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Article ; Online: Daily fluctuations in blood glucose with normal aging are inversely related to hippocampal synaptic mitochondrial proteins.

Braunstein, Paul W / Horovitz, David J / Hampton, Andreina M / Hollis, Fiona / Newman, Lori A / Enos, Reilly T / McQuail, Joseph A

Aging brain

2024 Volume 5, Page(s) 100116

Abstract: Defective brain glucose utilization is a hallmark of Alzheimer's disease (AD) while Type II diabetes and elevated blood glucose escalate the risk for AD in later life. Isolating contributions of normal aging from coincident metabolic or brain diseases ... ...

Abstract	Defective brain glucose utilization is a hallmark of Alzheimer's disease (AD) while Type II diabetes and elevated blood glucose escalate the risk for AD in later life. Isolating contributions of normal aging from coincident metabolic or brain diseases could lead to refined approaches to manage specific health risks and optimize treatments targeted to susceptible older individuals. We evaluated metabolic, neuroendocrine, and neurobiological differences between young adult (6 months) and aged (24 months) male rats. Compared to young adults, blood glucose was significantly greater in aged rats at the start of the dark phase of the day but not during the light phase. When challenged with physical restraint, a potent stressor, aged rats effected no change in blood glucose whereas blood glucose increased in young adults. Tissues were evaluated for markers of oxidative phosphorylation (OXPHOS), neuronal glucose transport, and synapses. Outright differences in protein levels between age groups were not evident, but circadian blood glucose was inversely related to OXPHOS proteins in hippocampal synaptosomes, independent of age. The neuronal glucose transporter, GLUT3, was positively associated with circadian blood glucose in young adults whereas aged rats tended to show the opposite trend. Our data demonstrate aging increases daily fluctuations in blood glucose and, at the level of individual differences, negatively associates with proteins related to synaptic OXPHOS. Our findings imply that glucose dyshomeostasis may exacerbate metabolic aspects of synaptic dysfunction that contribute to risk for age-related brain disorders.
Language	English
Publishing date	2024-04-05
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-9589
ISSN (online)	2589-9589
DOI	10.1016/j.nbas.2024.100116
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Article ; Online: Time-dependent changes in hippocampal and striatal glycogen long after maze training in male rats.

Scavuzzo, Claire J / Newman, Lori A / Gold, Paul E / Korol, Donna L

Neurobiology of learning and memory

2021 Volume 185, Page(s) 107537

Abstract: Long-lasting biological changes reflecting past experience have been studied in and typically attributed to neurons in the brain. Astrocytes, which are also present in large number in the brain, have recently been found to contribute critically to ... ...

Abstract	Long-lasting biological changes reflecting past experience have been studied in and typically attributed to neurons in the brain. Astrocytes, which are also present in large number in the brain, have recently been found to contribute critically to learning and memory processing. In the brain, glycogen is primarily found in astrocytes and is metabolized to lactate, which can be released from astrocytes. Here we report that astrocytes themselves have intrinsic neurochemical plasticity that alters the availability and provision of metabolic substrates long after an experience. Rats were trained to find food on one of two versions of a 4-arm maze: a hippocampus-sensitive place task and a striatum-sensitive response task. Remarkably, hippocampal glycogen content increased while striatal levels decreased during the 30 days after rats were trained to find food in the place version, but not the response version, of the maze tasks. A long-term consequence of the durable changes in glycogen stores was seen in task-by-site differences in extracellular lactate responses activated by testing on a working memory task administered 30 days after initial training, the time when differences in glycogen content were most robust. These results suggest that astrocytic plasticity initiated by a single experience may augment future availability of energy reserves, perhaps priming brain areas to process learning of subsequent experiences more effectively.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Astrocytes/physiology ; Corpus Striatum/metabolism ; Corpus Striatum/physiology ; Glycogen/metabolism ; Hippocampus/metabolism ; Hippocampus/physiology ; Lactic Acid/metabolism ; Male ; Maze Learning/physiology ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Lactic Acid (33X04XA5AT) ; Glycogen (9005-79-2)
Language	English
Publishing date	2021-10-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1223366-3
ISSN	1095-9564 ; 1074-7427
ISSN (online)	1095-9564
ISSN	1074-7427
DOI	10.1016/j.nlm.2021.107537
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Article ; Online: Training-induced elevations in extracellular lactate in hippocampus and striatum: Dissociations by cognitive strategy and type of reward.

Newman, Lori A / Scavuzzo, Claire J / Gold, Paul E / Korol, Donna L

Neurobiology of learning and memory

2016 Volume 137, Page(s) 142–153

Abstract: Recent evidence suggests that astrocytes convert glucose to lactate, which is released from the astrocytes and supports learning and memory. This report takes a multiple memory perspective to test the role of astrocytes in cognition using real-time ... ...

Abstract	Recent evidence suggests that astrocytes convert glucose to lactate, which is released from the astrocytes and supports learning and memory. This report takes a multiple memory perspective to test the role of astrocytes in cognition using real-time lactate measurements during learning and memory. Extracellular lactate levels in the hippocampus or striatum were determined with lactate biosensors while rats were learning place (hippocampus-sensitive) or response (striatum-sensitive) versions of T-mazes. In the first experiment, rats were trained on the place and response tasks to locate a food reward. Extracellular lactate levels in the hippocampus increased beyond those of feeding controls during place training but not during response training. However, striatal lactate levels did not increase beyond those of controls when rats were trained on either the place or the response version of the maze. Because food ingestion itself increased blood glucose and brain lactate levels, the contribution of feeding may have confounded the brain lactate measures. Therefore, we conducted a second similar experiment using water as the reward. A very different pattern of lactate responses to training emerged when water was used as the task reward. First, provision of water itself did not result in large increases in either brain or blood lactate levels. Moreover, extracellular lactate levels increased in the striatum during response but not place learning, whereas extracellular lactate levels in the hippocampus did not differ across tasks. The findings from the two experiments suggest that the relative engagement of the hippocampus and striatum dissociates not only by task but also by reward type. The divergent lactate responses of the hippocampus and striatum in place and response tasks under different reward conditions may reflect ethological constraints tied to foraging for food and water.
MeSH term(s)	Animals ; Blood Glucose ; Cognition/physiology ; Corpus Striatum/metabolism ; Hippocampus/metabolism ; Lactic Acid/metabolism ; Male ; Maze Learning/physiology ; Rats ; Rats, Sprague-Dawley ; Reward
Chemical Substances	Blood Glucose ; Lactic Acid (33X04XA5AT)
Language	English
Publishing date	2016-12-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	1223366-3
ISSN	1095-9564 ; 1074-7427
ISSN (online)	1095-9564
ISSN	1074-7427
DOI	10.1016/j.nlm.2016.12.001
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Article: Prenatal Protein Malnutrition Produces Resistance to Distraction Similar to Noradrenergic Deafferentation of the Prelimbic Cortex in a Sustained Attention Task.

Newman, Lori A / Baraiolo, Jaime / Mokler, David J / Rabinowitz, Arielle G / Galler, Janina R / McGaughy, Jill A

Frontiers in neuroscience

2019 Volume 13, Page(s) 123

Abstract: Exposure to malnutrition early in development increases likelihood of neuropsychiatric disorders, affective processing disorders, and attentional problems later in life. Many of these impairments are hypothesized to arise from impaired development of the ...

Abstract	Exposure to malnutrition early in development increases likelihood of neuropsychiatric disorders, affective processing disorders, and attentional problems later in life. Many of these impairments are hypothesized to arise from impaired development of the prefrontal cortex. The current experiments examine the impact of prenatal malnutrition on the noradrenergic and cholinergic axons in the prefrontal cortex to determine if these changes contribute to the attentional deficits seen in prenatal protein malnourished rats (6% casein vs. 25% casein). Because prenatally malnourished animals had significant decreases in noradrenergic fibers in the prelimbic cortex with spared innervation in the anterior cingulate cortex and showed no changes in acetylcholine innervation of the prefrontal cortex, we compared deficits produced by malnutrition to those produced in adult rats by noradrenergic lesions of the prelimbic cortex. All animals were able to perform the baseline sustained attention task accurately. However, with the addition of visual distractors to the sustained attention task, animals that were prenatally malnourished and those that were noradrenergically lesioned showed cognitive rigidity, i.e., were less distractible than control animals. All groups showed similar changes in behavior when exposed to withholding reinforcement, suggesting specific attentional impairments rather than global difficulties in understanding response rules, bottom-up perceptual problems, or cognitive impairments secondary to dysfunction in sensitivity to reinforcement contingencies. These data suggest that prenatal protein malnutrition leads to deficits in noradrenergic innervation of the prelimbic cortex associated with cognitive rigidity.
Language	English
Publishing date	2019-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2019.00123
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Article ; Online: Cognitive control and the anterior cingulate cortex: how conflicting stimuli affect attentional control in the rat.

Newman, Lori A / Creer, David J / McGaughy, Jill A

Journal of physiology, Paris

2014 Volume 109, Issue 1-3, Page(s) 95–103

Abstract: Converging evidence supports the hypothesis that the prefrontal cortex is critical for cognitive control. One prefrontal subregion, the anterior cingulate cortex, is hypothesized to be necessary to resolve response conflicts, disregard salient ... ...

Abstract	Converging evidence supports the hypothesis that the prefrontal cortex is critical for cognitive control. One prefrontal subregion, the anterior cingulate cortex, is hypothesized to be necessary to resolve response conflicts, disregard salient distractors and alter behavior in response to the generation of an error. These situations all involve goal-oriented monitoring of performance in order to effectively adjust cognitive processes. Several neuropsychological disorders, e.g., schizophrenia, attention deficit hyperactivity and obsessive compulsive disorder, are accompanied by morphological changes in the anterior cingulate cortex. These changes are hypothesized to underlie the impairments on tasks that require cognitive control found in these subjects. A novel conflict monitoring task was used to assess the effects on cognitive control of excitotoxic lesions to anterior cingulate cortex in rats. Prior to surgery all subjects showed improved accuracy on the second of two consecutive, incongruent trials. Lesions to the anterior cingulate cortex abolished this. Lesioned animals had difficulty in adjusting cognitive control on a trial-by-trial basis regardless of whether cognitive changes were increased or decreased. These results support a role for the anterior cingulate cortex in adjustments in cognitive control.
MeSH term(s)	Analysis of Variance ; Animals ; Attention/physiology ; Cognition/physiology ; Conflict, Psychological ; Discrimination, Psychological ; Excitatory Amino Acid Agonists/toxicity ; Gyrus Cinguli/injuries ; Gyrus Cinguli/physiology ; Ibotenic Acid/toxicity ; Male ; Photic Stimulation ; Rats ; Rats, Long-Evans
Chemical Substances	Excitatory Amino Acid Agonists ; Ibotenic Acid (2552-55-8)
Language	English
Publishing date	2014-07-19
Publishing country	France
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1141200-8
ISSN	1769-7115 ; 0928-4257
ISSN (online)	1769-7115
ISSN	0928-4257
DOI	10.1016/j.jphysparis.2014.06.004
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Article ; Online: Cholinergic modulation of visuospatial responding in central thalamus.

Newman, Lori A / Mair, Robert G

The European journal of neuroscience

2007 Volume 26, Issue 12, Page(s) 3543–3552

Abstract: Central thalamus has extensive connections with basal ganglia and frontal cortex that are thought to play a critical role in sensory-guided goal-directed behavior. Central thalamic activity is influenced by cholinergic projections from mesopontine nuclei. ...

Abstract	Central thalamus has extensive connections with basal ganglia and frontal cortex that are thought to play a critical role in sensory-guided goal-directed behavior. Central thalamic activity is influenced by cholinergic projections from mesopontine nuclei. To elucidate this function we trained rats to respond to lights in a reaction time (RT) task and compared effects of muscarinic (2.4, 7.3, 22 nmol scopolamine) and nicotinic (5.4, 16, 49, 98 nmol mecamylamine) antagonists with the GABA(A) agonist muscimol (0.1, 0.3, 1.0 nmol) in central thalamus. We compared this with subcutaneous (systemic) effects of mecamylamine (3.2, 9.7, 29 micromol/kg) and scopolamine (0.03, 0.09, 0.26 micromol/kg). Subcutaneous scopolamine increased omissions (failure to respond within a 3-s response window) at the highest dose tested. Subcutaneous mecamylamine increased omissions at the highest dose tested while impairing RT and per cent correct at lower doses. Intrathalamic injections of muscimol and mecamylamine decreased per cent correct at doses that did not affect omissions or RT. Intrathalamic scopolamine increased omissions and RT at doses that had little effect on per cent correct. Anatomical controls indicated that the effects of mecamylamine were localized in central thalamus and those of scopolamine were not. Drug effects did not interact with attention-demanding manipulations of stimulus duration, proximity of stimulus and response locations, or stimulus array size. These results are consistent with the hypothesis that central thalamus mediates decisional processes linking sensory stimuli with actions, downstream from systems that detect sensory signals. They also provide evidence that this function is specifically influenced by nicotinic cholinergic receptors.
MeSH term(s)	Animals ; Behavior, Animal/drug effects ; Behavior, Animal/radiation effects ; Choice Behavior/physiology ; Cholinergic Antagonists/administration & dosage ; Cholinergic Antagonists/pharmacology ; Dose-Response Relationship, Drug ; Drug Combinations ; GABA Agonists/administration & dosage ; GABA Agonists/pharmacology ; Injections ; Injections, Subcutaneous ; Light ; Male ; Mecamylamine/administration & dosage ; Mecamylamine/pharmacology ; Muscimol/administration & dosage ; Muscimol/pharmacology ; Nicotinic Antagonists/administration & dosage ; Nicotinic Antagonists/pharmacology ; Rats ; Rats, Long-Evans ; Reaction Time/drug effects ; Scopolamine Hydrobromide/administration & dosage ; Scopolamine Hydrobromide/pharmacology ; Space Perception/physiology ; Thalamus/drug effects ; Thalamus/physiology ; Thalamus/radiation effects ; Visual Perception/physiology
Chemical Substances	Cholinergic Antagonists ; Drug Combinations ; GABA Agonists ; Nicotinic Antagonists ; Muscimol (2763-96-4) ; Scopolamine Hydrobromide (451IFR0GXB) ; Mecamylamine (6EE945D3OK)
Language	English
Publishing date	2007-12
Publishing country	France
Document type	Comparative Study ; Journal Article
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/j.1460-9568.2007.05961.x
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Article ; Online: Lactate produced by glycogenolysis in astrocytes regulates memory processing.

Newman, Lori A / Korol, Donna L / Gold, Paul E

PloS one

2011 Volume 6, Issue 12, Page(s) e28427

Abstract: When administered either systemically or centrally, glucose is a potent enhancer of memory processes. Measures of glucose levels in extracellular fluid in the rat hippocampus during memory tests reveal that these levels are dynamic, decreasing in ... ...

Abstract	When administered either systemically or centrally, glucose is a potent enhancer of memory processes. Measures of glucose levels in extracellular fluid in the rat hippocampus during memory tests reveal that these levels are dynamic, decreasing in response to memory tasks and loads; exogenous glucose blocks these decreases and enhances memory. The present experiments test the hypothesis that glucose enhancement of memory is mediated by glycogen storage and then metabolism to lactate in astrocytes, which provide lactate to neurons as an energy substrate. Sensitive bioprobes were used to measure brain glucose and lactate levels in 1-sec samples. Extracellular glucose decreased and lactate increased while rats performed a spatial working memory task. Intrahippocampal infusions of lactate enhanced memory in this task. In addition, pharmacological inhibition of astrocytic glycogenolysis impaired memory and this impairment was reversed by administration of lactate or glucose, both of which can provide lactate to neurons in the absence of glycogenolysis. Pharmacological block of the monocarboxylate transporter responsible for lactate uptake into neurons also impaired memory and this impairment was not reversed by either glucose or lactate. These findings support the view that astrocytes regulate memory formation by controlling the provision of lactate to support neuronal functions.
MeSH term(s)	Animals ; Arabinose ; Astrocytes/cytology ; Astrocytes/drug effects ; Astrocytes/metabolism ; Biological Transport/drug effects ; Extracellular Space/drug effects ; Extracellular Space/metabolism ; Glucose/metabolism ; Glycogen/metabolism ; Glycogenolysis/drug effects ; Imino Furanoses ; Lactic Acid/biosynthesis ; Lactic Acid/metabolism ; Male ; Memory/drug effects ; Monocarboxylic Acid Transporters/metabolism ; Neurons/cytology ; Neurons/drug effects ; Neurons/metabolism ; Rats ; Rats, Sprague-Dawley ; Spatial Behavior/drug effects ; Spatial Behavior/physiology ; Sugar Alcohols/pharmacology
Chemical Substances	Imino Furanoses ; Monocarboxylic Acid Transporters ; Slc16a7 protein, rat ; Sugar Alcohols ; 1,4-dideoxy-1,4-iminoarabinitol (100937-53-9) ; Lactic Acid (33X04XA5AT) ; Glycogen (9005-79-2) ; Arabinose (B40ROO395Z) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2011-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0028427
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Article ; Online: Attentional effects of lesions to the anterior cingulate cortex: how prior reinforcement influences distractibility.

Newman, Lori A / McGaughy, Jill

Behavioral neuroscience

2011 Volume 125, Issue 3, Page(s) 360–371

Abstract: Morphological changes in the anterior cingulate cortex are found in subjects with schizophrenia, attention deficit hyperactivity disorder, and obsessive-compulsive disorder. These changes are hypothesized to underlie the impairments these individuals ... ...

Abstract	Morphological changes in the anterior cingulate cortex are found in subjects with schizophrenia, attention deficit hyperactivity disorder, and obsessive-compulsive disorder. These changes are hypothesized to underlie the impairments these individuals show on tasks that require cognitive control. The anterior cingulate cortex has previously been shown to be active in situations involving high conflict, presentation of salient, distracting stimuli, and error processing, that is, situations that occur when a shift in attention or responding is required. However, there is some uncertainty as to what specific role the anterior cingulate cortex plays in these situations. The current study used converging evidence from two behavioral paradigms to determine the effects of excitotoxic lesions in the anterior cingulate cortex on executive control. The first assay tests reversal learning, attentional set formation and shifting. The second assesses sustained attention with and without distractors. Animals with anterior cingulate cortex lesions were impaired during reinforcement reversals, discriminations that required subjects to disregard previously relevant stimulus attributes and showed a more rapid decline in attentional ability than Sham-Lesioned subjects when maintaining sustained attention for extended periods of time. These results are consistent with the hypothesis that the anterior cingulate cortex is involved in attending to stimulus attributes that currently predict reinforcement in the presence of previously relevant, salient distractors and maintaining sustained attention over prolonged time on task.
MeSH term(s)	Animals ; Attention/drug effects ; Attention/physiology ; Conditioning, Operant/drug effects ; Conditioning, Operant/physiology ; Cues ; Discrimination Learning/drug effects ; Discrimination Learning/physiology ; Executive Function/drug effects ; Executive Function/physiology ; Gyrus Cinguli/drug effects ; Gyrus Cinguli/physiology ; Ibotenic Acid/administration & dosage ; Ibotenic Acid/toxicity ; Male ; Microinjections ; Rats ; Rats, Long-Evans ; Reinforcement, Psychology ; Reversal Learning/drug effects ; Reversal Learning/physiology
Chemical Substances	Ibotenic Acid (2552-55-8)
Language	English
Publishing date	2011-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	230159-3
ISSN	1939-0084 ; 0735-7044
ISSN (online)	1939-0084
ISSN	0735-7044
DOI	10.1037/a0023250
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Article ; Online: Adolescent rats show cognitive rigidity in a test of attentional set shifting.

Newman, Lori A / McGaughy, Jill

Developmental psychobiology

2011 Volume 53, Issue 4, Page(s) 391–401

Abstract: As neuropsychiatric disorders such as schizophrenia, attention deficit disorder, and mood disorders all impact executive function and are likely to be diagnosed prior to adulthood, it is important to understand the normal ontogeny of executive function. ... ...

Abstract	As neuropsychiatric disorders such as schizophrenia, attention deficit disorder, and mood disorders all impact executive function and are likely to be diagnosed prior to adulthood, it is important to understand the normal ontogeny of executive function. Previous behavioral research has shown that adolescents' executive function is different than that of adults. In the present study, we use a previously validated cognitive test, the intradimensional/extradimensional (ID/ED) set-shifting task, to assess attentional set shifting and reversal learning in adolescent and adult, male, Long-Evans rats. These data suggest that adolescent rats are more cognitively rigid than adult rats and have impairments in the shifting, but not formation, of an attentional set. Adolescent rats are also more susceptible to distraction than adult rats when an irrelevant stimulus dimension is introduced as part of a complex stimulus. Moreover, we find that attentional set shifting becomes adult-like at an earlier age than reversal learning. As these functions are mediated by distinct prefrontal subregions, that is, the prelimbic and orbitofrontal cortices, respectively, we hypothesize that prefrontal cortical subregions show slightly different developmental trajectories.
MeSH term(s)	Analysis of Variance ; Animals ; Attention/physiology ; Behavior, Animal/physiology ; Cognition/physiology ; Male ; Rats ; Rats, Long-Evans ; Reversal Learning/physiology ; Set, Psychology
Language	English
Publishing date	2011-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	4107-5
ISSN	1098-2302 ; 0012-1630
ISSN (online)	1098-2302
ISSN	0012-1630
DOI	10.1002/dev.20537
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Article ; Online: Modulation of multiple memory systems: from neurotransmitters to metabolic substrates.

Gold, Paul E / Newman, Lori A / Scavuzzo, Claire J / Korol, Donna L

Hippocampus

2013 Volume 23, Issue 11, Page(s) 1053–1065

Abstract: This article reviews evidence showing that neurochemical modulators can regulate the relative participation of the hippocampus and striatum in learning and memory tasks. For example, relative release of acetylcholine increases in the hippocampus and ... ...

Abstract	This article reviews evidence showing that neurochemical modulators can regulate the relative participation of the hippocampus and striatum in learning and memory tasks. For example, relative release of acetylcholine increases in the hippocampus and striatum reflects the relative engagement of these brain systems during learning of place and response tasks. Acetylcholine release is regulated in part by available brain glucose levels, which themselves are dynamically modified during learning. Recent findings suggest that glucose acts through astrocytes to deliver lactate to neurons. Brain glycogen is contained in astrocytes and provides a capacity to deliver energy substrates to neurons when needed, a need that can be generated by training on tasks that target hippocampal and striatal processing mechanisms. These results integrate an increase in blood glucose after epinephrine release from the adrenal medulla with provision of brain energy substrates, including lactate released from astrocytes. Together, the availability of peripheral and central energy substrates regulate the processing of learning and memory within and across multiple neural systems. Dysfunctions of the physiological steps that modulate memory--from hormones to neurotransmitters to metabolic substrates--may contribute importantly to some of the cognitive impairments seen during normal aging and during neurodegenerative diseases.
MeSH term(s)	Acetylcholine/physiology ; Animals ; Astrocytes/metabolism ; Corpus Striatum/metabolism ; Corpus Striatum/physiology ; Glucose/metabolism ; Hippocampus/metabolism ; Hippocampus/physiology ; Lactic Acid/metabolism ; Learning/physiology ; Memory/physiology ; Neurons/metabolism ; Neurotransmitter Agents/physiology ; Rats ; Systems Biology
Chemical Substances	Neurotransmitter Agents ; Lactic Acid (33X04XA5AT) ; Glucose (IY9XDZ35W2) ; Acetylcholine (N9YNS0M02X)
Language	English
Publishing date	2013-05-31
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1074352-2
ISSN	1098-1063 ; 1050-9631
ISSN (online)	1098-1063
ISSN	1050-9631
DOI	10.1002/hipo.22182
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