Characterization of sensory and corticothalamic excitatory inputs to rat thalamocortical neurones <i>in vitro</i>

Turner, J. P.; Salt, Te

doi:10.1111/j.1469-7793.1998.829bj.x

Cited by 180 publications

(240 citation statements)

References 35 publications

(56 reference statements)

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“…In addition, we can distinguish retinal from cortical inputs by their short-term plasticity. Corticothalamic inputs facilitate in response to pairs of stimuli separated by 50 ms, whereas retinal inputs exhibit short-term synaptic depression (Turner and Salt, 1998;Granseth et al, 2002;Reichova and Sherman, 2004). Finally, the AMPAR EPSC decay kinetics of cortical inputs is relatively slower than that of retinal inputs: Ͼ5-6 ms (Alexander et al, 2006) versus 1.5-3 ms for retinal inputs (Chen and Regehr, 2000).…”

Section: Methodsmentioning

confidence: 99%

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Hooks

Chen²

2008

J. Neurosci.

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In the mammalian visual system, sensory experience is widely thought to sculpt cortical circuits during a precise critical period. In contrast, subcortical regions, such as the thalamus, were thought to develop at earlier ages in a vision-independent manner. Recent studies at the retinogeniculate synapse, however, have demonstrated an influence of vision on the formation of synaptic circuits in the thalamus. In mice, dark rearing from birth does not alter normal developmental maturation of the connection between retina and thalamus. However, deprivation 20 d after birth [postnatal day 20 (p20)] resulted in dramatic weakening of synaptic strength and an increase in the number of retinal inputs that innervate a thalamic relay neuron. Here, by quantifying changes in synaptic strength and connectivity in response to different time windows of deprivation, we find that several days of vision after eye opening is necessary for triggering experience-dependent plasticity. Shorter periods of visual experience do not permit similar experience-dependent synaptic reorganization. Furthermore, changes in connectivity are rapidly reversible simply by restoring normal vision. However, similar plasticity did not occur when shifting the onset of deprivation to p25. Although synapses still weakened, recruitment of additional retinal inputs no longer occurred. Therefore, synaptic circuits in the visual thalamus are unexpectedly malleable during a late developmental period, after the time when normal synapse elimination and pruning has occurred. This thalamic sensitive period overlaps temporally with experience-dependent changes in the cortex, suggesting that subcortical plasticity may influence cortical responses to sensory experience.

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Section: Methodsmentioning

confidence: 99%

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Hooks

Chen²

2008

J. Neurosci.

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“…mGlu1/mGlu5) receptors in several brain areas (Fitzjohn et al 1996;Doherty et al 1997;Pisani et al 1997;Martin et al 1998;Holohean et al 1999), as has modulation of AMPA-receptor-mediated responses (Cerne & Randic 1992;Bond & Lodge 1995;Jones & Headley 1995;Dev & Henley 1998;Calabresi et al 1999). In the VB, activation of mGlu1 receptors potentiates responses mediated via either AMPA or NMDA receptors in vivo ( gure 2) (Salt & Binns 2000), and it is probable that this is due to the direct effects of mGlu1 activation on neuronal membrane potential and resistance (McCormick & Von Krosigk 1992;Turner & Salt 1998) rather than a speci c interaction at the receptor level, or that the potentiation seen is a combination of these factors (Salt & Binns 2000). Thus, although the isolated corticothalamic synaptic potential (which can be attributed to mGlu1 receptors in vitro) appears to be rather small (Turner & Salt 2000b), it would be able to exert a profound in uence on ionotropic receptor-mediated responses, if the sensory stimulus was appropriate to recruit activity in the corticothalamic output.…”

Section: Sensory Responses Of Thalmic Relay Neurons In Vivo: Recruitmmentioning

confidence: 99%

“…A particular focus has been the function of mGlu1 receptors, as these have been localized postsynaptically in LGN predominantly beneath terminals of corticothalamic bres (Martin et al 1992;Vidnyanszky et al 1996;Godwin et al 1996). Activation of mGlu receptors in thalamic relay neurons causes a slow depolarizing response associated with an increase in membrane resistance, as seen in many other parts of the brain, probably due a reduction in a potassium conductance (McCormick & Von Krosigk 1992;Turner & Salt 1998;Hughes et al 2002), and this has been shown to be mediated speci cally via mGlu1 receptors ( gure 1) (Turner & Salt 2000b;Hughes et al 2002). Nevertheless, it is also evident that there is a substantial AMPA-receptor-mediated component to corticothalamic synapses in sensory relay nuclei (Turner & Salt 1998;Golshani et al 2001), a nding supported by ultrastructural evidence which indicates that there are AMPA receptor subunits which are predominantly GluR2/3 and GluR4 located postsynaptically at corticothalamic synapses in VB (Mineff & Weinberg 2000;Golshani et al 2001).…”

Section: Cortical Inputs To the Thalmic Relay Nucleimentioning

confidence: 99%

“…Activation of mGlu receptors in thalamic relay neurons causes a slow depolarizing response associated with an increase in membrane resistance, as seen in many other parts of the brain, probably due a reduction in a potassium conductance (McCormick & Von Krosigk 1992;Turner & Salt 1998;Hughes et al 2002), and this has been shown to be mediated speci cally via mGlu1 receptors ( gure 1) (Turner & Salt 2000b;Hughes et al 2002). Nevertheless, it is also evident that there is a substantial AMPA-receptor-mediated component to corticothalamic synapses in sensory relay nuclei (Turner & Salt 1998;Golshani et al 2001), a nding supported by ultrastructural evidence which indicates that there are AMPA receptor subunits which are predominantly GluR2/3 and GluR4 located postsynaptically at corticothalamic synapses in VB (Mineff & Weinberg 2000;Golshani et al 2001). More recently a low level of kainate receptor subunits (GluR5/6/7) has been found postsynaptically beneath corticothalamic synapses in VB, although initial in vitro electrophysiological evidence does not appear to indicate a synaptic role for these receptors (Bolea et al 2001 …”

Section: Cortical Inputs To the Thalmic Relay Nucleimentioning

confidence: 99%

“…(Abbreviations used: ATPA, (RS)-2-amino-3(3-hydroxy-5-t butylisoxazol-4-yl) propanionate; GYKI 52466, 1-(4-amino-phenyl)-4-methyl-7,8-methylene-dioxy-5H-2,3-benzodiazepine; SYM2206, (±)-4-(4-aminophenyl)-1,2-dihydro-1-methyl-2-propylcarbamoyl-6,7-methylenedioxyphthalazine.) (Abbreviations used: APDC, 2R,4R-4-aminopyrrolidine-2,4-decarboxylate; CCG-1, (2S,19S,29S)-2-(2-carboxycyclopropyl) glycine; CHPG, 2-chloro-5-hydroxyphenylglycine; 4CPG, (S)-4-carboxyphenylglycine; CPPG, a-cyclopropyl-4-phosphonophenylglycine; DHPG, 3,5-dihydroxyphenylglycine; l-AP4, l-2-amino-4-phosphonobutyric acid; l-SOP, l-serine-O-phosphate; LY341495, 2S-2-amino-2 (1S,2S-2-carboxcyclopropyl-1-yl)-3-(xanth-9-yl)propanoic acid; LY354740, (1) of NMDA receptors and non-NMDA ionotropic receptors (Salt 1986;Crunelli et al 1987;Sillito et al 1990;Salt & Eaton 1991;, and it has become clear that this re ects a fast EPSP/C component mediated by AMPA receptors in conjunction with an NMDAreceptor-mediated synaptic component (Paulsen & Heggelund 1994;Turner et al 1994;Turner & Salt 1998;Kielland & Heggelund 2001). These in vivo and in vitro electrophysiological ndings are supported by ultrastructural evidence showing the localization of NMDA and AMPA receptor subunits postsynaptic to sensory terminals (Liu 1997;Mineff & Weinberg 2000).…”

Section: Sensory Inputs To Thalamic Relay Nucleimentioning

confidence: 99%

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Glutamate receptor functions in sensory relay in the thalamus

Salt

2002

Phil. Trans. R. Soc. Lond. B

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It is known that glutamate is a major excitatory transmitter of sensory and cortical afferents to the thalamus. These actions are mediated via several distinct receptors with postsynaptic excitatory effects predominantly mediated by ionotropic receptors of the a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and N-methyl-d-aspartate varieties (NMDA). However, there are also other kinds of glutamate receptor present in the thalamus, notably the metabotropic and kainate types, and these may have more complex or subtle roles in sensory transmission. This paper describes recent electrophysiological experiments done in vitro and in vivo which aim to determine how the metabotropic and kainate receptor types can in uence transmission through the sensory thalamic relay. A particular focus will be how such mechanisms might operate under physiological conditions.

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Comparison of the ultrastructure of cortical and retinal terminals in the rat dorsal lateral geniculate and lateral posterior nuclei

Wang

Bickford

2003

J of Comparative Neurology

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We compared the ultrastructure and synaptic targets of terminals of cortical or retinal origin in the rat dorsal lateral geniculate nucleus (LGN) and lateral posterior nucleus (LPN). Following injections of biotinylated dextran amine (BDA) into cortical area 17, two types of corticothalamic terminals were labeled by anterograde transport. Type I terminals, found throughout the LGN and LPN, were small, drumstick-shaped terminals that extended from thin axons. At the ultrastructural level in both the LGN and LPN, labeled type I corticothalamic terminals were observed to be small profiles that contained densely packed round vesicles (RS profiles) and contacted small-caliber dendrites. In tissue stained for gamma amino butyric acid (GABA) using postembedding immunocytochemical techniques, most dendrites postsynaptic to type I corticothalamic terminals did not contain GABA (97%). Type II corticothalamic terminals, found only in the LPN, were large terminals that sometimes formed clusters. At the ultrastructural level, type II terminals were large profiles that contained round vesicles (RL profiles) and contacted large-caliber dendrites, most of which did not contain GABA (98%). Retinogeniculate terminals, identified by their distinctive pale mitochondria, were similar to type II corticothalamic terminals except that 26% of their postsynaptic targets were vesicle-containing profiles that contained GABA (F2 profiles). Our results suggest that type I corticothalamic terminals are very similar across nuclei but that the postsynaptic targets of RL profiles vary. Comparison of the responses to retinal inputs in the LGN and to layer V cortical inputs in the LPN may provide a unique opportunity to determine the function of interneurons in the modulation of retinal signals and, in addition, may provide insight into the signals relayed by cortical layer V.

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Characterization of sensory and corticothalamic excitatory inputs to rat thalamocortical neurones in vitro

Cited by 180 publications

References 35 publications

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Glutamate receptor functions in sensory relay in the thalamus

Comparison of the ultrastructure of cortical and retinal terminals in the rat dorsal lateral geniculate and lateral posterior nuclei

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