Reinstatement of festinating forward locomotion by antiserotonergic drugs in rats partially recovered from damage in the region of the nucleus reticularis tegmenti pontis

Rebecca M. Chesire, Jung Tung Cheng, Philip Teitelbaum

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5 Citations (Scopus)

Abstract

Damage in the region of the nucleus reticularis tegmenti pontis (NRTP) produces galloping festinating forward locomotion. Therefore, the NRTP is part of a system that normally inhibits locomotion. In operated rats that had partially recovered the ability to inhibit locomotion, presumably based on recovery of function in that inhibitory system, methysergide (45 or 60 mg/kg) or metergoline (5 or 10 mg/kg) reinstated such galloping. This suggests that serotonin systems blocked by these drugs may activate this system to inhibit locomotion. In haloperidol akinesia (a model of parkinsonian akinesia), NRTP destruction or inactivation also released festinating locomotion (3). We suggest that dopamine deficiency-induced akinesia may result from the unchecked action of the NRTP movement-inhibition system. This agrees with earlier findings by us that lateral hypothalamic damage-induced profound akinesia can be reversed by methysergide (4). Antiserotonergic drugs may therefore prove useful in alleviating parkinsonian akinesia.

Original languageEnglish (US)
Pages (from-to)286-294
Number of pages9
JournalExperimental Neurology
Volume77
Issue number2
DOIs
StatePublished - Aug 1982
Externally publishedYes

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Locomotion
Methysergide
Pharmaceutical Preparations
Metergoline
Recovery of Function
Haloperidol
Dopamine
Serotonin

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience

Cite this

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title = "Reinstatement of festinating forward locomotion by antiserotonergic drugs in rats partially recovered from damage in the region of the nucleus reticularis tegmenti pontis",
abstract = "Damage in the region of the nucleus reticularis tegmenti pontis (NRTP) produces galloping festinating forward locomotion. Therefore, the NRTP is part of a system that normally inhibits locomotion. In operated rats that had partially recovered the ability to inhibit locomotion, presumably based on recovery of function in that inhibitory system, methysergide (45 or 60 mg/kg) or metergoline (5 or 10 mg/kg) reinstated such galloping. This suggests that serotonin systems blocked by these drugs may activate this system to inhibit locomotion. In haloperidol akinesia (a model of parkinsonian akinesia), NRTP destruction or inactivation also released festinating locomotion (3). We suggest that dopamine deficiency-induced akinesia may result from the unchecked action of the NRTP movement-inhibition system. This agrees with earlier findings by us that lateral hypothalamic damage-induced profound akinesia can be reversed by methysergide (4). Antiserotonergic drugs may therefore prove useful in alleviating parkinsonian akinesia.",
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N2 - Damage in the region of the nucleus reticularis tegmenti pontis (NRTP) produces galloping festinating forward locomotion. Therefore, the NRTP is part of a system that normally inhibits locomotion. In operated rats that had partially recovered the ability to inhibit locomotion, presumably based on recovery of function in that inhibitory system, methysergide (45 or 60 mg/kg) or metergoline (5 or 10 mg/kg) reinstated such galloping. This suggests that serotonin systems blocked by these drugs may activate this system to inhibit locomotion. In haloperidol akinesia (a model of parkinsonian akinesia), NRTP destruction or inactivation also released festinating locomotion (3). We suggest that dopamine deficiency-induced akinesia may result from the unchecked action of the NRTP movement-inhibition system. This agrees with earlier findings by us that lateral hypothalamic damage-induced profound akinesia can be reversed by methysergide (4). Antiserotonergic drugs may therefore prove useful in alleviating parkinsonian akinesia.

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