Central modulation of formalin-induced acute peripheral inflammation & pain by some putative amino acid neurotransmitters in rats.

Possible central modulation of acute peripheral inflammation by putative amino acid neurotransmitters was investigated in rats by adopting formalin induced pedal inflammation as an experimental model. Out of five amino acids (GABA, glycine, DL-alanine, L-glutamic acid and L-aspartic acid) tested, intracerebroventricular (icv) administration of GABA and L-aspartic acid produced significant alteration in acute inflammation. GABA showed a significant attenuation of paw oedema and nociception whereas, L-aspartic acid produced significant increase in oedema volume along with marked hyperalgesia. In conclusion, the study confirms that CNS is capable of modulating peripheral inflammation.

Central noradrenergic & dopaminergic modulation of brewer's yeast-induced inflammation & nociception in rats.

The possibility of central noradrenergic and dopaminergic modulation of Brewer's yeast-induced peripheral inflammation was investigated in rats. Centrally administered noradrenaline (NA), amphetamine, which liberates NA and dopamine in the central nervous system and L-dopa, the precursor of dopamine significantly suppressed paw oedema. Conversely, the beta-adrenoceptor blocker, propranolol, catecholaminergic neuron degenerator, 6-hydroxydopamine (6-OHDA), dopaminergic antagonist, haloperidol and dopamine synthesis inhibitor, alpha-methyl para tyrosine (AMPT) augmented paw oedema. In addition, 6-OHDA and haloperidol produced significant reduction in pain threshold. The results of this study indicate that central NA and dopamine exert inhibitory effects on Brewer's yeast-induced peripheral inflammation.

Central serotonergic and histaminergic modulation of peripheral inflammation and nociception in rats.

Possible central serotonergic and histaminergic modulation of acute peripheral inflammation was investigated in rats, adopting the formaldehyde-induced acute pedal inflammation as an experimental model. Intracerebroventricular (icv) administration of central inhibitory neurotransmitter, serotonin and its precursor, 5-hydroxytryptophan (5-HTP) attenuated the oedema volume and exudate protein content alongwith augmentation in pain threshold. On the contrary, cyproheptadine, a 5-HT-receptor antagonist and selective serotonin synthesis inhibitor, parachlorophenylalanine (PCPA) produced oedema augmenting and pro-nociceptive effects besides elevating the protein content of the exudate. Centrally administered histamine attenuated pedal oedema, nociception as well as protein concentration in oedema fluid. Cimetidine, an H2 histaminergic receptor blocker did not produce any significant effect on inflammation.

Central noradrenergic and cholinergic modulation of formaldehyde-induced pedal inflammation and nociception in rats.

Possible central noradrenergic and cholinergic modulation of acute peripheral inflammation was investigated in rats, adopting the formaldehyde-induced pedal inflammation as the experimental model. Intracerebroventricularly (icv) administered noradrenaline (NA), alpha-adrenoceptor agonist, L-phenylephrine, alpha-2 adrenoceptor agonist, clonidine and non-selective beta-adrenoceptor blocker, propranolol, suppressed formaldehyde-induced inflammation producing a decrease in oedema volume and increase in pain threshold. Conversely, both noradrenergic neuron degenerator, 6-hydroxydopamine (6-OHDA) and non-selective alpha-adrenoceptor antagonist, phenoxybenzamine produced an increase in paw oedema along with an augmentation of pain. Significant oedema augmenting effects were also produced by central excitatory neurotransmitter, acetylcholine (ACh) on icv administration. ACh also produced pro-nociceptive action. An ACh antagonist, scopolamine and ACh synthesis inhibitor, hemicholinium-3 (HC) reduced pedal oedema and produced analgesia. The results of this study indicate that central NA exerts an inhibitory effect on peripheral oedema and pain whereas, ACh has an augmenting effect on formaldehyde-induced peripheral inflammation.