The evolving theory of basal forebrain functional—anatomical ‘macrosystems’

Zahm, Daniel S.

doi:10.1016/j.neubiorev.2005.06.003

Cited by 108 publications

(103 citation statements)

References 224 publications

(296 reference statements)

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“…Nor did Lindvall and Björkland 46 or Fallon and Loughlin 47,48 have much to say about A8 in their respective chapters on central dopamine-containing neuronal systems, and Fallon 50 intentionally omitted consideration of A8 in deference to a brief report on it in the same congress 49 . As it turns out, just as A9 is most closely associated with neostriatum and the somatomotor apparatus, and A10 with the ventral striatopallidum 36 , A8 appears to be closely related to extended amygdala, which, as noted above, a substantial literature ties closely to behaviors driven by fear and anxiety (see also Refs. [66][67][68].…”

mentioning

confidence: 83%

“…cited above). The likelihood that dopaminergic actions on association formation play out in several different basal forebrain macrosystems, including the dorsal and ventral striatopallidum, extended amygdala, and the septal-preoptic system 30,33,36,80 …”

mentioning

confidence: 99%

“…Macrosystem outputs diverge into [1] reentrant pathways to the forebrain, including cortex, via synaptic relays in the thalamus, forebrain and brainstem and [2] descending pathways to somatic and autonomic motor effectors, via relays in the hypothalamus, mesopontine tegmentum and caudal brainstem. Accompanying the host of basic similarities shared by macrosystems are a variety of features that distinguish them, such as the richness and extent of medium spiny neuronal intrinsic axonal arbors, the numbers and transmitter phenotypes of associated large interneurons and the quantity and indentities of neuropeptides, neuropeptide and transmitter receptors, and intracellular signaling cascades utilized 30,[34][35][36] . This paper takes a closer look at the dopaminergic innervation of macrosystems.…”

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confidence: 99%

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The Dopaminergic Projection System, Basal Forebrain Macrosystems, and Conditioned Stimuli

Zahm¹,

Trimble²

2008

CNS spectr.

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This review begins with a description of some problems that in recent years have beset an influential circuit model of fear-conditioning and goes on to look at neuroanatomy that might subserve conditioning viewed in a broader perspective, including not only fear, but also appetitive, conditioning. The paper then focuses on basal forebrain functional-anatomical systems, or macrosystems, as they have come to be called, which Lennart Heimer and colleagues described beginning in the 1970's. Yet more specific attention is then given to the relationships of the dorsal and ventral striatopallidal systems and extended amygdala with the dopaminergic mesotelencephalic projection systems, culminating with the hypothesis that all macrosystems contribute to behavioral conditioning.There is tremendous current interest in the neurobiological mechanisms underlying conditioned fear stemming in large part from an increasing prevalence in American culture of anxiety and panic disorders, not to mention PTSD 1 . By 2000, the relevant brain circuitry had seemed to be satisfactorily described 2 , but a number of serious caveats had been voiced the preceding year 3 , and an unraveling process accelerated thereafter. Indeed, current theory on the neural substrates of fear conditioning has entered into a state of reassessment 4 .The essential elements of fear conditioning are described by the observation that pairing neutral and fear-arousing stimuli causes the neutral one to gain meaning such that it can then drive an organism's voluntary and involuntary actions. Thus, behaviorally, rats exposed to a brief tone followed immediately by a footshock will soon, frequently after a single trial, come to "freeze" upon hearing the tone. In LeDoux's 2 model of this phenomenon, neuroplasticity reflecting the attachment of "significance" to a neutral stimulus, i.e., heralding the transformation of neutral to conditioned stimulus (CS), occurs in the amygdala, specifically its lateral nucleus (LA). According to LeDoux's model, LA projects to another part of the amygdala, the central nucleus (CeA), which, in turn sends out divergent descending projections to somatic and autonomic motor effectors in the brainstem, eliciting behavioral freezing and accompanying autonomic responses. Consistent with the model, [1] sensory inputs bearing information about the aversive and neutral (to be conditioned) stimuli converge in LA 5 , and [2] an increase in the efficacy of CS-related synapses corresponds to conditioning [6][7][8] . But, soon it was realized that the CeA consists of two parts, a medial division (CeAm) from which most of its descending projections arise and to which LA does not project, and a lateral one (CeAl) to which it does. While CeAl projects to CeAm and thus might serve as a relay interposed between LA and CeAm, the CeAl to CeAm projection is nearly exclusively inhibitiory (GABAergic) and thus would inhibit rather than activate outputs to brainstem. The model was accordingly adjusted to emphasize instead a projection from LA to amygda...

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confidence: 83%

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confidence: 99%

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confidence: 99%

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The Dopaminergic Projection System, Basal Forebrain Macrosystems, and Conditioned Stimuli

Zahm¹,

Trimble²

2008

CNS spectr.

Self Cite

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“…However, this circuit model may be too simplistic as recent studies provide evidence for additional structures to be involved in the regulation of general PIT. For instance, in rats there is little evidence for strong monosynaptic projections from the CeA to the VTA (Zahm et al 1999); thus, polysynaptic pathways linking the CeA and the VTA, for example, through the lateral hypothalamus or frontal cortex (Zahm 2006), may regulate PIT as well. In addition, the finding that lesions that disconnected the CeA from the VTA facilitated PIT relative to unilateral VTA lesions (El-Amamy and Holland 2007) is at variance with the notion that PIT requires direct interactions between both structures.…”

Section: Nac Core and Pavlovian-instrumental Transfermentioning

confidence: 99%

Dopamine D1 and D2 receptors in the nucleus accumbens core and shell mediate Pavlovian-instrumental transfer

Lex¹,

Hauber²

2008

Learn. Mem.

153

134

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Pavlovian stimuli previously paired with food can markedly elevate the rate of food-reinforced instrumental responding. This effect, termed Pavlovian-instrumental transfer (PIT), depends both on general activating and specific cueing properties of Pavlovian stimuli. Recent evidence suggests that the general activating properties of Pavlovian stimuli are mediated by mesoaccumbens dopamine systems; however, the role of NAC dopamine D1 and D2 receptors is still unknown. Here we examined the effects of a selective dopamine D1 and D2 receptor blockade in the shell and core subregion of the NAC on general PIT. Rats were trained to press a single lever for food, and the effect of a single Pavlovian stimulus previously associated with the same food on performance of that lever was measured in extinction. Results reveal that PIT, that is, the increase in instrumental responding during presentation of the Pavlovian stimulus, was reduced by microinjections of the dopamine D1 receptor antagonist SCH-23390 and, less pronounced, by microinjections of the dopamine D2 receptor antagonist raclopride into the NAC core or shell, respectively. Our data suggest that dopamine D1 and D2 receptors in the NAC core and shell mediate the general activating effects of Pavlovian stimuli on instrumental behavior.

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“…However, dopamine enhanced the PAS25-induced synapse-specific increase of cortical excitability. The similarity of the dopamine and ACh effects could be explained by the fact that dopaminergic and cholinergic neurons serve similar functions and are tightly interconnected in neuronal networks (Sarter et al, 1999;Zahm, 2006). They also provide, at least, a theoretical option for the application of dopamine in neurological disorders associated with cognitive deficits.…”

Section: Summary Of Cholinergic Modulation In Human Cortical Plasticitymentioning

confidence: 99%

Focusing Effect of Acetylcholine on Neuroplasticity in the Human Motor Cortex

Kuo¹,

Grosch²,

Fregni³

et al. 2007

J. Neurosci.

179

118

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Cholinergic neuromodulation is pivotal for arousal, attention, and cognitive processes. Loss or dysregulation of cholinergic inputs leads to cognitive impairments like those manifested in Alzheimer's disease. Such dysfunction can be at least partially restored by an increase of acetylcholine (ACh). In animal studies, ACh selectively facilitates long-term excitability changes induced by feed-forward afferent input. Consequently, it has been hypothesized that ACh enhances the signal-to-noise ratio of input processing. However, the neurophysiological foundation for its ability to enhance cognition in humans is not well documented. In this study we explore the effects of rivastigmine, a cholinesterase inhibitor, on global and synapse-specific forms of cortical plasticity induced by transcranial direct current stimulation (tDCS) and paired associative stimulation (PAS) on 10 -12 healthy subjects, respectively. Rivastigmine essentially blocked the induction of the global excitability enhancement elicited by anodal tDCS and revealed a tendency to first reduce and then stabilize cathodal tDCS-induced inhibitory aftereffects. However, ACh enhanced the synapse-specific excitability enhancement produced by facilitatory PAS and consolidated the inhibitory PAS-induced excitability diminution. These findings are in line with a cholinergic focusing effect that optimizes the detection of relevant signals during information processing in humans.

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The evolving theory of basal forebrain functional—anatomical ‘macrosystems’

Cited by 108 publications

References 224 publications

The Dopaminergic Projection System, Basal Forebrain Macrosystems, and Conditioned Stimuli

The Dopaminergic Projection System, Basal Forebrain Macrosystems, and Conditioned Stimuli

Dopamine D1 and D2 receptors in the nucleus accumbens core and shell mediate Pavlovian-instrumental transfer

Focusing Effect of Acetylcholine on Neuroplasticity in the Human Motor Cortex

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