Lesions of the Diagonal Band of Broca Enhance Drinking in the Rat

Sullivan, Margaret J.; Cunningham, J. Thomas; D, Mazzella; Allen, Andrew M.; Nissen, R.; Renaud, Leo P.

doi:10.1046/j.1365-2826.2003.01066.x

Cited by 11 publications

(6 citation statements)

References 29 publications

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“…Dopamine projections into V1, however, are relatively sparse (46). Another possibility is that cholinergic nuclei, which are known to be involved in the satiation of thirst (47,48) and which project into V1 (49,50) could signal reward to the visual cortex. Effects similar to the reported voltage sensitivity of G protein coupled ACh receptors (51) could provide a biochemical mechanism of reward inhibition.…”

Section: Discussionmentioning

confidence: 99%

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Gavornik

Shuler

Loewenstein

et al. 2009

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

124

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The ability to represent time is an essential component of cognition but its neural basis is unknown. Although extensively studied both behaviorally and electrophysiologically, a general theoretical framework describing the elementary neural mechanisms used by the brain to learn temporal representations is lacking. It is commonly believed that the underlying cellular mechanisms reside in high order cortical regions but recent studies show sustained neural activity in primary sensory cortices that can represent the timing of expected reward. Here, we show that local cortical networks can learn temporal representations through a simple framework predicated on reward dependent expression of synaptic plasticity. We assert that temporal representations are stored in the lateral synaptic connections between neurons and demonstrate that reward-modulated plasticity is sufficient to learn these representations. We implement our model numerically to explain reward-time learning in the primary visual cortex (V1), demonstrate experimental support, and suggest additional experimentally verifiable predictions. reinforcment learning ͉ visual cortex O ur brains process time with such instinctual ease that the difficulty of defining what time is, in a neural sense, seems paradoxical. There is a rich literature in experimental neuroscience describing the temporal dynamics of both cellular and system-level neuronal processes and many insightful psychophysical studies have revealed perceptual correlates of time. Despite this, and the clear importance of accurate temporal processing at all levels of behavior, we still know little about how time is represented or used by the brain (1). Temporal processing is classically understood as a higher order function, and although there is some disagreement (2, 3), it is often argued that dedicated structures or regions in the brain are responsible for representing time (4). Because different mechanisms are likely responsible for computing timing at different time scales (1,5,6), and because there is evidence for modality specific temporal mechanisms (7), an alternative possibility is that timing processes develop locally within different brain regions.Recent evidence indicates that temporal representations are expressed in primary sensory cortices (8-10) and that rewardbased reinforcement can affect the form of stimulus driven activity in the primary somatosensory cortex (11-13). In particular, Shuler and Bear (9) showed that neurons in rat primary visual cortex can develop persistent activity, evoked by brief visual stimuli, that robustly represents the temporal interval between a visual stimulus and paired reward (Fig. 1). A mechanistic framework capable of describing how a neural substrate can learn the observed temporal representations does not exist.Here, we explain how these temporal signals can be encoded in recurrent excitatory synaptic connections and how a local network can learn specific temporal instantiations through reward modulated plasticity. Although our model is potentially ...

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Section: Discussionmentioning

confidence: 99%

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Gavornik

Shuler

Loewenstein

et al. 2009

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

124

View full text Add to dashboard Cite

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“…Two milliliters of plasma were removed from the sample, placed in a conical centrifuge tube, and kept in an ultracold freezer (Ϫ80°C) until it was shipped on dry ice to the RIA core at the University of Iowa for measurement of AVP concentration. AVP concentration was determined using a specific radioimmunoassay after an acetone-petroleum ether extraction, as previously described (23,43). The antibody to AVP (courtesy Dr. Willis Samson, St. Louis University; Ref.…”

Section: Methodsmentioning

confidence: 99%

Effects of water deprivation and rehydration on c-Fos and FosB staining in the rat supraoptic nucleus and lamina terminalis region

Ji¹,

Fleming²,

Penny³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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We studied cFos and FosB staining in the supraoptic nucleus (SON) the organum vasculosum of the lamina terminalis (OVLT) and the median preoptic nucleus (MnPO) in adult male rats after water deprivation (24 h, n = 11; 48 h, n = 12) and water deprivation with rehydration (22 h + water, n = 11; 46 h + water, n = 10). Control rats (n = 15) had water available ad libitum. Separate sets of serial sections from each brain were processed for immunocytochemistry using primary antibodies against either c-Fos or FosB protein. Plasma osmolality, vasopressin, hematocrit, and plasma proteins were measured in separate groups (n = 6-7). The number of c-Fos-positive cells in the SON was significantly increased after 24 and 48 h of water deprivation. In contrast, rehydrated groups were not different from control. Water deprivation significantly increased c-Fos staining in both the OVLT and the MnPO, but c-Fos staining was not altered by rehydration. FosB staining in the SON was significantly increased only by 48-h water deprivation, and this effect was significantly decreased by rehydration. In the MnPO and OVLT, FosB staining was significantly increased by water deprivation, and, like c-Fos staining, these increases were not affected by rehydration. Water deprivation significantly increased osmolality and hematocrit, as well as plasma protein and vasopressin concentrations. Plasma measurements from rehydrated rats were not different from control. We conclude that water deprivation and rehydration differentially affect c-Fos and FosB staining in a region-dependent manner.

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“…Dopamine, which is often characterized as a modulatory reward signal (Schultz 1998), is an obvious candidate. Dopamine projections to V1 are relatively sparse (Papadopoulos et al 1989), however, whereas cholinergic projections from the basal forebrain are robust and are known to be responsive to thirst satiation (Sullivan et al 2003). The cholinergic system is also well-documented to play an important role in learning and memory (Hasselmo 2006), and subsequent experiments designed to test the theoretical predictions described above showed definitively that cholinergic activity is necessary to learn interval timing in V1 (Chubykin et al 2013).…”

Section: Rodent V1 Reports Reward Timingmentioning

confidence: 99%

Higher brain functions served by the lowly rodent primary visual cortex

Gavornik

Bear

2014

Learn. Mem.

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It has been more than 50 years since the first description of ocular dominance plasticity-the profound modification of primary visual cortex (V1) following temporary monocular deprivation. This discovery immediately attracted the intense interest of neurobiologists focused on the general question of how experience and deprivation modify the brain as a potential substrate for learning and memory. The pace of discovery has quickened considerably in recent years as mice have become the preferred species to study visual cortical plasticity, and new studies have overturned the dogma that primary sensory cortex is immutable after a developmental critical period. Recent work has shown that, in addition to ocular dominance plasticity, adult visual cortex exhibits several forms of response modification previously considered the exclusive province of higher cortical areas. These "higher brain functions" include neural reports of stimulus familiarity, reward-timing prediction, and spatiotemporal sequence learning. Primary visual cortex can no longer be viewed as a simple visual feature detector with static properties determined during early development. Rodent V1 is a rich and dynamic cortical area in which functions normally associated only with "higher" brain regions can be studied at the mechanistic level.

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Lesions of the Diagonal Band of Broca Enhance Drinking in the Rat

Cited by 11 publications

References 29 publications

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Learning reward timing in cortex through reward dependent expression of synaptic plasticity

Effects of water deprivation and rehydration on c-Fos and FosB staining in the rat supraoptic nucleus and lamina terminalis region

Higher brain functions served by the lowly rodent primary visual cortex

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