Developmental modulation of synaptic transmission by acetylcholine in the primary visual cortex

2006 ◽  
Vol 1095 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Nicola Kuczewski ◽  
Eugenio Aztiria ◽  
Luciano Domenici
2019 ◽  
Author(s):  
XiangLing Liu ◽  
Rui Zhang ◽  
ZiXuan Song ◽  
JingLi Wang ◽  
Li Zhang ◽  
...  

Abstract Background :The occurrence of amblyopia is closely related to the glutamate receptors in visual cortex. The expression of metabotropic glutamate receptor 1 (mGluR1) in the visual cortex of rats with amblyopia has been proved to decrease, however, the role of mGluR1 in the synaptic transmission of visual cortex is not clear. This study aimed to investigate the effect of group I mGluR on the synaptic transmission efficiency in the primary visual cortex of monocular deprivation amblyopia rat. Methods The 14-day-old rads were rangomly divided intonormal control group and form-deprivation group,with 8 rats in each group. The eyelids of the left eye were sutured to establish the monocular form- deprivation amblyopia rat model,The rats visual cortex slices were prepared and incubated in artificial cerebrospinal fluid . Four groups of drugs that it is 3,5-dihydroxyphenylglycine( DHPG), LY367385, 2-methyl-6( phenyl acetylene) pyridine hydrochloride( MPEP) and DHPG, LY367385and MPEP and DHPG were added to every group, respectively.The extracellular recording technique was used to record the field excitatory postsynaptic potential (fEPSP) in the visual cortex. Results: After application of DHPG, the fEPSP-slope of the visual cortex was significantly increased in both normal rats and monocular deprivation amblyopia rats (P<0.001), but the increase of normal group was significantly higher than that of amblyopia group (P<0.05). Application of LY367385, a selective mGluR1 blocker or Application of MPEP, an mGluR5 blocker can partially reduce the DHPG-induced fEPSP-slope in both normal group and amblyopia group. Conclusions:These results demonstrate that the effect of modulation of group I mGluR (mGluR1, 5) on the synaptic transmission was reduced in the visual cortex of monocular deprivation amblyopia rat. found that agonist DHPG of Group I mGluRs increased synaptic transmission efficiency of neurons in visual cortex of normal rats and monocular form deprivation rats.


1990 ◽  
Vol 64 (5) ◽  
pp. 1484-1501 ◽  
Author(s):  
R. B. Langdon ◽  
M. Sur

1. We have recorded profiles of the spatial distributions of extracellular field potentials in transverse slices of rat primary visual cortex. Responses were evoked by electrical stimulation near the white matter/layer VI border and sampled from layers I to V along the radial axis orthogonal to the laminae and intersecting the stimulation site ("on-beam" recording). To assess the activity of "horizontal" connections, we also recorded profiles along axes parallel to the cortical lamination ("off-beam" recording), usually in layer III. Overall, our goal was to extend understanding of the physiology and organization of neocortical circuitry and to provide a basis for comparisons of data from different experiments and experimenters when neocortical field potentials are used in studies of plasticity and pharmacology. 2. Responses were highly specific with respect to the cortical layers. We distinguish four major components: two kinds of population spike ("S1" and "S2") and two slower waveforms ("W1" and "W2"). The latter appear to represent flow of current in apical dendrites of the supragranular layers. Component W1, the earliest slow component, is a synaptically driven field potential dipole that is positive in layer I and negative in layer II. Based on estimates of current source densities (CSDs), we attribute this to entry of depolarizing current into dendrites and/or cell somata in layer II, ascending intradendritic current, and passive depolarization of inactive dendritic membrane in layer I. Component W1 rises during the 20 ms after stimulation and falls during the 50-100 ms thereafter. Component W2 is also positive in layer I but maximally negative in layer III. It rises for approximately 100 ms after stimulation and decays during the following 400-800 ms. 3. Component S1 does not depend on synaptic transmission because it persists during the application of glutamate receptor antagonists or medium that is low in Ca2+. This component is largest in layer III, radial to the site of stimulation. There, it is a negative deflection, typically 1-2 mV in amplitude and lasting roughly 2 ms, with a latency to peak between 2 and 4.5 ms. Component S1 is most likely a population spike due to synchronized firing of cell somata activated antidromically via unmyelinated efferent axons. 4. Component S2 is a short (less than 20 ms) burst of population spikes specifically in layer III. Individual S2 spikes closely resemble S1 spikes, and we propose that the same neuronal population generates both. However, S2 spikes require glutamatergic synaptic transmission.(ABSTRACT TRUNCATED AT 400 WORDS)


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