The Experts below are selected from a list of 19002 Experts worldwide ranked by ideXlab platform
Laszlo Zaborszky - One of the best experts on this subject based on the ideXlab platform.
-
Chapter 28 – The Basal Forebrain Cholinergic Projection System in Mice
The Mouse Nervous System, 2012Co-Authors: Laszlo Zaborszky, Anthony N. Van Den Pol, Erika GyengesiAbstract:Publisher Summary The Basal Forebrain is composed of an affiliation of heterogeneous structures and includes the medial septum, ventral pallidum (VP), diagonal band nuclei, substantia innominata/extended amygdala, and peripallidal regions. The Basal Forebrain is located close to the medial and ventral surfaces of the cerebral hemispheres that develop from the subpallium. This highly complex brain region has been implicated in cortical activation, attention, motivation, memory, and neuropsychiatric disorders such as Alzheimer's disease Parkinson's disease, schizophrenia, and drug abuse. The Basal Forebrain contains a heterogeneous mixture of cell types that differ in transmitter content, morphology, and projection pattern. One of the most prominent features of the mammalian Basal Forebrain is the presence of a collection of aggregated and non-aggregated, large, hyperchromic neurons, many of them containing choline acetyl transferase (ChAT), the critical enzyme in the synthesis of acetylcholine (ACh); these neurons project to the cerebral cortex. Single unit studies in anesthetized and behaving rats showed that identified cholinergic neurons increase their firing during cortical EEG activation. Activity of Basal Forebrain cholinergic neurons is associated with an increase in cortical release of ACh. Cortical ACh release is high during wakefulness and rapid eye movement (REM) sleep and is low during non-REM sleep that is characterized by EEG delta power with periodic oscillations of medium-frequency high amplitude spindles. Against the relatively “diffuse” termination of the ascending brainstem and hypothalamic axons in the Basal Forebrain, the restricted input from the prefrontal cortex to Basal Forebrain neurons, including specific clusters, might be instrumental in communicating state-related changes from Basal Forebrain neurons to specific posterior sensory areas to modulate selective cognitive processes.
-
Sleep-wake mechanisms and Basal Forebrain circuitry.
Frontiers in bioscience : a journal and virtual library, 2003Co-Authors: Laszlo Zaborszky, Alvaro DuqueAbstract:The seminal studies by von Economo in humans (1) and by Nauta (2) in rats implicated specific Basal Forebrain areas at the preoptic level as important in sleep regulation. In the last two decades, studies employing recording of single neurons and monitoring of sleep parameters with subsequent chemical and electron microscopic identification of the synaptic input-output relations of these recorded neurons, provided an increasingly detailed understanding of the function of specific neurotransmitters and corresponding chemically specific neuronal circuits in the Forebrain in relation to sleep-wake states. In this review, first the electrophysiology of cholinergic and parvalbumin-containing GABAergic Basalo-cortical projection neurons is described, followed by an examination of possible functional interconnections between Basal Forebrain neuropeptide Y- (NPY) and somatostatin-containing putative interneurons and cholinergic projection neurons. A survey of various inputs to Basal Forebrain neurons that show state-related changes is then discussed in relation to their possible effects via Basal Forebrain circuitry on cortical activity. This treatise suggests that cholinergic and GABAergic projection neurons of the Basal Forebrain are anatomically in a unique position to enable the channeling of specific cellular and homeostatic states from different subcortical systems to the cortical mantle to modulate behavioral adaptation and cognitive functions.
-
Local synaptic connections of Basal Forebrain neurons
Behavioural brain research, 2000Co-Authors: Laszlo Zaborszky, Alvaro DuqueAbstract:Single, biocytin filled neurons in combination with immunocytochemistry and retrograde tracing as well as material with traditional double-immunolabeling were used at the light and electron microscopic levels to study the neural circuitry within the Basal Forebrain. Cholinergic neurons projecting to the frontal cortex exhibited extensive local collaterals terminating on non-cholinergic, (possible GABAergic) neurons within the Basal Forebrain. Elaborate axon arbors confined to the Basal Forebrain region also originated from NPY, somatostatin and other non-cholinergic interneurons. It is proposed that putative interneurons together with local collaterals from projection neurons contribute to regional integrative processing in the Basal Forebrain that may participate in more selective functions, such as attention and cortical plasticity.
-
The Basal Forebrain corticopetal system revisited
Annals of the New York Academy of Sciences, 1999Co-Authors: Laszlo Zaborszky, Kevin C.h. Pang, J. Somogyi, Zoltan Nadasdy, Imre KallóAbstract:The medial septum, diagonal bands, ventral pallidum, substantia innominata, globus pallidus, and internal capsule contain a heterogeneous population of neurons, including cholinergic and noncholinergic (mostly GABA containing), corticopetal projection neurons, and interneurons. This highly complex brain region, which constitutes a significant part of the Basal Forebrain has been implicated in attention, motivation, learning, as well as in a number of neuropsychiatric disorders, such as Alzheimer's disease, Parkinson's disease, and schizophrenia. Part of the difficulty in understanding the functions of the Basal Forebrain, as well as the aberrant information-processing characteristics of these disease states lies in the fact that the organizational principles of this brain area remained largely elusive. On the basis of new anatomical data, it is proposed that a large part of the Basal Forebrain corticopetal system be organized into longitudinal bands. Considering the topographic organization of cortical afferents to different divisions of the prefrontal cortex and a similar topographic projection of these prefrontal areas to Basal Forebrain regions, it is suggested that several functionally segregated cortico-prefronto-Basal Forebrain-cortical circuits exist. It is envisaged that such specific "triangular" circuits could amplify selective attentional processing in posterior sensory cortical areas.
-
Cortical input to the Basal Forebrain
Neuroscience, 1997Co-Authors: Laszlo Zaborszky, Ronald P.a. Gaykema, D.j. Swanson, William E. CullinanAbstract:The arborization pattern and postsynaptic targets of corticofugal axons in Basal Forebrain areas have been studied by the combination of anatomical tract-tracing and pre- and postembedding immunocytochemistry. The anterograde neuronal tracer Phaseolus vulgaris leucoagglutinin was iontophoretically delivered into different neocortical (frontal, parietal, occipital), allocortical (piriform) and mesocortical (insular, prefrontal) areas in rats. To identify the transmitter phenotype in pre- or postsynaptic elements, the tracer staining was combined with immunolabeling for either glutamate or GABA, or with immunolabeling for choline acetyltransferase or parvalbumin. Tracer injections into medial and ventral prefrontal areas gave rise to dense terminal arborizations in extended Basal Forebrain areas, particularly in the horizontal limb of the diagonal band and the region ventral to it. Terminals were also found to a lesser extent in the ventral part of the substantia innominata and in ventral pallidal areas adjoining ventral striatal territories. Similarly, labeled fibers from the piriform and insular cortices were found to reach lateral and ventral parts of the substantia innominata, where terminal varicosities were evident. In contrast, descending fibers from neocortical areas were smooth, devoid of terminal varicosities, and restricted to the myelinated fascicles of the internal capsule en route to more caudal targets. Ultrastructural studies obtained indicated that corticofugal axon terminals in the Basal Forebrain areas form synaptic contact primarily with dendritic spines or small dendritic branches (89%); the remaining axon terminals established synapses with dendritic shafts. All tracer labeled axon terminals were immunonegative for GABA, and in the cases investigated, were found to contain glutamate immunoreactivity. In material stained for the anterograde tracer and choline acetyltransferase, a total of 63 Phaseolus vulgaris leucoagglutinin varicosities closely associated with cholinergic profiles were selected for electron microscopic analysis. From this material, 37 varicosities were identified as establishing asymmetric synaptic contacts with neurons that were immunonegative for choline acetyltransferase, including spines and small dendrites (87%) or dendritic shafts (13%). Unequivocal evidence for synaptic interactions between tracer labeled terminals and cholinergic profiles could not be obtained in the remaining cases. From material stained for the anterograde tracer and parvalbumin, 40% of the labeled terminals investigated were found to establish synapses with parvalbumin-positive elements; these contacts were on dendritic shafts and were of the asymmetrical type. The present data suggest that corticofugal axons innervate Forebrain neurons that are primarily inhibitory and non-cholinergic; local Forebrain axonal arborizations of these cells may represent a mechanism by which prefrontal cortical areas control Basal Forebrain cholinergic neurons outside the traditional boundaries of pallidal areas.
Didier De Saint Jan - One of the best experts on this subject based on the ideXlab platform.
-
Basal Forebrain GABAergic innervation of olfactory bulb periglomerular interneurons.
The Journal of physiology, 2019Co-Authors: Alvaro Sanz Diez, Marion Najac, Didier De Saint JanAbstract:KEY POINTS Basal Forebrain long-range projections to the olfactory bulb are important for olfactory sensitivity and odour discrimination. Using optogenetics, it was confirmed that Basal Forebrain afferents mediate IPSCs on granule and deep short axon cells. It was also shown that they selectively innervate specific subtypes of periglomerular (PG) cells. Three different subtypes of type 2 PG cells receive GABAergic IPSCs from the Basal Forebrain but not from other PG cells. Type 1 PG cells, in contrast, do not receive inputs from the Basal Forebrain but do receive inhibition from other PG cells. These results shed new light on the complexity and specificity of glomerular inhibitory circuits, as well as on their modulation by the Basal Forebrain. ABSTRACT Olfactory bulb circuits are dominated by multiple inhibitory pathways that finely tune the activity of mitral and tufted cells, the principal neurons, and regulate odour discrimination. Granule cells mediate interglomerular lateral inhibition between mitral and tufted cells' lateral dendrites whereas diverse subtypes of periglomerular (PG) cells mediate intraglomerular lateral inhibition between their apical dendrites. Deep short axon cells form broad intrabulbar inhibitory circuits that regulate both populations of interneurons. Little is known about the extrabulbar GABAergic circuits that control the activity of these various interneurons. We examined this question using patch-clamp recordings and optogenetics in olfactory bulb slices from transgenic mice. We showed that axonal projections emanating from diverse Basal Forebrain GABAergic neurons densely project in all layers of the olfactory bulb. These long-range GABAergic projections provide a prominent synaptic input on granule and short axon cells in deep layers as well as on selective subtypes of PG cells. Specifically, three different subclasses of type 2 PG cells receive robust and target-specific Basal Forebrain inputs but have little local interactions with other PG cells. In contrast, type 1 PG cells are not innervated by Basal Forebrain fibres but do interact with other PG cells. Thus, attention-regulated Basal Forebrain inputs regulate inhibition in all layers of the olfactory bulb with a previously overlooked synaptic complexity that further defines interneuron subclasses.
-
Basal Forebrain gabaergic innervation of olfactory bulb periglomerular interneurons
bioRxiv, 2018Co-Authors: Alvaro Sanz Diez, Marion Najac, Didier De Saint JanAbstract:Olfactory bulb circuits are dominated by multiple inhibitory pathways that finely tune the activity of mitral and tufted cells, the principal neurons, and regulate odor discrimination. Granule cells mediate interglomerular lateral inhibition between mitral and tufted cells lateral dendrites whereas diverse subtypes of periglomerular (PG) cells mediate intraglomerular lateral inhibition between their apical dendrites. Deep short axon cells form broad intrabulbar inhibitory circuits that regulate both populations of interneurons. Little is known about the extrabulbar GABAergic circuits that control the activity of these various interneurons. We examined this question using patch-clamp recordings and optogenetics in olfactory bulb slices from transgenic mice. We show that axonal projections emanating from diverse Basal Forebrain GABAergic neurons densely project in all layers of the olfactory bulb. These long-range GABAergic projections provide a prominent synaptic input on granule and short axon cells in deep layers as well as on selective subtypes of PG cells. Specifically, three different subclasses of type 2 PG cells receive robust and target-specific Basal Forebrain inputs but have little local interactions with other PG cells. In contrast, type 1 PG cells are not innervated by Basal Forebrain fibers but do interact with other PG cells. Thus, attention-regulated Basal Forebrain inputs regulate inhibition in all layers of the olfactory bulb with a previously overlooked synaptic complexity that further defines interneuron subclasses.
-
Basal Forebrain control of olfactory bulb interneurons
bioRxiv, 2017Co-Authors: Alvaro Sanz Diez, Marion Najac, Didier De Saint JanAbstract:Olfactory bulb circuits transform a spatially organized olfactory sensory input into a temporal output code in mitral and tufted cells. Various GABAergic interneurons modulate this early processing. However, little is known about the GABAergic circuits that regulate the activity of olfactory bulb interneurons. We examined this question using patch-clamp recording and optogenetics in olfactory bulb slices. We found that long-range centrifugal projections from the Basal Forebrain provide a prominent GABAergic synaptic input on most subtypes of periglomerular (PG) cells, deep short axon cells and granule cells. We also demonstrate that Basal Forebrain inputs have specific properties and distinct functional impacts depending on the postsynaptic PG cell subtype. Thus, centrifugal GABAergic afferents may excite, inhibit or sequentially inhibit and excite distinct PG cells using co-transmission of acetylcholine. Together, these results reinforce the idea that Basal Forebrain projections have multiple, complex and so far overlooked implications on olfactory bulb processing.
Alvaro Sanz Diez - One of the best experts on this subject based on the ideXlab platform.
-
Basal Forebrain GABAergic innervation of olfactory bulb periglomerular interneurons.
The Journal of physiology, 2019Co-Authors: Alvaro Sanz Diez, Marion Najac, Didier De Saint JanAbstract:KEY POINTS Basal Forebrain long-range projections to the olfactory bulb are important for olfactory sensitivity and odour discrimination. Using optogenetics, it was confirmed that Basal Forebrain afferents mediate IPSCs on granule and deep short axon cells. It was also shown that they selectively innervate specific subtypes of periglomerular (PG) cells. Three different subtypes of type 2 PG cells receive GABAergic IPSCs from the Basal Forebrain but not from other PG cells. Type 1 PG cells, in contrast, do not receive inputs from the Basal Forebrain but do receive inhibition from other PG cells. These results shed new light on the complexity and specificity of glomerular inhibitory circuits, as well as on their modulation by the Basal Forebrain. ABSTRACT Olfactory bulb circuits are dominated by multiple inhibitory pathways that finely tune the activity of mitral and tufted cells, the principal neurons, and regulate odour discrimination. Granule cells mediate interglomerular lateral inhibition between mitral and tufted cells' lateral dendrites whereas diverse subtypes of periglomerular (PG) cells mediate intraglomerular lateral inhibition between their apical dendrites. Deep short axon cells form broad intrabulbar inhibitory circuits that regulate both populations of interneurons. Little is known about the extrabulbar GABAergic circuits that control the activity of these various interneurons. We examined this question using patch-clamp recordings and optogenetics in olfactory bulb slices from transgenic mice. We showed that axonal projections emanating from diverse Basal Forebrain GABAergic neurons densely project in all layers of the olfactory bulb. These long-range GABAergic projections provide a prominent synaptic input on granule and short axon cells in deep layers as well as on selective subtypes of PG cells. Specifically, three different subclasses of type 2 PG cells receive robust and target-specific Basal Forebrain inputs but have little local interactions with other PG cells. In contrast, type 1 PG cells are not innervated by Basal Forebrain fibres but do interact with other PG cells. Thus, attention-regulated Basal Forebrain inputs regulate inhibition in all layers of the olfactory bulb with a previously overlooked synaptic complexity that further defines interneuron subclasses.
-
Basal Forebrain gabaergic innervation of olfactory bulb periglomerular interneurons
bioRxiv, 2018Co-Authors: Alvaro Sanz Diez, Marion Najac, Didier De Saint JanAbstract:Olfactory bulb circuits are dominated by multiple inhibitory pathways that finely tune the activity of mitral and tufted cells, the principal neurons, and regulate odor discrimination. Granule cells mediate interglomerular lateral inhibition between mitral and tufted cells lateral dendrites whereas diverse subtypes of periglomerular (PG) cells mediate intraglomerular lateral inhibition between their apical dendrites. Deep short axon cells form broad intrabulbar inhibitory circuits that regulate both populations of interneurons. Little is known about the extrabulbar GABAergic circuits that control the activity of these various interneurons. We examined this question using patch-clamp recordings and optogenetics in olfactory bulb slices from transgenic mice. We show that axonal projections emanating from diverse Basal Forebrain GABAergic neurons densely project in all layers of the olfactory bulb. These long-range GABAergic projections provide a prominent synaptic input on granule and short axon cells in deep layers as well as on selective subtypes of PG cells. Specifically, three different subclasses of type 2 PG cells receive robust and target-specific Basal Forebrain inputs but have little local interactions with other PG cells. In contrast, type 1 PG cells are not innervated by Basal Forebrain fibers but do interact with other PG cells. Thus, attention-regulated Basal Forebrain inputs regulate inhibition in all layers of the olfactory bulb with a previously overlooked synaptic complexity that further defines interneuron subclasses.
-
Basal Forebrain control of olfactory bulb interneurons
bioRxiv, 2017Co-Authors: Alvaro Sanz Diez, Marion Najac, Didier De Saint JanAbstract:Olfactory bulb circuits transform a spatially organized olfactory sensory input into a temporal output code in mitral and tufted cells. Various GABAergic interneurons modulate this early processing. However, little is known about the GABAergic circuits that regulate the activity of olfactory bulb interneurons. We examined this question using patch-clamp recording and optogenetics in olfactory bulb slices. We found that long-range centrifugal projections from the Basal Forebrain provide a prominent GABAergic synaptic input on most subtypes of periglomerular (PG) cells, deep short axon cells and granule cells. We also demonstrate that Basal Forebrain inputs have specific properties and distinct functional impacts depending on the postsynaptic PG cell subtype. Thus, centrifugal GABAergic afferents may excite, inhibit or sequentially inhibit and excite distinct PG cells using co-transmission of acetylcholine. Together, these results reinforce the idea that Basal Forebrain projections have multiple, complex and so far overlooked implications on olfactory bulb processing.
John P Bruno - One of the best experts on this subject based on the ideXlab platform.
-
The neglected constituent of the Basal Forebrain corticopetal projection system: GABAergic projections
European Journal of Neuroscience, 2002Co-Authors: Martin Sarter, John P BrunoAbstract:At least half of the Basal Forebrain neurons which project to the cortex are GABAergic. Whilst hypotheses about the attentional functions mediated by the cholinergic component of this corticopetal projection system have been substantiated in recent years, knowledge about the functional contributions of its GABAergic branch has remained extremely scarce. The possibility that Basal Forebrain GABAergic neurons that project to the cortex are selectively contacted by corticofugal projections suggests that the functions of the GABAergic branch can be conceptualized in terms of mediating executive aspects of cognitive performance, including the switching between multiple input sources and response rules. Such speculations gain preliminary support from the effects of excitotoxic lesions that preferentially, but not selectively, target the noncholinergic component of the Basal Forebrain corticopetal system, on performance in tasks involving demands on cognitive flexibility. Progress in understanding the cognitive functions of the Basal Forebrain system depends on evidence regarding its main noncholinergic components, and the generation of such evidence is contingent on the development of methods to manipulate and monitor selectively the activity of the GABAergic corticopetal projections.
-
Amphetamine-stimulated cortical acetylcholine release: role of the Basal Forebrain
Brain research, 2001Co-Authors: H. Moore Arnold, Martin Sarter, Jim R. Fadel, John P BrunoAbstract:Abstract Systemic administration of amphetamine results in increases in the release of acetylcholine in the cortex. Basal Forebrain mediation of this effect was examined in three experiments using microdialysis in freely-moving rats. Experiment 1 examined whether dopamine receptor activity within the Basal Forebrain was necessary for amphetamine-induced increase in cortical acetylcholine by examining whether intra-Basalis perfusion of dopamine antagonists attenuates this increase. Systemic administration of 2.0 mg/kg amphetamine increased dopamine efflux within the Basal Forebrain nearly 700% above Basal levels. However, the increase in cortical acetylcholine efflux following amphetamine administration was unaffected by intra-Basalis perfusions of high concentrations of D1- (100 μM SCH 23390) or D2-like (100 μM sulpiride) dopamine receptor antagonists. Experiments 2 and 3 determined whether glutamatergic or GABAergic local modulation of the excitability of the Basal Forebrain cholinergic neurons influences the ability of systemic amphetamine to increase cortical acetylcholine efflux. In Experiment 2, perfusion of kynurenate (1.0 mM), a non-selective glutamate receptor antagonist, into the Basal Forebrain attenuated the increase in cortical acetylcholine produced by amphetamine. Experiment 3 revealed that positive modulation of GABAergic transmission by bilateral intra-Basalis infusion of the benzodiazepine receptor agonist chlordiazepoxide (40 μg/hemisphere) also attenuated the amphetamine-stimulated increase in cortical acetylcholine efflux. These data suggest that amphetamine increases cortical acetylcholine release via a complex neuronal network rather than simply increasing Basal Forebrain D1 or D2 receptor activity.
-
Basal Forebrain glutamatergic modulation of cortical acetylcholine release
Synapse (New York N.Y.), 2001Co-Authors: J. Fadel, Martin Sarter, John P BrunoAbstract:The mediation of cortical ACh release by Basal Forebrain glutamate receptors was studied in awake rats fitted with microdialysis probes in medial prefrontal cortex and ipsilateral Basal Forebrain. Repeated presentation of a stimulus consisting of exposure to darkness with the opportunity to consume a sweetened cereal resulted in a transient increase in cortical ACh efflux. This stimulated release was dependent on Basal Forebrain glutamate receptor activity as intraBasalis perfusion with the ionotropic glutamate receptor antagonist kynurenate (1.0 mM) markedly attenuated darkness/cereal-induced ACh release. Activation of AMPA/kainate receptors by intraBasalis perfusion of kainate (100 microM) was sufficient to increase cortical ACh efflux even under Basal (nonstimulated) conditions. This effect of kainate was blocked by coperfusion with the antagonist DNQX (0.1-5.0 mM). Stimulation of NMDA receptors with intraBasalis perfusion of NMDA (50 or 200 microM) did not increase Basal cortical ACh efflux. However, perfusion of NMDA in rats following exposure to the darkness/cereal stimulus resulted in a potentiation of both the magnitude and duration of stimulated cortical ACh efflux. Moreover, intraBasalis perfusion of the higher dose of NMDA resulted in a rapid increase in cortical ACh efflux even before presentation of the darkness/cereal stimulus, suggesting an anticipatory change in the excitability of Basal Forebrain cholinergic neurons. These data demonstrate that Basal Forebrain glutamate receptors contribute to the stimulation of cortical ACh efflux in response to behavioral stimuli. The specific roles of Basal Forebrain glutamate receptor subtypes in mediating cortical ACh release differ and depend on the level of activity of Basal Forebrain cholinergic neurons.
Daniel B Polley - One of the best experts on this subject based on the ideXlab platform.
-
the cholinergic Basal Forebrain links auditory stimuli with delayed reinforcement to support learning
Neuron, 2019Co-Authors: Blaise Robert, Daniel B PolleyAbstract:Summary Animals learn to fear conditioned sound stimuli (CSs) that accompany aversive unconditioned stimuli (USs). Auditory cortex (ACx) circuits reorganize to support auditory fear learning when CS-evoked activity temporally overlaps with US-evoked acetylcholine release from the Basal Forebrain. Here we describe robust fear learning and acetylcholine-dependent ACx plasticity even when the US is delayed by several seconds following CS offset. A 5-s CS-US gap was not bridged by persistent CS-evoked spiking throughout the trace period. Instead, within minutes following the start of conditioning, optogenetically identified Basal Forebrain neurons that encode the aversive US scaled up responses to the CS and increased functional coupling with the ACx. Over several days of conditioning, bulk imaging of cholinergic Basal Forebrain neurons revealed sustained sound-evoked activity that filled in the 5-s silent gap preceding the US. These findings identify a plasticity in the Basal Forebrain that supports learned associations between sensory stimuli and delayed reinforcement.
-
the cholinergic Basal Forebrain links sensory stimuli with delayed reinforcement to support learning
bioRxiv, 2019Co-Authors: Daniel B PolleyAbstract:Animals learn to fear conditioned sound stimuli (CS) that accompany aversive unconditioned stimuli (US). Auditory cortex (ACx) circuits reorganize to support auditory fear learning when CS-evoked activity temporally overlaps with US-evoked acetylcholine (ACh) release from the Basal Forebrain. Here, we describe robust fear learning and ACh-dependent ACx plasticity even when the US is delayed by several seconds following CS offset. A 5s CS-US gap was not bridged by persistent CS-evoked spiking throughout the trace period. Instead, within minutes following the start of conditioning, optogenetically identified Basal Forebrain neurons that encode the aversive US scaled up responses to the CS and increased functional coupling with ACx. Over several days of conditioning, bulk imaging of cholinergic Basal Forebrain neurons revealed sustained sound-evoked activity that filled in the 5s silent gap preceding the US. These findings identify a plasticity in the Basal Forebrain that supports learned associations between sensory stimuli and delayed reinforcement.
