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Central serotonin receptor sensitivity in rats with experimental allergic encephalomyelitis
Research Communications in Chemical Pathology and Pharmacology
|November 1, 1980
Summary
Experimental allergic encephalomyelitis (EAE) causes motor deficits by impairing serotonin neurotransmission. This study in rats found EAE-induced paraplegia disrupts serotonin pathways, affecting motor control.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Experimental allergic encephalomyelitis (EAE) is an autoimmune disease that causes central nervous system inflammation and motor deficits.
- Serotonin plays a crucial role in regulating motor activity and other neurological functions.
- Understanding the impact of EAE on serotonergic pathways is vital for developing effective treatments.
Purpose of the Study:
- To investigate the effects of EAE-induced paraplegia on serotonin-mediated bulbospinal motor activities in rats.
- To determine if serotonergic neurotransmission is impaired during the acute paralytic stage of EAE.
- To correlate motor deficits in EAE with alterations in serotonergic pathways.
Main Methods:
- Induction of EAE in rats to create a model of paraplegia.
- Administration of monoamine oxidase inhibitors and L-tryptophan to assess serotonin syndrome components.
- Evaluation of specific motor responses, including Straub tail, hindlimb abduction, rigidity, head weaving, and forepaw treading.
- Assessment of head tremor and sensory hyper-reactivity.
- Examination of serotonergically-evoked automatic swallowing activity in anesthetized EAE rats using receptor agonists, precursor, reuptake blocker, and antagonist.
Main Results:
- EAE-induced paraplegia failed to elicit typical serotonin syndrome components like Straub tail, hindlimb abduction, or rigidity.
- Altered but present motor responses, including lateral head weaving and forepaw treading, were observed at spinal segments above the paraplegia level.
- Head tremor and sensory hyper-reactivity remained unimpaired in EAE rats.
- Serotonergically-evoked automatic swallowing activity in anesthetized EAE rats was not significantly changed.
Conclusions:
- EAE-induced impairment of serotonergic neurotransmission is closely linked to the motor deficits observed during the acute paralytic phase.
- Specific bulbospinal motor activities mediated by serotonin are disrupted in EAE.
- While some serotonergic functions remain intact, the overall integrity of serotonergic pathways is compromised in EAE-related paralysis.