Electrophysiological Properties and Input-Output Organization of Callosal Neurons in Cat Association Cortex

2003 ◽  
Vol 89 (3) ◽  
pp. 1402-1413 ◽  
Author(s):  
Youssouf Cissé ◽  
François Grenier ◽  
Igor Timofeev ◽  
Mircea Steriade
Keyword(s):  
Cortical Cell ◽  
Association Cortex ◽  
Thalamic Nuclei ◽  
Postsynaptic Potentials ◽  
Electrophysiological Properties ◽  
Cortical Areas ◽  
Pathway Data ◽  
Antidromic Responses ◽  
Contralateral Cortex ◽  
Current Steps

Intracellular recordings from association cortical areas 5 and 7 were performed in cats under barbiturate or ketamine-xylazine anesthesia to investigate the activities of different classes of neurons involved in callosal pathways, which were electrophysiologically characterized by depolarizing current steps. Excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and/or antidromic responses were elicited by stimulating homotopic sites in the contralateral cortical areas. Differential features of EPSPs related to latencies, amplitudes, and slopes were detected in closely located (50 μm or less) neurons recorded in succession along the same electrode track. In contrast to synchronous thalamocortical volleys that excited most neurons within a cortical column, stimuli applied to homotopic sites in the contralateral cortex activated neurons at restricted cortical depths. Median latencies of callosally evoked EPSPs were 1.5 to 4 ms in various cortical cell-classes. Fast-rhythmic-bursting neurons displayed EPSPs whose amplitudes were threefold larger, and latencies two- or threefold shorter, than those found in the three other cellular classes. Converging callosal and thalamic inputs were recorded in the same cortical neuron. EPSPs or IPSPs were elicited by stimulating foci spaced by <1 mm in the contralateral cortex. In the overwhelming majority of neurons, latencies of antidromic responses were between 1.2 and 3.1 ms; however, some callosal neurons had much longer latencies, ≤18.5 ms. Some neurons were excited monosynaptically through the callosal pathway and identified antidromically from appropriate thalamic nuclei, thus revealing a callosal-corticothalamic pathway. Data are discussed in relation to the commissural spread of fast and slow normal oscillations as well as paroxysmal activities.

The mamillothalamic pathways: my first encounter with the thalamus

2017 ◽  
Author(s):  
Ray Guillery
Keyword(s):  
Sensory Input ◽  
Great Success ◽  
Cortical Lesions ◽  
Head Direction ◽  
Thalamic Nuclei ◽  
Sensory Pathways ◽  
Cortical Areas ◽  
Thalamic Relay ◽  
The Many

My thesis studies had stimulated an interest in the mamillothalamic pathways but also some puzzlement because we knew nothing about the nature of the messages passing along these pathways. Several laboratories were studying the thalamic relay of sensory pathways with great success during my post-doctoral years. Each sensory relay could be understood in terms of the appropriate sensory input, but we had no way of knowing the meaning of the mamillothalamic messages. I introduce these nuclei as an example of the many thalamic nuclei about whose input functions we still know little or nothing. Early clinical studies of mamillary lesions had suggested a role in memory formation, whereas evidence from cortical lesions suggested a role in emotional experiences. Studies of the smallest of the three nuclei forming these pathways then showed it to be concerned with sensing head direction, relevant but not sufficient for defining an animal’s position in space. More recent studies based on studies of cortical activity or cortical damage have provided a plethora of suggestions: as so often, the answers reported depend on the questions asked. That simple conclusion is relevant for all transthalamic pathways. The evidence introduced in Chapter 1, that thalamocortical messages have dual meanings, suggests that we need to rethink our questions. It may prove useful to look at the motor outputs of relevant cortical areas to get clues about some appropriate questions.

scholarly journals Subcortical circuits mediate communication between primary sensory cortical areas in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Michael Lohse ◽  
Johannes C. Dahmen ◽  
Victoria M. Bajo ◽  
Andrew J. King
Keyword(s):  
Cortical Neurons ◽  
Common Property ◽  
Primary Auditory Cortex ◽  
Facilitatory Effect ◽  
Thalamic Nuclei ◽  
Auditory Midbrain ◽  
Cortical Areas ◽  
Auditory Responses ◽  
Evoked Activity

AbstractIntegration of information across the senses is critical for perception and is a common property of neurons in the cerebral cortex, where it is thought to arise primarily from corticocortical connections. Much less is known about the role of subcortical circuits in shaping the multisensory properties of cortical neurons. We show that stimulation of the whiskers causes widespread suppression of sound-evoked activity in mouse primary auditory cortex (A1). This suppression depends on the primary somatosensory cortex (S1), and is implemented through a descending circuit that links S1, via the auditory midbrain, with thalamic neurons that project to A1. Furthermore, a direct pathway from S1 has a facilitatory effect on auditory responses in higher-order thalamic nuclei that project to other brain areas. Crossmodal corticofugal projections to the auditory midbrain and thalamus therefore play a pivotal role in integrating multisensory signals and in enabling communication between different sensory cortical areas.

Somatosensory cortical efferent neurons of the awake rabbit: latencies to activation via supra--and subthreshold receptive fields

1996 ◽  
Vol 75 (4) ◽  
pp. 1753-1759 ◽  
Author(s):  
H. A. Swadlow ◽  
T. P. Hicks
Keyword(s):  
High Speed ◽  
Receptive Fields ◽  
Cortical Cell ◽  
Sensory Stimulation ◽  
Inhibitory Response ◽  
Postsynaptic Potentials ◽  
Peripheral Stimulation ◽  
Efferent Neurons ◽  
Excitatory Component ◽  
Peripheral Sensory

1. Latencies to peripheral sensory stimulation were examined in four classes of antidromically identified efferent neurons in the primary somatosensory cortex (S1) of awake rabbits. Both suprathreshold responses (action potentials) and subthreshold responses were examined. Subthreshold responses were examined by monitoring the thresholds of efferent neurons to juxtasomal current pulses (JSCPs) delivered through the recording microelectrode (usually 1-3 microA). Through the use of this method, excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) were manifested as decreases and increases in threshold, respectively. Efferent populations examined included callosal (CC) neurons, ipsilateral corticocortical (C-IC) neurons, and descending corticofugal neurons of layer 5 (CF-5) and layer 6 (CF-6). Very brief air puffs (rise and fall times 0.6 ms) were delivered to the receptor periphery via a high-speed solenoid valve. 2. Whereas all CF-5 neurons had demonstrable suprathreshold excitatory and/or inhibitory responses to peripheral stimulation, most CC, C-IC, and CF-6 neurons did not. CC and CF-6 neurons that yielded no suprathreshold response to the stimulus had lower axonal conduction velocities than those that did respond (P < 0.0001 in both cases). However, subthreshold receptive fields could be demonstrated in many of the otherwise unresponsive CC (81%), C-IC (88%), and CF-6 (43%) neurons. The subthreshold responses usually consisted of an initial excitatory component (a decrease in the threshold to the JSCP) and a subsequent long-duration (> 80 ms) inhibitory component. A few neurons (1 CC, 1 C-IC, and 5 CF-6) showed an initial short latency inhibitory response in the absence of any excitatory component. 3. Some CC and C-IC neurons yielded supra- and/or subthreshold responses to peripheral stimulation at latencies of 6.1-7 ms. All such neurons were found at intermediate cortical depths (thought to correspond to deep layer 2-3 through layer 5). It is argued that such latencies are indicative of monosynaptic activation via thalamic afferents. Very superficial CC and C-IC neurons, and all CF-6 neurons responded to latencies of > 7 ms. All CF-5 neurons responded to latencies of > 8 ms, although many were found at the same depth as the deeper CC and C-IC neurons that responded at monosynaptic latencies. These results indicate that cortical cell type as well as laminar position are important factors that determine the sequence of intracortical neuronal activation after peripheral sensory stimulation.

Absence of a Prevalent Laminar Distribution of IPSPs in Association Cortical Neurons of Cat

1997 ◽  
Vol 78 (5) ◽  
pp. 2742-2753 ◽  
Author(s):  
Diego Contreras ◽  
Niklaus Dürmüller ◽  
Mircea Steriade
Keyword(s):  
Cortical Neurons ◽  
Feedback Inhibition ◽  
Anterior Part ◽  
Cortical Stimulation ◽  
Association Cortex ◽  
Postsynaptic Potentials ◽  
Thalamic Stimulation ◽  
Laminar Distribution ◽  
Deep Layers

Contreras, Diego, Niklaus Dürmüller, and Mircea Steriade. Absence of a prevalent laminar distribution of IPSPs in association cortical neurons of cat. J. Neurophysiol. 78: 2742–2753, 1997. The depth distribution of inhibitory postsynaptic potentials (IPSPs) was studied in cat suprasylvian (association) cortex in vivo. Single and dual simultaneous intracellular recordings from cortical neurons were performed in the anterior part of suprasylvian gyrus (area 5). Synaptic responses were obtained by stimulating the suprasylvian cortex, 2–3 mm anterior to the recording site, as well as the thalamic lateral posterior (LP) nucleus. Neurons were recorded from layers 2 to 6 and were classified as regular spiking (RS, n = 132), intrinsically bursting (IB, n = 24), and fast spiking (FS, n = 4). Most IB cells were located in deep layers (below 0.7 mm, n = 19), but we also found some IB cells more superficially (between 0.2 and 0.5 mm, n = 5). Deeply lying corticothalamic neurons were identified by their antidromic invasion on thalamic stimulation. Neurons responded with a combination of excitatory postsynaptic potentials (EPSPs) and IPSPs to both cortical and thalamic stimulation. No consistent relation was found between cell type or cell depth and the amplitude or duration of the IPSPs. In response to thalamic stimulation, RS cells had IPSPs of 7.9 ± 0.9 (SE) mV amplitude and 88.9 ± 6.4 ms duration. In IB cells, IPSPs elicited by thalamic stimulation had 7.4 ± 1.3 mV amplitude and 84.7 ± 14.3 ms duration. The differences between the two (RS and IB) groups were not statistically significant. Compared with thalamically elicited inhibitory responses, cortical stimulation evoked IPSPs with higher amplitude (12.3 ± 1.7 mV) and longer duration (117 ± 17.3 ms) at all depths. Both cortically and thalamically evoked IPSPs were predominantly monophasic. Injections of Cl− fully reversed thalamically as well as cortically evoked IPSPs and revealed additional late synaptic components in response to cortical stimulation. These data show that the amount of feed forward and feedback inhibition to cat's cortical association cells is not orderly distributed to distinct layers. Thus local cortical microcircuitry goes beyond the simplified structure determined by cortical layers.

Duodenal neurons provide nicotinic fast synaptic input to sphincter of Oddi neurons in guinea pig

1999 ◽  
Vol 277 (1) ◽  
pp. G226-G234 ◽  
Author(s):  
Gary M. Mawe ◽  
Audra L. Kennedy
Keyword(s):  
Synaptic Input ◽  
Sphincter Of Oddi ◽  
Duodenal Mucosa ◽  
Postsynaptic Potentials ◽  
Chemical Coding ◽  
Neural Connections ◽  
Inhibitory Postsynaptic Potentials ◽  
Neural Communication ◽  
Antidromic Responses ◽  
Synaptic Responses

We have investigated the existence of neural connections between the duodenum and the sphincter of Oddi (SO). Stimulation of duodenal myenteric fiber bundles elicited synaptic responses in SO neurons, which included nicotinic fast excitatory postsynaptic potentials (EPSPs), slow EPSPs, and α2-adrenoreceptor-mediated inhibitory postsynaptic potentials. After 48 h in organ culture, when extrinsic fibers had diminished, only the fast EPSPs persisted. Duodenal mucosal stimulation also elicited nicotinic fast EPSPs in SO neurons. There was no association between the SO neurons that received duodenal input and their chemical coding. A reciprocal projection also exists from the SO to the duodenum. In acute and cultured preparations, duodenal myenteric stimulation caused antidromic responses in 20% of SO neurons. Furthermore, 45.6 ± 10.5 neurons in SO ganglia were retrogradely labeled from dye application sites in the duodenum. It is proposed that bidirectional neural communication occurs between the duodenum and the SO and that duodenal neurons provide excitatory fast synaptic input to SO neurons through a reflex that can be activated at the duodenal mucosa.

scholarly journals Structural Brain Architectures Match Intrinsic Functional Networks and Vary across Domains: A Study from 15 000+ Individuals

2020 ◽  
Vol 30 (10) ◽  
pp. 5460-5470 ◽  
Author(s):  
Na Luo ◽  
Jing Sui ◽  
Anees Abrol ◽  
Jiayu Chen ◽  
Jessica A Turner ◽  
...  
Keyword(s):  
Interindividual Variability ◽  
Association Cortex ◽  
Functional Networks ◽  
Functional Domains ◽  
Network Module ◽  
Replication Cohort ◽  
Discovery Cohort ◽  
Cortical Areas ◽  
Frontoparietal Network ◽  
Structural Networks

Abstract Brain structural networks have been shown to consistently organize in functionally meaningful architectures covering the entire brain. However, to what extent brain structural architectures match the intrinsic functional networks in different functional domains remains under explored. In this study, based on independent component analysis, we revealed 45 pairs of structural-functional (S-F) component maps, distributing across nine functional domains, in both a discovery cohort (n = 6005) and a replication cohort (UK Biobank, n = 9214), providing a well-match multimodal spatial map template for public use. Further network module analysis suggested that unimodal cortical areas (e.g., somatomotor and visual networks) indicate higher S-F coherence, while heteromodal association cortices, especially the frontoparietal network (FPN), exhibit more S-F divergence. Collectively, these results suggest that the expanding and maturing brain association cortex demonstrates a higher degree of changes compared with unimodal cortex, which may lead to higher interindividual variability and lower S-F coherence.

scholarly journals Thiamine Deficiency Induced Neurochemical, Neuroanatomical, and Neuropsychological Alterations: A Reappraisal

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Raffaele Nardone ◽  
Yvonne Höller ◽  
Monica Storti ◽  
Monica Christova ◽  
Frediano Tezzon ◽  
...  
Keyword(s):  
Thiamine Deficiency ◽  
Cortical Cell ◽  
Cell Loss ◽  
Brain Regions ◽  
Experimental Models ◽  
Neurological Sequela ◽  
Thalamic Nuclei ◽  
Chronic Alcoholic ◽  
Ethanol Abuse ◽  
And Function

Nutritional deficiency can cause, mainly in chronic alcoholic subjects, the Wernicke encephalopathy and its chronic neurological sequela, the Wernicke-Korsakoff syndrome (WKS). Long-term chronic ethanol abuse results in hippocampal and cortical cell loss. Thiamine deficiency also alters principally hippocampal- and frontal cortical-dependent neurochemistry; moreover in WKS patients, important pathological damage to the diencephalon can occur. In fact, the amnesic syndrome typical for WKS is mainly due to the damage in the diencephalic-hippocampal circuitry, including thalamic nuclei and mammillary bodies. The loss of cholinergic cells in the basal forebrain region results in decreased cholinergic input to the hippocampus and the cortex and reduced choline acetyltransferase and acetylcholinesterase activities and function, as well as in acetylcholine receptor downregulation within these brain regions. In this narrative review, we will focus on the neurochemical, neuroanatomical, and neuropsychological studies shedding light on the effects of thiamine deficiency in experimental models and in humans.

scholarly journals Primary Graviceptive System and Astasia: Case Report and Literature Review

2021 ◽  
Author(s):  
Ko-Ting Chen ◽  
Sheng-Yao Huang ◽  
Yi-Jye Chen
Keyword(s):  
English Literature ◽  
Vestibular Nuclei ◽  
Subcortical White Matter ◽  
Upright Posture ◽  
Neural Pathways ◽  
Thalamic Nuclei ◽  
Cortical Areas ◽  
Cortical Projections ◽  
Contralateral Projection ◽  
Motor Strength

Abstract Purpose of ReviewAstasia refers to the inability to maintain upright posture during standing, despite having full motor strength. However, the pathophysiology and neural pathways of astasia remains unclear.Recent FindingsWe analyzed 26, including ours, non-psychogenic astasia patients in English literature. Seventy-three percent of them were man, 73% were associated with other neurologic symptoms and 62% of reported lesions were at right side. Contralateral lateropulsion was very common followed by retropulsion while describing astasia. Infarction (54%) was the most commonly reported cause. Thalamus (65%) was the most commonly reported location. Infarction being the mostly likely to recover (mean:10.6 days), while lesions at brainstem had longer time to recover (mean: 61.6 days).SummaryThe underlying interrupted pathway may be the primary graviceptive system, which composed of at least five unilateral and contralateral projection fibers from vestibular nuclei to thalamic nuclei, and thalamo-cortical projections including subcortical white matter tracts and cortical areas.

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