ABSTRACT
Stimulation of the mamillary nuclei of the rat hypothalamus induced increases in the permeability of forelimb skin microvessels. This effect was not seen in rats stimulated after administration of capsaicin at a dose (150 mg/kg) sufficient to deplete vasoactive neuropeptides from the peripheral nerve terminals of capsaicin-sensitive neurons. These data indicate a role for the mamillary nuclei in central mechanisms modulating the effector functions of primary capsaicin-sensitive neurons.
Subject(s)
Capillary Permeability/physiology , Capsaicin/pharmacology , Hypothalamus/physiology , Mammillary Bodies/physiology , Skin/blood supply , Animals , Capillary Permeability/drug effects , Electric Stimulation , Forelimb/blood supply , Forelimb/physiology , Hypothalamus/cytology , Male , Neurons/drug effects , Neurons/physiology , Rats , Rats, Wistar , Regional Blood Flow/drug effects , Regional Blood Flow/physiology , Skin/drug effectsABSTRACT
Contralateral increased exudation of plasma proteins, as measured by Evans Blue leakage into the fore paws, was produced by unilateral electrocoagulation of the mamillary nuclei in rats. Ten days after adult capsaicin pretreatment (increasing doses/4 days total 200 mg/kg, s.c.) the unilateral destruction of these nuclei did not evoke any changes of skin blood vessel permeability in both contralateral and unilateral paws. The findings show that the central nervous system may modulate the capsaicin-sensitive peptidergic neuron action on blood vessel permeability.
Subject(s)
Capillary Permeability/physiology , Capsaicin/pharmacology , Mammillary Bodies/physiology , Skin/blood supply , Animals , Blood Proteins/metabolism , Coloring Agents , Evans Blue , Male , Rats , Rats, Wistar , Reference ValuesABSTRACT
The results of the present study, in the rat and cat, indicate that not only a lesion of peripheral nerve or capsaicin pretreatment but also pharmacological deafferentation with local anaesthetic or disruption of the connections between primary sensory neurons and the central nervous system are effective in producing dystrophic changes in tissues. These effects of deafferentation do not seem to depend on the sympathetic or parasympathetic efferents. Dystrophic changes are connected with microcirculation disturbances: slow down of local blood flow, elevation of the vascular permeability, oedema and leucocyte infiltration. The findings indicate that capsaicin-sensitive primary sensory neurons are the afferent part of some reflex arrangement which participates in the regulation of microcirculation and the maintenance of trophic processes in peripheral tissues. The efferent part of this arrangement is unknown.
Subject(s)
Neurons, Afferent/physiology , Animals , Atropine/pharmacology , Capsaicin/pharmacology , Cats , Electrocoagulation , Female , Ganglia, Sympathetic/physiology , Histocytochemistry , Liver/anatomy & histology , Liver/innervation , Male , Microinjections , Ophthalmic Nerve/physiology , RNA/metabolism , Rats , Rats, Inbred Strains , Regional Blood Flow/drug effects , Stereotaxic TechniquesABSTRACT
Subcutaneous injection of 50 mg/kg capsaicin to newborn rats resulted in a marked decrease of heat pain sensitivity and neurogenic inflammation. There was, however, no significant difference between capsaicin-pretreated and control rats in the severity of neuroparalytic keratitis after surgical deafferentation of the eye. Retrobulbar injection of 100 microliters of 0.5% capsaicin produced keratitis-like corneal changes. These changes were not prevented by previous pretreatment with a total subcutaneous dose of 200 mg/kg capsaicin. The findings indicate that corneal changes after deafferentation are not due to excessive release of substance P and other neuropeptides from the degenerating afferent fibres.
