoding sheds light on exploring homeostatic mechanisms in other cell types.

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Short-term cerebral ischemia causes the dysfunction of interneurons and more excitation of pyramidal neurons in rats

Cited by 98 publications

References 22 publications

Imaging rapid redistribution of sensory-evoked depolarization through existing cortical pathways after targeted stroke in mice

Imaging rapid redistribution of sensory-evoked depolarization through existing cortical pathways after targeted stroke in mice

Gain and fidelity of transmission patterns at cortical excitatory unitary synapses improve spike encoding

Homeostasis established by coordination of subcellular compartment plasticity improves spike encoding

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