Amino acids are still as exciting as ever

Carpenter, Kate J.; Dickenson, Anthony H.

doi:10.1016/s1471-4892(01)00009-1

Cited by 22 publications

(10 citation statements)

References 52 publications

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“…“best sites”) that appeared to initiate locomotor activity with the shortest and least variable cycle times. Specifically, the types of excitatory amino acid (EAA) receptors present at the “best site” for each locomotor area were determined by pressure ejection of each of the following agents (Carpenter and Dickerson, 2001): (N-methyl D-aspartate (NMDA, 0.5 mM); kainate (KA, 0.25 mM); or α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA, 1 mM) (all from Sigma Chemical). These agents were dissolved in lamprey Ringer’s solution (pH = 7.2 – 7.4), and Fast Green was added to visualize the ejection bolus.…”

Section: Methodsmentioning

confidence: 99%

Localization, pharmacology, and organization of brain locomotor areas in larval lamprey

Jackson

McClellan

2011

Neuroscience

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In larval lamprey, spinal locomotor activity can be initiated by pharmacological microstimulation from the following higher order brain locomotor areas (Paggett et al., 2004; Jackson et al., 2007): rostrolateral rhombencephalon (RLR); ventromedial diencephalon (VMD); or dorsolateral mesencephalon (DLM). In the present study, pharmacological microstimulation with excitatory amino acids (EAAs) or their agonists in the brains of in vitro brain/spinal cord preparations was used to determine the sizes, pharmacology, and organization of these locomotor areas. First, the RLR, DLM and VMD locomotor areas were confined to relatively small areas of the brain, and stimulation as little as 50 μm outside these areas was ineffective or elicited tonic or uncoordinated motor activity. Second, pharmacological stimulation with NMDA, kainate, or AMPA in the VMD or DLM reliably initiated well-coordinated spinal locomotor activity. In the RLR, stimulation with all three ionotropic EAA receptor agonists could initiate spinal locomotor activity, but NMDA or AMPA was more reliable than kainate. Third, with synaptic transmission blocked only in the brain, stimulation in the RLR, VMD, or DLM no longer initiated spinal locomotor activity, suggesting that these locomotor areas do not directly activate spinal locomotor networks. Fourth, following a complete transection at the mesencephalon-rhombencephalon border, stimulation in the RLR no longer initiated spinal motor activity. Thus, the RLR locomotor area does not appear able to initiate spinal locomotor activity by neural circuits confined entirely within the rhombencephalon but requires more rostral neural centers, such as those in the VMD and DLM, as previously proposed (Paggett et al., 2004).

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Section: Methodsmentioning

confidence: 99%

Localization, pharmacology, and organization of brain locomotor areas in larval lamprey

Jackson

McClellan

2011

Neuroscience

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“…However, NMDA receptor-dependent synaptic plasticity plays a role not only in pathological conditions such as chronic pain, but also in cognition and functions such as learning and memory (McMahon et al 1993). The wide spread localization of the receptor and the complex role of glutamate signaling in the CNS implies that nonselective NMDA receptor blockers may cause serious and unacceptable side effects (Carpenter and Dickenson 2001;.…”

Section: Nmda Receptorsmentioning

confidence: 99%

Effect of spinal cord stimulation in an animal model of neuropathic pain relates to degree of tactile “allodynia”

et al. 2006

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“…Recently, specific neuroprotective effects of acamprosate 25 together with radioligand binding studies 26 have been used to suggest that the drug can inhibit metabotropic glutamate receptors (mGluRs). This is an attractive hypothesis because mGluRs have wide‐ranging effects on glutamate release and NMDA receptor function, 27 thus explaining the myriad of previously reported effects of acamprosate on the glutamatergic system. It would also resolve some structural questions because N‐acetyl aspartyl glutamate (the transmitter candidate that shows closest structural homology with acamprosate) is suggested to be a relatively selective agonist for mGluRs 16 .…”

Section: Acamprosatementioning

confidence: 99%

Pharmacological Mechanisms of Naltrexone and Acamprosate in the Prevention of Relapse in Alcohol Dependence

Littleton

Zieglgänsberger

2003

American J Addict

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Naltrexone and acamprosate may ultimately prove to be useful additions to pharmacotherapy for alcoholism by reducing relapse. Naltrexone is a relatively selective competitive antagonist at mu-opioid receptors, and this activity may explain its anti-relapse action either because endogenous opioids are involved in the positively reinforcing effects of alcohol and/or because these same transmitters are involved in the conditioned anticipation of these effects. In contrast, the pharmacology of acamprosate is still poorly understood. This is not surprising because it is a small flexible molecule with similarities to several neuro-active amino acids and is used in high doses. All these factors suggest that it may have multiple actions. Currently, the best explanation for the effects of acamprosate seems to be that it inhibits the glutamatergic transmitter system involved in both the negative reinforcing effects of alcohol and the conditioned ''pseudo-withdrawal'' that may be important in cue-induced relapse. (Am J Addict 2003;12[Suppl 1]:S3^S11) S3

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Amino acids are still as exciting as ever

Cited by 22 publications

References 52 publications

Localization, pharmacology, and organization of brain locomotor areas in larval lamprey

Localization, pharmacology, and organization of brain locomotor areas in larval lamprey

Effect of spinal cord stimulation in an animal model of neuropathic pain relates to degree of tactile “allodynia”

Pharmacological Mechanisms of Naltrexone and Acamprosate in the Prevention of Relapse in Alcohol Dependence

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