Bacterial melanin improves cognitive impairment induced by cerebral hypoperfusion in rats.

The effect of bacterial melanin (BM) solution on learning and memory impairment induced by chronic cerebral hypoperfusion in rats was studied. Male rats were injected intramuscularly with BM solution on the second day after bilateral permanent occlusion of the common carotid artery. Rats received 6 mg/ml (170 mg/kg) BM and performed significantly better in cognition tests compared with controls. The present findings demonstrate that the beneficial effects of BM injection on cognitive functions may be due to preventing neuropathological alterations, suppressing the inflammation process, stimulating vascularization and inhibiting oxidative damage. Obtained data suggest that BM has therapeutic potential for the treatment of neurodegeneration caused by ischemia.

Bacterial melanin increases electrical activity of neurons in Substantia Nigra pars compacta.

Bacterial melanin (BM) has been used in different series of experiments as a neuroprotector. It facilitates recovery and regeneration processes after CNS lesions. The action of BM after Substantia Nigra destruction is of major interest. Electrophysiological study tries to reveal the effects of this substance on the electrical activity of Substantia Nigra pars compacta (SNc) neurons. The substance significantly increases the firing rate of SN cdopaminergic neurons. BM increases the rate of excitatory responses after high frequency tetanic stimulation of ipsilateral caudate­putamen. Overall increase in firing rate of SN neurons can contribute to recovery processes after neuronal degeneration in SN.

Effects of bacterial melanin on movement, posture, and skilled balancing deficits after unilateral destruction of substantia nigra pars compacta in rats.

Sixteen adult male rats were initially trained to an instrumental conditioned reflex (ICR) and subjected to unilateral destruction of substantia nigra pars compacta. Part of the animals was injected with bacterial melanin solution on the next day of destruction. The other 8 rats served as the control group. Recovery rates for ICR and dynamics of paralyzed hindlimb movements were studied in both groups. Conditioned reflex and contralateral to lesion hindlimb movements recovered faster in rats injected with bacterial melanin after the destruction.

Effects of bacterial melanin on motor recovery and regeneration after unilateral destruction of Substantia Nigra pars compacta in rats.

We examined the potential neuroprotective action of bacterial melanin (BM) in rats after unilateral destruction of Substantia Nigra pars compacta (SNc) dopaminergic neurons. 24 rats were initially trained to an instrumental conditioned reflex (ICR) and then subjected to unilateral electrolytic destruction of SNc. Unilateral deficit in balancing hindlimb movements was observed in all rats after the destruction. On the next day after the destruction part of the animals (n=12) was intramuscularly injected with BM solution at the concentration 6 mg/ml (0.17 g/kg). The other 12 operated rats served as a control group. On the second day after the operation the testing of instrumental conditioned reflex was resumed in both groups. Comparison of recovery periods for the ICR in both groups showed that recovery of the reflex and balancing hindlimb movements in melanin treated rats took place in three postoperative testing days, whereas in control group the recovery was not complete after 23 testing days. Electrophysiological study was conducted in 12 intact rats to show the effects of BM on the activity of SNc neurons. The firing rate of neurons was significantly increased by the BM injection. Morpho-histochemical study of brain sections was conducted after the completion of behavioral experiments. In melanin injected rats the study revealed absence of destruction or electrode trace in Substantia Nigra pars compacta of melanin injected rats. BM stimulates regeneration and microcirculation in SNc. Increased electrical activity of SN neurons and regenerative efforts induced by BM accelerate motor recovery after unilateral SNc destruction.