Large layer VI neurons of monkey striate cortex (Meynert cells) project to the superior colliculus

After injections of the enzyme horseradish peroxidase (HRP) into the superior colliculus of macaque monkeys, labelled cells in the neocortex were found to be restricted to layer V in all areas except striate visual cortex. In striate visual cortex, cortico-tectal cells were found both in layer V and in layer VI. The labelled cells in the two layers belonged to morphologically different populations: those of layer V were the common pyramidal cells and those of layer VI were identified as solitary cells of Meynert. This finding may provide new insights into the physiology of the cortico-collicular pathways. It also shows that the striate area in primates differs, with respect to cortico-tectal laminar specificity, from other neocortex.

2002 ◽  
Vol 357 (1428) ◽  
pp. 1793-1808 ◽  
Author(s):  
N.J. Bannister ◽  
J.C. Nelson ◽  
J.J.B. Jack

The principal target of lateral geniculate nucleus in the cat visual cortex is the stellate neurons of layer 4. In previously reported work with intracellular recording and extracellular stimulation in slices of visual cortex, three general classes of fast excitatory synaptic potentials (EPSPs) in layer 4a spiny stellate neurons were identified. One of these classes, characterized by large and relatively invariant amplitudes (mean 1.7 mV, average coefficient of variation (CV) 0.083) were attributed to the action of geniculate axons because, unlike the other two classes, they could not be matched by intracortical inputs, using paired recording. We have examined in detail the properties of this synaptic input in twelve examples, selecting for study those EPSPs where there was secure extracellular stimulation of the single fibre input to a pair of stimuli 50 ms apart. In our analysis, we conclude that the depression that these inputs show to the second stimulus is entirely postsynaptic, since the evidence strongly suggests that the probability of transmitter release at the synaptic site(s) remains 1.0 for both stimuli. We argue that the most plausible explanation for this postsynaptic depression is a reduction in the average probability of opening the synaptic channels. Using a simple biochemical analysis (c.f. Sigworth plot), it is then possible to calculate the number of synaptic channels and their probability of opening, for each of the 12 connections. The EPSPs had a mean amplitude of 1.91 mV (±1.3 mV SD) and a mean CV of 0.067 (± 0.022). The calculated number of channels ranged from 20 to 158 (59.4 ± 48.7) and their probability of opening to the first EPSP had an average of 0.83 (± 0.09), with an average depression of the probability to 0.60 for the second EPSP. Geniculate afferents also terminate in layer 6. Intracellular recordings were also made in the upper part of this layer and a total of 51 EPSPs were recorded from pyramidal cells of three principal types. Amongst this dataset we sought EPSPs with similar properties to those characterized in layer 4a. Three examples were found, which is a much lower percentage (6%) than the incidence of putative geniculate EPSPs found in layer 4a (42%).


2004 ◽  
Vol 91 (2) ◽  
pp. 1097-1101 ◽  
Author(s):  
Simon Rumpel ◽  
Gunnar Kattenstroth ◽  
Kurt Gottmann

Central glutamatergic synapses are thought to initially form as immature, so-called silent synapses showing exclusively N-methyl-d-aspartate receptor-mediated synaptic transmission. Postsynaptic insertion of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors during further development leads to a conversion into functional, mature synapses. Here, we tested the hypothesis that, according to the “inside first–outside last” pattern of neocortical layer formation and synaptogenesis, pyramidal cells in the superficial layers might show a higher fraction of silent synapses compared with pyramidal cells in the deep layers. We performed an electrophysiological analysis of glutamatergic synapses in acute rat visual cortex slices during postnatal development. In layer VI pyramidal neurons the incidence of silent synapses was high during the first postnatal week and strongly declined during further development. Surprisingly, in superficial cortical plate pyramidal neurons (immature layers II/III), the fraction of silent synapses was initially very low and increased up to the second postnatal week. Thereafter, a similar decline as found in layer VI pyramidal neurons was observed. Thus the developmental regulation of silent synapses was clearly different in pyramidal neurons from different neocortical layers. The almost complete absence of silent synapses at early stages in layer II/III pyramidal neurons indicates that an initially formed subset of synapses is constitutively functional. This might be important to enable spontaneous activity and latter activity-dependent maturation of synapses.


1997 ◽  
Vol 9 (4) ◽  
pp. 857-862 ◽  
Author(s):  
Diego Ruano ◽  
David Perrais ◽  
Jean Rosier ◽  
Nicole Ropert

2017 ◽  
Author(s):  
Yevgenij Yanovsky ◽  
Jurij Brankačk

summaryThe relative electrical conductivity gradient with depth was estimated in the frontal cortex of anaesthetized rats. Current source density (CSD) approximations of field potentials evoked by ventromedial thalamic stimulations with an assumed homogeneous electrical conductivity of the neocortical tissue were compared to those with correction for the estimated conductivity gradient. In spite of the cellular heterogeneity the electrical conductivity of the frontal cortical tissue was found to be fairly homogeneous inside the superficial (layers I through IV) or deep layers (V- VI). The relative conductivity increased twofold at the transition between superficial and deep layers. Regardless of this changes CSD analysis of the field potentials evoked by ventromedial thalamic stimulation revealed negligible differences between estimations ignoring the conductivity and those taking the conductivity into account. No sinks or sources appeared or disappeared. Both CSD approximations revealed: 1) a strong sink in layer I representing most likely summed monosynaptic EPSPs of the ventromedial thalamic afferents; 2) a strong sink in layer VI, probably representing summed disynaptic EPSPs on dendrites of layer VI pyramidal cells, generated by axons of upper layer pyramidal cells; and 3) a sink in lower layer V representing probably threesynaptic summed EPSPs on dendrites of layer V pyramidal cells.


1988 ◽  
Vol 60 (2) ◽  
pp. 798-828 ◽  
Author(s):  
J. Kruger ◽  
F. Aiple

1. In the infragranular layers of the striate cortex of three monkeys, we studied tangential neuronal interactions by analyzing cross-correlograms calculated from spike trains recorded with 30 closely spaced microelectrodes. 2. There are two major types of correlogram structures--"narrow" peaks a few milliseconds wide, sometimes accompanied by small lateral troughs, and "broad" peaks approximately 30- to 100-ms wide. Isolated troughs are rare. Both types of structures are superimposed in the same correlograms; they are not due to shared optical stimulation. 3. In layer VI, narrow peaks are largest in a short lateral range of approximately 220 micron, and they depend on ocularity. In layer V, the lateral range is greater, and the dependency on ocularity is weak. 4. In addition, narrow peaks are largest at distances of 160 micron if the angles of preferred orientation are similar. In layer VI, however, at tangential distances of 300-400 micron, peaks are smaller, and troughs are found more often, for neuron pairs with parallel orientations compared with those with orthogonal orientations. From the agreement of this finding with a cooperative theory, we conclude that orientation selectivity is shaped by collective interactions. 5. Broad peaks always depend on ocularity, and the associated lateral interaction range exceeds the maximum of 1 mm investigated. Their size sharply decreases with receptive-field distance. 6. Average mutual delays of spikes of neuron pairs, manifest as lateral displacements of broad peaks, are interdependent; the delay between neurons 1 and 3 is the sum of that of neurons 1 and 2 and of neurons 2 and 3. This feature permits to rank the neurons on a "delay scale." 7. We conclude from 5 and 6 above that broad peaks partly result from intraretinal interactions whose effects are transmitted to the cortex via slow and fast pathways. 8. Lateral troughs adjacent to narrow peaks provide evidence that neurons at the "slow" end of the delay scale inhibit those at the "fast" end, and to a lesser extent, nondirectional neurons inhibit directional ones.


2008 ◽  
Vol 99 (2) ◽  
pp. 950-957 ◽  
Author(s):  
Yoshifumi Ueta ◽  
Ryo Yamamoto ◽  
Shigeki Sugiura ◽  
Kaoru Inokuchi ◽  
Nobuo Kato

Homer1a/Vesl-1S is an activity-dependently induced member of the scaffold protein family Homer/Vesl, which is known to link group I metabotropic glutamate receptors (mGluRs) to endoplasmic calcium release channels and to regulate them. Here we studied roles of Homer 1a in inducing long-term depression (LTD) in rat visual cortex slices. Homer 1a protein was injected by diffusion from whole cell patch pipettes. In layer VI pyramidal cells, LTD was reduced in magnitude with Homer 1a. LTD in layer VI was suppressed by applying antagonists of mGluR5, a subtype of group I mGluRs expressed with higher density than mGluR1 in neocortex pyramidal cells, or inositol-1,4,5-triphosphate receptors (IP3Rs) but not that against N-methyl-d-aspartate receptors (NMDARs). In layer II/III or layer V, Homer 1a injection was unable to affect LTD, which is mostly dependent on NMDARs and not on group I mGluRs in these layers. To examine the effects of endogenous Homer 1a, electroconvulsive shock (ECS) was applied. Homer 1a thereby induced, as did Homer 1a injection, reduced LTD magnitude in layer VI pyramidal cells and failed to do so in layer II/III or layer V pyramidal cells. These results indicate that both exo- and endogenous Homer 1a suppressed LTD in a cortical layer-specific manner, and its layer-specificity may be explained by the high affinity of Homer 1a to group I mGluRs.


1994 ◽  
Vol 72 (2) ◽  
pp. 578-591 ◽  
Author(s):  
Y. Kang ◽  
F. Kayano

1. Intracellular recordings were made from layer VI pyramidal cells in in vitro slice preparations of the cat motor cortex (area 4 gamma). Layer VI pyramidal cells were identified morphologically by intracellular injection of biocytin. 2. Of 22 layer VI pyramidal cells examined, single action potentials were followed by depolarizing afterpotentials (DAP) in 9 cells, but were not followed by DAP in the remaining 13 cells. The amplitude of DAP was 3.4 +/- 1.4 mV (mean +/- SD, n = 9) when measured from the negative peak of fast afterhyperpolarization to the peak of DAP. 3. In response to depolarizing current pulses with a duration of 300–400 ms, pyramidal cells showing DAP displayed a train of action potentials in a phasic-tonic pattern without any appreciable adaptation in the tonic firing, whereas pyramidal cells lacking DAP exhibited a weak adaptation after phasic firing. Anomalous rectification was seen in both pyramidal cells showing DAP and those lacking DAP. 4. Repetitive doublet or triplet spiking was induced in DAP-showing pyramidal cells in response to a depolarizing current pulse after injecting strong depolarizing current pulses of 400 ms duration at 1 Hz for 30–60 s, but was never induced in DAP-lacking pyramidal cells. Doublet/triplet spiking lasted 5–10 min and returned to the original single spiking. An application of CsCl induced a burst firing in DAP-showing pyramidal cells. 5. In the nine pyramidal cells showing DAP, seven cells had shorter apical dendrites that arborized extensively at layer V and terminated in the middle part of layer III. In the 13 pyramidal cells lacking DAP, 11 cells had longer apical dendrites that arborized less frequently and extended into layer II or I. Main axons could be traced into the deep white matter in 17 of the 22 layer VI pyramidal cells examined. 6. Ascending recurrent axon collaterals were more prominent in pyramidal cells with longer apical dendrites than in pyramidal cells with shorter apical dendrites. The terminal bouton-like swelling observed along the recurrent axon collaterals arising from the pyramidal cells with longer apical dendrite were distributed most densely at the level between the bottom part of layer III and the top part of layer V. In contrast, those arising from the pyramidal cells with shorter apical dendrite were distributed mainly at the levels of layers V and VI.(ABSTRACT TRUNCATED AT 400 WORDS)


2002 ◽  
Vol 88 (2) ◽  
pp. 740-750 ◽  
Author(s):  
Zixiu Xiang ◽  
John R. Huguenard ◽  
David A. Prince

Properties of GABAA receptor-mediated unitary inhibitory postsynaptic currents (uIPSCs) in pyramidal (P) cells, evoked by fast spiking (FS) and low-threshold spike (LTS) subtypes of interneurons in layer V of rat visual cortex slices were examined using dual whole cell recordings. uIPSCs evoked by FS cells were larger and faster rising than those evoked by LTS cells, consistent with the known primary projections of FS and LTS cell axons to perisomatic and distal dendritic areas of layer V pyramidal cells, respectively, and the resulting electrotonic attenuation for LTS-P synaptic events. Unexpectedly, the decay time constants for LTS-P and FS-P uIPSCs were not significantly different. Modeling results were consistent with differences in the underlying GABAAreceptor–mediated conductance at LTS-P and FS-P synapses. Paired-pulse depression (PPD), present at both synapses, was associated with an increase in failure rate and a decrease in coefficient of variation, indicating that presynaptic mechanisms were involved. Furthermore, the second and first uIPSC amplitudes during PPD were not inversely correlated, suggesting that PPD at both synapses is independent of previous release and might not result from depletion of the releasable pool of synaptic vesicles. Short, 20-Hz trains of action potentials in presynaptic interneurons evoked trains of uIPSCs with exponentially decreasing amplitudes at both FS-P and LTS-P synapses. FS-P uIPSC amplitudes declined more slowly than those of LTS-P uIPSCs. Thus FS and LTS cells, with their differences in firing properties, synaptic connectivity with layer V P cells, and short-term synaptic dynamics, might play distinct roles in regulating the input-output relationship of the P cells.


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