A comparison of the analgesic and behavioral effects of [D-Ala2] met-enkephalinamide and morphine in the mesencephalic reticular formation of rats

Haigler, Henry J.; Spring, Denise D.

doi:10.1016/0024-3205(78)90500-3

Cited by 30 publications

(2 citation statements)

References 16 publications

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“…The most exhaustive studies refer to opioid receptors, namely the µ‐opioid subtype which has been shown to play a major role in the hypoalgesia induced by morphine injected intracerebroventriculary (i.c.v. ; Gogas et al ., 1996) into the periaqueductal grey (PAG; Jensen & Yaksh, 1986), mesencephalic reticular formation (Haiger & Spring, 1978) or rostroventromedial medulla (RVM; Levy & Proudfit, 1979; Azami et al ., 1982; Yaksh & Melzach, 1999). More recently, other receptors have been shown to be important for supraspinal pain control.…”

Section: Introductionmentioning

confidence: 99%

Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABA_B, µ‐opioid and NK‐1 receptors

Pinto

Lima

Castro-Lopes

et al. 2003

Eur J of Neuroscience

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Modulation of nociceptive transmission at the brainstem involves several neurochemical systems. The precise location and specific characteristics of nociceptive neurons activated in each system was never reported. In this study, the presence of GABA(B), mu-opioid, and neurokinin-1 (NK-1) receptors in brainstem nociceptive neurons was investigated by double-immunocytochemical detection of each receptor and noxious-evoked induction of the c-fos proto-oncogene. Noxious cutaneous mechanical stimulation significantly increased the proportions of neurons double-labelled for Fos and GABA(B) receptors in several brainstem regions, namely, the reticular formation of the caudal ventrolateral medulla (VLMlat and VLMrf), lateral reticular nucleus, spinal trigeminal nucleus, pars caudalis (Sp5C), nucleus of the solitary tract, dorsal reticular nucleus, ventral reticular nucleus, raphe obscurus nucleus and dorsal parabrachial nucleus (DPB). For mu-opioid receptors, the proportions of double-labelled neurons in noxious-stimulated animals were higher than in controls only in the VLMlat, VLMrf, Sp5C, DPB and A5 noradrenergic cell group. As for the NK-1 receptor, no significant differences were found between control and stimulated animals. According to these results, neurons expressing GABA(B), mu-opioid and NK-1 receptors at several pain control centres of the brainstem are differentially involved in processing nociceptive mechanical input. The data provide the definition of new supraspinal targets for selective modulation of nociceptive neurons in order to define better strategies of pain control.

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Section: Introductionmentioning

confidence: 99%

Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABA_B, µ‐opioid and NK‐1 receptors

Pinto

Lima

Castro-Lopes

et al. 2003

Eur J of Neuroscience

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“…There is evidence that points to the MRF as a possible site of interaction between morphine and the combined MFB-LH/MRF stimulation. The microiontophoretic application of either morphine or the synthetic opioid peptide met-enkephalinamide into the MRF significantly increases tail flick latency (Haigler and Mittleman, 1978; Haigler and Spring, 1978). Morphine infusion into the MRF also attenuates the response to the hemostat pinch test.…”

Section: Discussionmentioning

confidence: 99%

Medial forebrain stimulation enhances intracranial nociception and attenuates morphine analgesia suggesting the existence of an endogenous opioid antagonist

Kornetsky

Knapp

Tozier

et al. 2010

Pharmacology Biochemistry and Behavior

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The purpose of this experiment was to test in the rat the hypotheses that activation of the brain reward system would attenuate the effects of intracranial nociceptive stimulation and would potentiate the antinociceptive effects of morphine. In this experiment pain (nociception) was generated by electrical stimulation of a brain pain pathway, the mesencephalic reticular formation (MRF) of the rat. Reward pathway stimulation was to the medial forebrain bundle at the level of the lateral hypothalamus (MFB-LH). Current thresholds for escape from MRF stimulation were determined using a modification of the psychophysical methods of limits. MRF stimulation was delivered concurrently with different intensities of non-contingent MFB-LH stimulation. The effects of morphine and saline were determined under all stimulation conditions. Contrary to expectation MFB-LH stimulation significantly lowered MRF stimulation escape thresholds. Morphine administration elevated MRF thresholds in the absence of MFB-LH stimulation. However, this effect was blocked by concurrent MFB-LH stimulation. These findings, which mimic the effects of the opiate antagonist naloxone, i.e., potentiating of pain and antagonism of morphine’s analgesic effects, suggest the presence of an endogenous opiate receptor antagonist.

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Neurotensin: Topographical distribution of brain sites involoved in hypothermia and antinociception

Kalivas¹,

Jennes²,

Nemeroff

et al. 1982

J of Comparative Neurology

105

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When administered into the cerebroventricular system of the rat, neurotensin (NT) produces a variety of effects, including a decrease in colonic temperature and an increase in nociceptive threshold. The previous study described in detail the localization of immunohistochemical NT in the rat brain. In this study, bilateral injections of NT were made into 223 separate loci in the rat brain an a map was generated showing the brain regions where NT produced a decline in colonic temperature and an increase in hot plate response latency. It was found that some of the brain areas which contain immunohistochemically identified NT responded to locally administered NT. Further, most NT-sensitive brain loci contain NT cell bodies as well as fibers. Areas in the brain where NT produced an antinociceptive response were not the same areas where NT evoked hypothermia. An antinociceptive response was consistently produced after NT injection into the nucleus amygdaloideus centralis, rostral area praeoptica medialis, the ventral thalamus dorsomedial and medial to the lemniscus medialis, rostral mesencephalic periventricular gray, and medial pontine formatio reticularis. Less-consistent antinociception was also observed in the mesencephalic formatio reticularis and the caudal diagonal band of Broca. Hypothermia was induced by NT in the area praeoptica medialis contiguous with the area anterior hypothalami, nucleus ventralis tegmenti (Tsai), floor of the fourth ventricle, and tractus spinalis nervi trigemini. Less profound hypothermia was also produced in the posterior hypothalamus. The fact that all these responsive brain areas contain NT indicates that the microinjection of NT may be mimicking the effects of endogenously released NT, thus supporting the possible physiological significance of NT as an endogenous modulator of body temperature or nociceptive sensory information.

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A comparison of the analgesic and behavioral effects of [D-Ala2] met-enkephalinamide and morphine in the mesencephalic reticular formation of rats

Cited by 30 publications

References 16 publications

Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABA_B, µ‐opioid and NK‐1 receptors

Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABA_B, µ‐opioid and NK‐1 receptors

Medial forebrain stimulation enhances intracranial nociception and attenuates morphine analgesia suggesting the existence of an endogenous opioid antagonist

Neurotensin: Topographical distribution of brain sites involoved in hypothermia and antinociception

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A comparison of the analgesic and behavioral effects of [D-Ala2] met-enkephalinamide and morphine in the mesencephalic reticular formation of rats

Cited by 30 publications

References 16 publications

Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABAB, µ‐opioid and NK‐1 receptors

Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABAB, µ‐opioid and NK‐1 receptors

Medial forebrain stimulation enhances intracranial nociception and attenuates morphine analgesia suggesting the existence of an endogenous opioid antagonist

Neurotensin: Topographical distribution of brain sites involoved in hypothermia and antinociception

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Product

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Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABA_B, µ‐opioid and NK‐1 receptors

Noxious‐evoked c‐fos expression in brainstem neurons immunoreactive for GABA_B, µ‐opioid and NK‐1 receptors