Antinociception and behavioral changes induced by carbachol microinjected into identified sites of the rat brain

Klamt, Jyrson Guilherme; Prado, Wiliam A.

doi:10.1016/0006-8993(91)90593-k

Cited by 61 publications

(29 citation statements)

References 59 publications

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“…Microinjection of a κ-opioid agonist (13) or neurotensin (14) into the amygdala evokes antinociception. A similar effect was demonstrated in the rat tail flick test following microinjection of carbachol into various amygdaloid nuclei, including the CE and the medial (ME) nuclei (15,16). Microinjection of morphine into the corticomedial subdivision of the amygdala is effective in the flinch-jump (17,18) and hot plate (19) tests.…”

Section: Introductionsupporting

confidence: 52%

Antinociception induced by stimulating amygdaloid nuclei in rats: changes produced by systemically administered antagonists

Oliveira

Prado

1998

Braz J Med Biol Res

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The antinociceptive effects of stimulating the medial (ME) and central (CE) nuclei of the amygdala in rats were evaluated by the changes in the latency for the tail withdrawal reflex to noxious heating of the skin. A 30-s period of sine-wave stimulation of the ME or CE produced a significant and short increase in the duration of tail flick latency. A 15-s period of stimulation was ineffective. Repeated stimulation of these nuclei at 48-h intervals produced progressively smaller effects. The antinociception evoked from the ME was significantly reduced by the previous systemic administration of naloxone, methysergide, atropine, phenoxybenzamine, and propranolol, but not by mecamylamine, all given at the dose of 1.0 mg/kg. Previous systemic administration of naloxone, atropine, and propranolol, but not methysergide, phenoxybenzamine, or mecamylamine, was effective against the effects of stimulating the CE. We conclude that the antinociceptive effects of stimulating the ME involve at least opioid, serotonergic, adrenergic, and muscarinic cholinergic descending mechanisms. The effects of stimulating the CE involve at least opioid, ß-adrenergic, and muscarinic cholinergic descending mechanisms.Correspondence

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Section: Introductionsupporting

confidence: 52%

Antinociception induced by stimulating amygdaloid nuclei in rats: changes produced by systemically administered antagonists

Oliveira

Prado

1998

Braz J Med Biol Res

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“…In the first set, carbachol 125 nmol in 0.5 µl normal saline, a dose previously determined to provide optimum antinociception in a lightly anesthetized acute preparation (Holden and Naleway, 2001;Holden et al, 2005), or normal saline for control was microinjected into the LH, and nociceptive responses were measured. Carbachol is a nonselective cholinergic receptor agonist that resists the actions of cholinesterase and produces activation of neurons at a number of intracerebral sites (Klamt and Prado, 1991). The LH contains both muscarinic and nicotinic receptors (Rainbow et al, 1984;Cortes et al, 1986;Oki et al, 2005), and we have shown that the actions of carbachol are mediated by cholinergic receptor activity in the LH (Holden et al, 2005).…”

Section: Introductionmentioning

confidence: 75%

Lateral hypothalamic-induced antinociception may be mediated by a substance P connection with the rostral ventromedial medulla

Holden

Pizzi

2008

Brain Research

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“…Pain-induced changes in Ach release in the HF Apart from the above described behavioral [29,217] and electrophysiological evidence [56,57,74,75,[145][146][147] concerning the roles of cholinergic inputs in hippocampal processing of painful information, Aloisi's lab has addressed pain-elicited changes in Ach release or activity of Ach-synthesizing enzyme, ChAT, in the HF in response to persistent pain stimulation. At first,…”

Section: 5mentioning

confidence: 99%

Roles of the hippocampal formation in pain information processing

2009

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Abstract:Pain is a complex experience consisting of sensory-discriminative, affective-motivational, and cognitive-evaluative dimensions. Now it has been gradually known that noxious information is processed by a widely-distributed, hierarchicallyinterconnected neural network, referred to as neuromatrix, in the brain. Thus, identifying the multiple neural networks subserving these functional aspects and harnessing this knowledge to manipulate the pain response in new and beneficial ways are challenging tasks. Albeit with elaborate research efforts on the cortical responses to painful stimuli or clinical pain, involvement of the hippocampal formation (HF) in pain is still a matter of controversy. Here, we integrate previous animal and human studies from the viewpoint of HF and pain, sequentially representing anatomical, behavioral, electrophysiological, molecular/ biochemical and functional imaging evidence supporting the role of HF in pain processing. At last, we further expound on the relationship between pain and memory and present some unresolved issues.

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Antinociception and behavioral changes induced by carbachol microinjected into identified sites of the rat brain

Cited by 61 publications

References 59 publications

Antinociception induced by stimulating amygdaloid nuclei in rats: changes produced by systemically administered antagonists

Antinociception induced by stimulating amygdaloid nuclei in rats: changes produced by systemically administered antagonists

Lateral hypothalamic-induced antinociception may be mediated by a substance P connection with the rostral ventromedial medulla

Roles of the hippocampal formation in pain information processing

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