The Contribution of Basal Forebrain to Limbic — Motor Integration and the Mediation of Motivation to Action

Mogenson, Gordon J.; Yang, Charles R.

doi:10.1007/978-1-4757-0145-6_14

Cited by 203 publications

(135 citation statements)

References 90 publications

(96 reference statements)

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“…Concerning NAc-VP interaction, many have noted that reciprocal inhibitory GABAergic projections tend to enforce opposite polarity of events within NAc vs. VP so that hyperpolarization in neurons of the NAc accompanies depolarization in neurons of the VP and vice versa (5,87,88). An expectation from that reciprocal inhibition view would be that excitatory peaks of VP firing observed here might have corresponded to inhibitory pauses of NAc neurons, which have been suggested to signal reward (20,24,88,89).…”

Section: Reward Component Separation By Population Segregation and Fimentioning

confidence: 99%

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Smith

Berridge

Aldridge

2011

Proc. Natl. Acad. Sci. U.S.A.

349

330

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Multiple signals for reward-hedonic impact, motivation, and learned associative prediction-are funneled through brain mesocorticolimbic circuits involving the nucleus accumbens and ventral pallidum. Here, we show how the hedonic "liking" and motivation "wanting" signals for a sweet reward are distinctly modulated and tracked in this circuit separately from signals for Pavlovian predictions (learning). Animals first learned to associate a fixed sequence of Pavlovian cues with sucrose reward. Subsequent intraaccumbens microinjections of an opioid-stimulating drug increased the hedonic liking impact of sucrose in behavior and firing signals of ventral pallidum neurons, and likewise, they increased incentive salience signals in firing to the reward-proximal incentive cue (but did not alter firing signals to the learned prediction value of a reward-distal cue). Microinjection of a dopamine-stimulating drug instead enhanced only the motivation component but did not alter hedonic impact or learned prediction signals. Different dedicated neuronal subpopulations in the ventral pallidum tracked signal enhancements for hedonic impact vs. incentive salience, and a faster firing pattern also distinguished incentive signals from slower hedonic signals, even for a third overlapping population. These results reveal separate neural representations of wanting, liking, and prediction components of the same reward within the nucleus accumbens to ventral pallidum segment of mesocorticolimbic circuitry.addiction | obesity | limbic | reinforcement | striatum

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Section: Reward Component Separation By Population Segregation and Fimentioning

confidence: 99%

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Smith

Berridge

Aldridge

2011

Proc. Natl. Acad. Sci. U.S.A.

349

330

View full text Add to dashboard Cite

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“…As suggested by the anatomy of the VP and its associated structures, recent electrophysiological studies have demonstrated that the VP integrates information flow among distinct limbic and basal ganglia systems (Chrobak and Napier, 1993;Maslowski-Cobuzzi and Napier, 1994;Mitrovic and Napier, 1998). Consistent with this role, the VP influences motivational (Richardson and DeLong, 1991), cognitive (Chrobak et al, 1991;Wilson, 1991), and motor (Mogenson and Yang, 1991) behaviors. Thus, a better definition of its influence on the VP may delineate a clearer understanding of the functional repertoire of the STN, as well as the putative deficits that may occur with dysfunction of this structure.…”

mentioning

confidence: 90%

Regulation of Limbic Information Outflow by the Subthalamic Nucleus: Excitatory Amino Acid Projections to the Ventral Pallidum

et al. 2001

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The subthalamic nucleus (STN), a component of the basal ganglia motor system, sends an excitatory amino acid (EAA)-containing projection to the ventral pallidum (VP), a major limbic system output region. The VP contains both NMDA and AMPA subtypes of EAA receptors. To characterize the physiology of the subthalamic pathway to the VP, and to determine the influence of EAA receptor subtypes, in vivo intracellular recordings, and in vivo extracellular recordings combined with microiontophoresis, were made from VP neurons in anesthetized rats. Of the intracellularly recorded neurons, 86% responded to STN stimulation, and these displayed EPSPs with an onset of 8.7 msec, consistent with a monosynaptic input. The EPSPs evoked in spontaneously firing neurons were nearly twice the amplitude of those in nonfiring cells (13.1 vs 6.8 mV, respectively). As neurons were depolarized by current injection, the latency for spiking decreased from 24.2 to 14.2 msec, although EPSP latency was unaffected. Eighty-seven percent of the extracellularly recorded VP neurons responded to STN stimulation with a rapid and robust enhancement of spiking; the response onset, like the EPSP onset, equaled 8.7 msec. Firing rate was enhanced by NMDA in 94% of the STN-excited cells, and AMPA increased firing in 94% as well. The NMDA-selective antagonist AP-5 attenuated 67% of the STN-evoked excitatory responses, and the AMPA-selective antagonist CNQX attenuated 52%. Both antagonists attenuated 33% of responses, and 78% were attenuated by at least one. This evidence suggests that a great majority of VP neurons are directly influenced by STN activation and that both NMDA and non-NMDA receptors are involved. Moreover, the VP response to STN stimulation appears to be strongly dependent on the depolarization state of the neuron.Key words: ventral pallidum; subthalamic nucleus; basal ganglia; NMDA; AMPA; CNQX; electrophysiology The subthalamic nucleus (STN) is a basal ganglia structure involved in processes related to both normal motor function and movement disorders (Albin et al., 1989;Graybiel et al., 1994). Damage to the STN can result in hemiballismus (Whittier and Mettler, 1949;Guridi and Obeso, 1997), whereas surgically placed lesions of the STN in Parkinson's disease patients reverse many of the motor symptoms associated with this pathology (Guridi and Obeso, 1997). STN function may not be limited to effects on motor systems, for excitotoxic lesions of the STN in rats induce deficits in attentional tasks (Baunez and Robbins, 1997). It is plausible that the nonmotor functions of the STN reflect its reciprocal projections with the ventral pallidum (VP) (Groenewegen and Berendse, 1990), a brain region that serves as a major output from the limbic (ventral) striatum (Heimer et al., 1985). As suggested by the anatomy of the VP and its associated structures, recent electrophysiological studies have demonstrated that the VP integrates information flow among distinct limbic and basal ganglia systems (Chrobak and Napier, 1993;Maslowski-Cobuzzi and Napier,...

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“…Since accumbal cells are mostly inhibitory, accumbal targets would be disinhibited. It is thought that as a result, locomotor mechanisms normally inhibited by the nucleus accumbens become activated (Mogenson and Yang, 1991), possibly allowing the animal to approach (or consume, or investigate) or run away from the stimulus source.…”

Section: Properties Of Vta Cells That Supply Dopaminergic Input To Thmentioning

confidence: 99%

Storage, recall, and novelty detection of sequences by the hippocampus: Elaborating on the SOCRATIC model to account for normal and aberrant effects of dopamine

2001

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ABSTRACT:In order to understand how the molecular or cellular defects that underlie a disease of the nervous system lead to the observable symptoms, it is necessary to develop a large-scale neural model. Such a model must specify how specific molecular processes contribute to neuronal function, how neurons contribute to network function, and how networks interact to produce behavior. This is a challenging undertaking, but some limited progress has been made in understanding the memory functions of the hippocampus with this degree of detail. There is increasing evidence that the hippocampus has a special role in the learning of sequences and the linkage of specific memories to context. In the first part of this paper, we review a model (the SOCRATIC model) that describes how the dentate and CA3 hippocampal regions could store and recall memory sequences in context. A major line of evidence for sequence recall is the "phase precession" of hippocampal place cells. In the second part of the paper, we review the evidence for theta-gamma phase coding. According to a framework that incorporates this form of coding, the phase precession is interpreted as cued recall of a discrete sequence of items from long-term memory. The third part of the paper deals with the issue of how the hippocampus could learn memory sequences. We show that if multiple items can be active within a theta cycle through the action of a short-term "buffer," NMDA-dependent plasticity can lead to the learning of sequences presented at realistic item separation intervals. The evidence for such a buffer function is reviewed. An important underlying issue is whether the hippocampal circuitry is configured differently for learning and recall. We argue that there are indeed separate states for learning and recall, but that both involve theta oscillations, albeit in possibly different forms. This raises the question of how neuromodulatory input might switch the hippocampus between learning and recall states and more generally how different neuromodulatory inputs reconfigure the hippocampus for different functions. In the fifth part of this paper we review our studies of dopamine and dopamine/NMDA interactions in the control of synaptic function. Our results show that dopamine dramatically reduces the direct cortical input to CA1 (the perforant path input), while having little effect on the input from CA3. In order to interpret the functional consequences of this pathway-specific modulation, it is necessary to understand the function of CA1 and the role of dopaminergic input from the ventral tegmental area (VTA). In the sixth part of this paper we consider several possibilities and address the issue of how dopamine hyperfunction or NMDA hypofunction, abnormalities that may underlie schizophrenia, might lead to the symptoms of the disease. Relevant to this issue is the demonstrated role of the hippocampus in novelty detection, a function that is likely to depend on sequence recall by the hippocampus. Novelty signals are generated when reality does not match ...

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The Contribution of Basal Forebrain to Limbic — Motor Integration and the Mediation of Motivation to Action

Cited by 203 publications

References 90 publications

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Regulation of Limbic Information Outflow by the Subthalamic Nucleus: Excitatory Amino Acid Projections to the Ventral Pallidum

Storage, recall, and novelty detection of sequences by the hippocampus: Elaborating on the SOCRATIC model to account for normal and aberrant effects of dopamine

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