Formalin pain is expressed in decerebrate rats but not attenuated by morphine

Matthies, Brigitte K.; Franklin, Keith B.J.

doi:10.1016/0304-3959(92)90261-9

Cited by 132 publications

(48 citation statements)

References 35 publications

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“…Similarly, intra-Ce injection of muscimol did not change baseline nociceptive scores (data not shown). These results suggest that Ce inactivation does not affect baseline behavioral responses to formalin injection and are consistent with the observation that behavioral responses to formalin are intact in decerebrate rats (Matthies and Franklin, 1992).…”

Section: Hyperalgesia As a Confound To The Present Resultssupporting

confidence: 76%

A Lateralized Deficit in Morphine Antinociception after Unilateral Inactivation of the Central Amygdala

Manning

1998

J. Neurosci.

124

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The amygdala is a forebrain region that is receiving increasing attention as a modulator of pain sensation. The amygdala contributes to antinociception elicited by both psychological factors (e.g., fear) and exogenous opioid agonists. Unlike the midbrain periaqueductal gray matter (PAG) or rostral ventromedial medulla, the amygdala is a pain-modulating region that has clear bilateral representation in the brain, making it possible to determine whether pain-modulating effects of this region are lateralized with respect to the peripheral origin of noxious stimulation. Unilateral inactivation of the central nucleus of the amygdala (Ce) plus adjacent portions of the basolateral amygdaloid complex (with either the excitotoxin NMDA or the GABA A agonist muscimol) reduced the ability of morphine to suppress prolonged, formalin-induced pain derived from the hindpaw ipsilateral, but not contralateral, to the inactivated region. This effect was evident regardless of the nociceptive scoring method used (weighted scores or flinch-frequency method) and was not accompanied by a concurrent reduction in morphine-induced hyperlocomotion. Unilateral lesions restricted to the basolateral amygdaloid complex (i.e., not including the Ce) did not reduce the ability of morphine to suppress formalin-induced pain derived from either hindpaw. The results constitute the first report of a lateralized deficit in opioid antinociception after unilateral inactivation of a specific brain area and show the first clear neuroanatomical dissociation between antinociceptive and motor effects of systemically administered morphine in the rat. The amygdala appears to modulate nociceptive signals entering the ipsilateral spinal dorsal horn, probably through monosynaptic connections with ipsilateral portions of the PAG.

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Section: Hyperalgesia As a Confound To The Present Resultssupporting

confidence: 76%

A Lateralized Deficit in Morphine Antinociception after Unilateral Inactivation of the Central Amygdala

Manning

1998

J. Neurosci.

124

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“…Interactions between GABA and opioids in other regions may be important as well. Opiates can inhibit uptake and the subsequent release of GABA in cortical slices (Bradford et al, 1986), and it is possible that antinociceptive effects of opiates at the level of the cortex (Matthies and Franklin, 1992;Burkey et al, 1996) are mediated through changes in GABA release. The GABAergic neurons of the striatum are thought to trigger motor activity by disinhibiting output circuits of the basal ganglia (for review, see Angulo and McEwen, 1994).…”

Section: Relationship Of -Opioid Receptors To Gabaergic Neurons In Thmentioning

confidence: 99%

Relationship of ?- and ?-opioid receptors to GABAergic neurons in the central nervous system, including antinociceptive brainstem circuits

1998

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Inhibition of neurons containing gamma-aminobutyric acid (GABA) may underlie some of the excitatory effects of opioids in the central nervous system (CNS). In the present study, we examined the relationship of the cloned mu- and delta-opioid receptors (MOR1 and DOR1, respectively) to GABAergic neurons in brain and spinal cord. This was done by combining immunofluorescent staining for MOR1 or DOR1 with that for GABA or glutamic acid decarboxylase (GAD); fluorescent retrograde tract-tracing was used in some cases to identify neurons with particular projections. In rats, cells double labeled for GABA and MOR1 were observed in layers II-VI of the parietal cortex and in layers II-IV of the piriform cortex. In the hippocampus, double labeling was observed in the dentate gyrus and in regions CA1 and CA3. Double labeling was very prominent in the striatum and in the reticular nucleus of the thalamus; it was also observed in other portions of the diencephalon. However, double labeling for GABA and MOR1 was never observed in the cerebellar cortex. Cells double labeled for GABA and MOR1 were common in the periaqueductal gray (PAG) and the medial rostral ventral medulla (RVM) of both rats and monkeys, suggesting that involvement of GABAergic neurons with supraspinal opioid antinociception may extend to primates. In the RVM of rats, many of those double-labeled neurons were retrogradely labeled from the dorsal spinal cord. In contrast, double-labeled neurons in the PAG were almost never retrogradely labeled from the RVM. No unequivocal examples of double labeling for DOR1 and GAD were found in any region of the CNS that we examined in either rats or monkeys. However, GABAergic neurons were often apposed by DOR1 immunoreactive varicosities. Our findings suggest that activation of mu-opioid receptors directly modulates the activity of GABAergic neurons throughout the CNS, including neurons involved in the supraspinal component of opioid analgesia. In contrast, delta-opioid receptors appear to be positioned to modulate the activity of GABAergic neurons indirectly.

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“…However, such a selective decrease in a particular behavior was not observed in the present study. Spinal transection and transections through various brain regions did not diminish acute and tonic phase licking and flinching responses to hind paw formalin injection (Matthies and Franklin, 1992;Coderre et al, 1994). Despite the absence of increased overt pain symptoms, the increased levels and segmental expansion of Fos-IR following spinal transection may be indicative of exaggerated activity in spinal nociceptive processing.…”

Section: Discussionmentioning

confidence: 89%

“…1). "Complex" or "integrated" behaviors such as licking are observed even in decerebrate rats (Grill and Norgren, 1978;Matthies and Franklin, 1992). A biphasic pattern was also observed in the rate of discharge of lumbar dorsal horn neurons following formalin injection in rats with an acute transection of the thoracic spinal cord (Pitcher and Henry, 2002).…”

Section: Discussionmentioning

confidence: 92%

Expansion of formalin-evoked Fos-immunoreactivity in rats with a spinal cord injury

Castellanos

Daniels

Morales

et al. 2007

Neuroscience Research

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Peripheral tissue injury as well as spinal cord injury (SCI) may lead to sensitization of dorsal horn neurons and alterations in nociceptive processing. Thus, peripheral injuries experienced by SCI patients, even if not initially perceived, could result in a persistent and widespread activation of dorsal horn neurons and emerge as chronic pain with interventive repair or modest recovery from SCI. To visualize the spinal neuron response to peripheral tissue injury following complete SCI in rats, the neural transcription factor Fos was quantitated in the spinal cord. Two weeks following either a complete transection of the spinal cord at the level of T8 or a sham surgery (laminectomy), rats were injected with formalin into the left hind paw. Sham-operated rats demonstrated biphasic hind paw pain-related behavior following formalin injection, but transected rats displayed fewer behaviors in the second (tonic) phase. Stereological analysis of the sham group revealed that the extent of formalininduced Fos expression was within the lumbar dorsal horn, with numerous Fos-like immunoreactive profiles in the ipsilateral dorsal horn and some contralateral immunoreactive profiles. In contrast, the level of Fos-like immunoreactivity in the transected group was significantly elevated and expanded in range compared to the sham group, with increases observed in the normal laminar distribution regions, as well as multisegmentally through sacral levels and increases in the contralateral dorsal horn segments. The data demonstrate that widespread activation of spinal, especially dorsal horn, neurons following peripheral insult can occur in the injured spinal cord, despite reduced pain responsiveness, and suggests that exaggerated pain may emerge as spinal recovery or repair progresses.

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Formalin pain is expressed in decerebrate rats but not attenuated by morphine

Cited by 132 publications

References 35 publications

A Lateralized Deficit in Morphine Antinociception after Unilateral Inactivation of the Central Amygdala

A Lateralized Deficit in Morphine Antinociception after Unilateral Inactivation of the Central Amygdala

Relationship of ?- and ?-opioid receptors to GABAergic neurons in the central nervous system, including antinociceptive brainstem circuits

Expansion of formalin-evoked Fos-immunoreactivity in rats with a spinal cord injury

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