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Jianhua Cang

Publications and source records attributed to Jianhua Cang.

7 recordsLinked to original sources
PubMed2006

Intrinsic ON responses of the retinal OFF pathway are suppressed by the ON pathway.

Parallel ON and OFF pathways conduct visual signals from bipolar cells in the retina to higher centers in the brain. ON responses are thought to originate by exclusive use of metabotropic glutamate receptor 6 (mGluR6) expressed in retinal ON bipolar cells. Paradoxically, we find ON responses in retinal ganglion cells of mGluR6-null mice, but they occur at long latency. The long-latency ON responses are not blocked by metabotropic glutamate or cholinergic receptor antagonists and are not produced by activation of receptive field surrounds. We show that these longer-latency ON responses are initiated in the OFF pathways. Our results expose a previously unrecognized intrinsic property of OFF retinal pathways that generates responses to light onset. In mGluR6-null mice, long-latency ON responses are observed in the visual cortex, indicating that they can be conducted reliably to higher visual areas. In wild-type (WT) mice, APB (DL-2-amino-4-phosphonobutyric acid), an mGluR6 agonist, blocks normal, short-latency ON responses but unmasks longer-latency ones. We find that these potentially confusing ON responses in the OFF pathway are actively suppressed in WT mice via two pharmacologically separable retinal circuits that are activated by the ON system in the retina. Consequently, we propose that a major function of the signaling of the ON pathway to the OFF pathway is suppression of these mistimed, and therefore inappropriate, light-evoked responses.

Action Potentials↗
PubMed2005

Development of precise maps in visual cortex requires patterned spontaneous activity in the retina.

The visual cortex is organized into retinotopic maps that preserve an orderly representation of the visual world, achieved by topographically precise inputs from the lateral geniculate nucleus. We show here that geniculocortical mapping is imprecise when the waves of spontaneous activity in the retina during the first postnatal week are disrupted genetically. This anatomical mapping defect is present by postnatal day 8 and has functional consequences, as revealed by optical imaging and microelectrode recording in adults. Pharmacological disruption of these retinal waves during the first week phenocopies the mapping defect, confirming both the site and the timing of the disruption in neural activity responsible for the defect. Analysis shows that the geniculocortical miswiring is not a trivial or necessary consequence of the retinogeniculate defect. Our findings demonstrate that disrupting early spontaneous activity in the eye alters thalamic connections to the cortex.

Animals↗
PubMed2005

Ephrin-as guide the formation of functional maps in the visual cortex.

Ephrin-As and their receptors, EphAs, are expressed in the developing cortex where they may act to organize thalamic inputs. Here, we map the visual cortex (V1) in mice deficient for ephrin-A2, -A3, and -A5 functionally, using intrinsic signal optical imaging and microelectrode recording, and structurally, by anatomical tracing of thalamocortical projections. V1 is shifted medially, rotated, and compressed and its internal organization is degraded. Expressing ephrin-A5 ectopically by in utero electroporation in the lateral cortex shifts the map of V1 medially, and expression within V1 disrupts its internal organization. These findings indicate that interactions between gradients of EphA/ephrin-A in the cortex guide map formation, but that factors other than redundant ephrin-As are responsible for the remnant map. Together with earlier work on the retinogeniculate map, the current findings show that the same molecular interactions may operate at successive stages of the visual pathway to organize maps.

Aging↗
PubMed2003

In vivo whole-cell recording of odor-evoked synaptic transmission in the rat olfactory bulb.

One of the first steps in the coding of olfactory information is the transformation of synaptic input to action potential firing in mitral and tufted (M/T) cells of the mammalian olfactory bulb. However, little is known regarding the synaptic mechanisms underlying this process in vivo. In this study, we examined odor-evoked response patterns of M/T and granule cells using whole-cell recording in anesthetized, freely breathing rats. We find that odor-evoked excitatory responses in M/T cells typically consist of bursts of action potentials coupled to the approximately 2 Hz respiration rhythm. Odor-evoked, rhythmic M/T cell excitation is reliable during odor presentation (2-4 sec); in contrast, both excitatory responses of granule cells and M/T cell lateral inhibition adapt quickly after the first respiration cycle in the presence of odorants. We also find that the amplitude and initial slope of odor-evoked synaptic excitation play an important role in regulating the timing of M/T cell spikes. Furthermore, differences in odor concentration alter the shape of odor-evoked excitatory synaptic responses, the latency of M/T cell spikes, and the timing of M/T cell lateral inhibition.

Action Potentials↗
PubMed2002

Model for intersegmental coordination of leech swimming: central and sensory mechanisms.

Sensory feedback as well as the coupling signals within the CNS are essential for leeches to produce intersegmental phase relationships in body movements appropriate for swimming behavior. To study the interactions between the central pattern generator (CPG) and peripheral feedback in controlling intersegmental coordination, we have constructed a computational model for the leech swimming system with physiologically realistic parameters. First, the leech swimming CPG is simulated by a chain of phase oscillators coupled by three channels of coordinating signals. The activity phase, the projection direction, and the phase response curve (PRC) of each channel are based on the identified intersegmental interneuron network. Output of this largely constrained model produces stable coordination in the simulated CPG with average phase lags of 8-10 degrees/segment in the period range from 0.5 to 1.5 s, similar to those observed in isolated nerve cords. The model also replicates the experimental finding that shorter chains of leech nerve cords have larger phase lags per segment. Sensory inputs, represented by stretch receptors, were subsequently incorporated into the CPG model. Each stretch receptor with its associated PRC, which was defined to mimic the experimental results of phase-dependent phase shifts of the central oscillator by the ventral stretch receptor, can alter the phase of the local central oscillator. Finally, mechanical interactions between the muscles from neighboring segments were simulated by PRCs linking adjacent stretch receptors. This model shows that interactions between neighboring muscles could globally increase the phase lags to the larger value required for the one-wavelength body form observed in freely swimming leeches. The full model also replicates the experimental observation that leeches with severed nerve cords have larger intersegmental phase lags than intact animals. The similarities between physiological and simulation results demonstrate that we have established a realistic model for the central and peripheral control of intersegmental coordination of leech swimming.

Animals↗
PubMedDate not supplied

Optical imaging of the intrinsic signal as a measure of cortical plasticity in the mouse.

The responses of cells in the visual cortex to stimulation of the two eyes changes dramatically following a period of monocular visual deprivation (MD) during a critical period in early life. This phenomenon, referred to as ocular dominance (OD) plasticity, is a widespread model for understanding cortical plasticity. In this study, we designed stimulus patterns and quantification methods to analyze OD in the mouse visual cortex using optical imaging of intrinsic signals. Using periodically drifting bars restricted to the binocular portion of the visual field, we obtained cortical maps for both contralateral (C) and ipsilateral (I) eyes and computed OD maps as (C - I)/(C + I). We defined the OD index (ODI) for individual animals as the mean of the OD map. The ODI obtained from an imaging session of less than 30 min gives reliable measures of OD for both normal and monocularly deprived mice under Nembutal anesthesia. Surprisingly, urethane anesthesia, which yields excellent topographic maps, did not produce consistent OD findings. Normal Nembutal-anesthetized mice have positive ODI (0.22 +/- 0.01), confirming a contralateral bias in the binocular zone. For mice monocularly deprived during the critical period, the ODI of the cortex contralateral to the deprived eye shifted negatively towards the nondeprived, ipsilateral eye (ODI after 2-day MD: 0.12 +/- 0.02, 4-day: 0.03 +/- 0.03, and 6- to 7-day MD: -0.01 +/- 0.04). The ODI shift induced by 4-day MD appeared to be near maximal, consistent with previous findings using single-unit recordings. We have thus established optical imaging of intrinsic signals as a fast and reliable screening method to study OD plasticity in the mouse.

Animals↗