Naloxone modulates the behavioral effects of cholinergic agonists and antagonists

@article{Walker2006NaloxoneMT,
  title={Naloxone modulates the behavioral effects of cholinergic agonists and antagonists},
  author={David L. Walker and Timothy McGlynn and Christina Grey and Michael E. Ragozzino and Paul E. Gold},
  journal={Psychopharmacology},
  year={2006},
  volume={105},
  pages={57-62}
}
Peripheral glucose administration enhances memory in rodents and humans. Recent findings suggest that glucose may affect behavior, in part, by augmenting central cholinergic functions and by attenuating central opiate functions. The present experiments examined interactions between an opiate antagonist, naloxone, and cholinergic agents to determine whether the effects would parallel those found with glucose. Three behavioral measures were assessed: tremors, hyperactivity, and spontaneous… Expand
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References

SHOWING 1-10 OF 50 REFERENCES
Glucose and physostigmine effects on morphine- and amphetamine-induced increases in locomotor activity in mice.
TLDR
The attenuation of morphine-induced hyperactivity demonstrates a similarity between glucose and cholinergic agonists, and also indicates that glucose may inhibit, directly or indirectly, opiate functions. Expand
Scopolamine- and morphine-induced impairments of spontaneous alternation performance in mice: reversal with glucose and with cholinergic and adrenergic agonists.
TLDR
The present experiments examined the possibility that peripheral glucose administration might reverse scopolamine- and morphine-induced impairments in a spontaneous alternation task, and found that central cholinergic systems may contribute to glucose and epinephrine effects on memory storage. Expand
Possible interaction between central cholinergic muscarinic and opioid peptidergic systems during memory consolidation in mice.
TLDR
The results suggest that naloxone facilitated retention as a function of its opiate antagonist properties, and an inhibitory modulatory role for endogenous opioid systems on the activity of central cholinergic muscarinic systems during memory consolidation is suggested. Expand
Blood glucose and brain function: interactions with CNS cholinergic systems.
TLDR
Findings indicate that glucose can facilitate the actions of a cholinergic agonist on two behaviors, locomotor activity and tremors, adding support to the view that circulating glucose levels can modulate central Cholinergic function. Expand
Attenuation of scopolamine-induced amnesia in mice
TLDR
The results support the value of scopolamine as a model of age-related memory impairments, but suggest further that these memory deficits may be particularly susceptible to attenuation with non-cholinergic treatments. Expand
Systemic naloxone administration potentiates locus coeruleus noradrenergic neuronal activity under stressful but not non-stressful conditions
TLDR
Indices of behavioral distress, vocalization and struggling, were also found to be significantly increased in animals given naloxone during stress, suggesting that endogenous opioids have a moderating influence upon the level of activity of the LC which operates only under specific conditions such as stress. Expand
Inhibition of acetylcholine turnover in rat hippocampus by intraseptal injections of β-endorphin and morphine
TLDR
The data suggest that opiate agonists decrease hippocampal TRACh by regulating septal cholinergic neurons, and that this effect is not associated with analgesia. Expand
Actions of enkephalin, μ and partial agonist analgesics on acetylcholine turnover in rat brain
TLDR
The actions of μ agonists, partial agonists and enkephalin analogues on the turnover rate of acetylcholine (TRAch) indicate that κ receptor mediated analgesia may involve different neural substrates from those of μagonists and supports the concept of multiple opiate receptors within the CNS. Expand
Attenuation of scopolamine-induced impairment of spontaneous alternation behaviour by antagonist but not inverse agonist and agonist β-carbolines
TLDR
It is hypothesized that the interaction of antagonist β-carbolines with scopolamine is based on a direct GABA-ergic control of cholinergic neurotransmission, and suggests an ability of antagonists β- carbolines to antagonize amnestic properties of scopolamines. Expand
Reversal of scopolamine-induced amnesia of passive avoidance by pre- and post-training naloxone
  • D. Rush
  • Psychology, Medicine
  • Psychopharmacology
  • 2004
TLDR
Control experiments indicated that neither an increase in pain sensitivity nor an induced aversive state appear to be responsible for the influence of naloxone on the scopolamine-induced retention deficit, extending previous findings implicating a cholinergic-opioid interaction in memory processes. Expand
...
1
2
3
4
5
...