Morphine Excitation in the Cerebral Cortex

Bioulac, Bernard; Jp, Lund; Puil, E.

doi:10.1139/y75-096

Cited by 24 publications

(1 citation statement)

References 6 publications

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“…The ability of morphine to dampen extracellular glutamate levels is likely mediated by opioid receptors located presynaptically on glutamatergic terminals. Morphine can also act postsynaptically to suppress glutamate-evoked neuronal excitation [280][281][282][283]. The resulting decrease in neuronal activity is reflected by other studies showing that the stimulatory effects of acute morphine on the expression of immediate-early genes such as c-fos and c-jun in the dorsal and ventral striatum is blocked by NMDA and/or AMPA receptor antagonists [284][285][286].…”

Section: Glutamate and Opiatesmentioning

confidence: 92%

Glutamatergic substrates of drug addiction and alcoholism

Gass

Olive

2008

Biochemical Pharmacology

437

367

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The past two decades have witnessed a dramatic accumulation of evidence indicating that the excitatory amino acid glutamate plays an important role in drug addiction and alcoholism. The purpose of this review is to summarize findings on glutamatergic substrates of addiction, surveying data from both human and animal studies. The effects of various drugs of abuse on glutamatergic neurotransmission are discussed, as are the effects of pharmacological or genetic manipulation of various components of glutamate transmission on drug reinforcement, conditioned reward, extinction, and relapse-like behavior. In addition, glutamatergic agents that are currently in use or are undergoing testing in clinical trials for the treatment of addiction are discussed, including acamprosate, N-acetylcysteine, modafinil, topiramate, lamotrigine, gabapentin and memantine. All drugs of abuse appear to modulate glutamatergic transmission, albeit by different mechanisms, and this modulation of glutamate transmission is believed to result in long-lasting neuroplastic changes in the brain that may contribute to the perseveration of drug-seeking behavior and drug-associated memories. In general, attenuation of glutamatergic transmission reduces drug reward, reinforcement, and relapse-like behavior. On the other hand, potentiation of glutamatergic transmission appears to facilitate the extinction of drug-seeking behavior. However, attempts at identifying genetic polymorphisms in components of glutamate transmission in humans have yielded only a limited number of candidate genes that may serve as risk factors for the development of addiction. Nonetheless, manipulation of glutamatergic neurotransmission appears to be a promising avenue of research in developing improved therapeutic agents for the treatment of drug addiction and alcoholism.

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Section: Glutamate and Opiatesmentioning

confidence: 92%

Glutamatergic substrates of drug addiction and alcoholism

Gass

Olive

2008

Biochemical Pharmacology

437

367

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Dose effects of morphine on the spontaneous unit activity recorded from the thalamus, hypothalamus, septum, hippocampus, reticular formation, central gray, and caudate nucleus

Dafny¹,

Burks²,

Bergmann³

1983

J of Neuroscience Research

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Spontaneous activity was recorded from 652 units in 8 subcortical structures of unanesthetized rats. Recordings were obtained in central gray, mesencephalic reticular formation, parafasciculus thalami, caudate nucleus, anterior and ventromedial hypothalamus, lateral septum, and dorsal hippocampus. Eighty recordings were obtained from untreated animals and 80 from saline-injected controls, none of which showed any significant changes of unit activity during the 4- 5-hr observation period. The effect of morphine, given in 5 incremental doses from 0.5 to 30.0 mg/kg ip, was followed in 492 units. Morphine enhanced or depressed spontaneous discharge rates, or caused biphasic effects, ie enhancement alternating with depression and vice versa. Naloxone induced increase in firing after either effect of morphine, or reduced spontaneous activity after morphine-induced increases. However, when morphine reduced neuronal discharges, naloxone never caused further depression. In 86 units, morphine at any dosage failed to alter neuronal activity, but in 54 of these units naloxone nevertheless induced alterations in firing rates. The pattern of responses to morphine differed between all 8 brain regions examined and was characteristic for each individual structure. This is the first systematic study describing the dose-response characteristics of morphine in 8 brain sites recorded simultaneously. Furthermore, it utilized freely behaving animals without the interference of anesthetics, which are themselves known to interact with opiates. The variety of response patterns seen supports the neuropharmacological evidence for multiple opiate receptors or multiple sites of opiate action.

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Opioids and Sensory Processing in the Central Nervous System

Duggan¹,

Fleetwood-Walker²

1993

Opioids

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Morphine Excitation in the Cerebral Cortex

Cited by 24 publications

References 6 publications

Glutamatergic substrates of drug addiction and alcoholism

Glutamatergic substrates of drug addiction and alcoholism

Dose effects of morphine on the spontaneous unit activity recorded from the thalamus, hypothalamus, septum, hippocampus, reticular formation, central gray, and caudate nucleus

Opioids and Sensory Processing in the Central Nervous System

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