SYNAPTIC RESPONSES OF SUPERIOR CERVICAL GANGLION NEURONS OF RATS WITH EXPERIMENTAL DIABETES MELLITUS

Excitatory postsynaptic potentials (EPSP) were recorded from the superior cervical ganglion neurons (SCG) in the rats with experimental streptozotocininduced diabetes (ESD). EPSP was inducted by electrical stimulation of the cervical sympathetic trunk. It was founded that the average value of the EPSP time constant decay in the rats with ESD was 15% higher. At the same time, the amplitudes of EPSP of SCG neurons and the hexamethonium blocking effect in the rats with ESD on 30th day after streptozotocin injection didn’t differ significantly from those in control rats. This may indicate specific functional disorders associated as with steady-state elevated blood glucose level in rats as SCG neurons nicotinic cholinergic receptors.

Neonicotinoids disrupt circadian rhythms and sleep in honey bees

Honey bees are critical pollinators in ecosystems and agriculture, but their numbers have significantly declined. Declines in pollinator populations are thought to be due to multiple factors including habitat loss, climate change, increased vulnerability to disease and parasites, and pesticide use. Neonicotinoid pesticides are agonists of insect nicotinic cholinergic receptors, and sub-lethal exposures are linked to reduced honey bee hive survival. Honey bees are highly dependent on circadian clocks to regulate critical behaviors, such as foraging orientation and navigation, time-memory for food sources, sleep, and learning/memory processes. Because circadian clock neurons in insects receive light input through cholinergic signaling we tested for effects of neonicotinoids on honey bee circadian rhythms and sleep. Neonicotinoid ingestion by feeding over several days results in neonicotinoid accumulation in the bee brain, disrupts circadian rhythmicity in many individual bees, shifts the timing of behavioral circadian rhythms in bees that remain rhythmic, and impairs sleep. Neonicotinoids and light input act synergistically to disrupt bee circadian behavior, and neonicotinoids directly stimulate wake-promoting clock neurons in the fruit fly brain. Neonicotinoids disrupt honey bee circadian rhythms and sleep, likely by aberrant stimulation of clock neurons, to potentially impair honey bee navigation, time-memory, and social communication.

Neonicotinoids Disrupt Circadian Rhythms and Sleep in Honey Bees

Honey bees are critical pollinators in ecosystems and agriculture, but their numbers have significantly declined. Declines in pollinator populations are thought to be due to multiple factors including habitat loss, climate change, increased vulnerability to disease and parasites, and pesticide use. Neonicotinoid pesticides are agonists of insect nicotinic cholinergic receptors, and sub-lethal exposures are linked to reduced honey bee hive survival. Honey bees are highly dependent on circadian clocks to regulate critical behaviors, such as foraging orientation and navigation, time-memory for food sources, sleep, and learning/ memory processes. Because circadian clock neurons in insects receive light input through cholinergic signaling we tested for effects of neonicotinoids on honey bee circadian rhythms and sleep. Neonicotinoid ingestion by feeding over several days results in neonicotinoid accumulation in the bee brain, disrupts circadian rhythmicity in many individual bees, shifts the timing of behavioral circadian rhythms in bees that remain rhythmic, and impairs sleep. Neonicotinoids and light input act synergistically to disrupt bee circadian behavior, and neonicotinoids directly stimulate wake-promoting clock neurons in the fruit fly brain. Neonicotinoids disrupt honey bee circadian rhythms and sleep, likely by aberrant stimulation of clock neurons, to potentially impair honey bee navigation, time-memory, and social communication.

EFFECTS OF PRENATAL PASSIVE SMOKING ON CHOLINERGIC MECHANISMS SIMULATION RESPIRATORY RHYTHM IN NEONATAL RATS (IN VITRO)

Both active and passive smoking increases the risk of sudden death of the newborn. Researchers are actively studying the effect of chronic nicotine infusion, as one of the leading neurogenic factors of tobacco smoke on cholinergic mechanisms of respiratory control. In this paper, using a fumigation model of passive smoking, tested the assumption that second-hand smoke that is transferred in the prenatal period, changes the expression mediated by nicotinic receptors activating influence of the cholinergic system of the brain stem to the processes of the respiratory activity of the neural network generation. It is found that the fumigation of tobacco smoke pregnant rats decreases their progeny respiratory sensitivity to the action of a neural network and exogenous nicotine increases cholinergic part tonic effect mediated by nicotinic cholinergic receptors in the modulation of respiratory rhythm. The study uses data obtained from 40 brain stem-spinal cord preparations (BSP) of the newborn rats. The experimental group was 22, and the control group was 18 newborn rats. In the processing of neurograms, the duration of the cycle of respiratory activity, duration, and the amplitude of inspiratory discharges were measured. To describe the peaks of the respiratory discharge spectrum, the following parameters were used: the peak frequency and the peak power spectral density of the peak. Analysis of the statistical differences was made using Student’s t-test for mean values. Differences were considered significant at p<0.05. Our results confirm the presence for exogenous nicotine of powerful activating effect on the generation frequency, amplitude and duration of inspiratory discharges of the BSP of newborn rats in the control group. It is established that an increase in the amplitude of the inspiratory discharges is accompanied by an increase in the spectral power density in the mid-frequency range of their spectrograms. In the BSP of the brain of newborn rats with prenatal exposure to tobacco smoke, exogenous nicotine increased only the frequency of inspiratory discharge generation. The amplitude of the inspiratory discharges and the power of the mid-frequency oscillations under the influence of exogenous nicotine in the BSP of the experimental group was significantly reduced. Mecamylamine, a selective blocker of nAChR, added to the perfusate of the BSP of the control group, caused a significant increase in the amplitude and duration of the inspiratory discharges, without significantly changing the duration of the respiratory cycle. At the same time, in BSP of newborn rats subjected to prenatal exposure to tobacco smoke, nAChR blockade resulted in an increase in the duration of the respiratory cycle. Thus, our study showed that fumigation of pregnant rats with tobacco smoke reduces the sensitivity of the respiratory neural network to the action of exogenous nicotine in early postnatal period and increases the involvement of tonic cholinergic effect mediated by nicotinic cholinergic receptors in modulating the respiratory rhythm.

Nurr1, Pitx3, and α7 nAChRs mRNA Expression in Nigral Tissue of Rats with Pedunculopontine Neurotoxic Lesion

Background and Objectives: The knowledge that the cholinergic neurons from pedunculopontine nucleus (PPN) are vulnerable to the degeneration in early stages of the Parkinson disease progression has opened new perspectives to the development of experimental model focused in pontine lesions that could increase the risk of nigral degeneration. In this context it is known that PPN lesioned rats exhibit early changes in the gene expression of proteins responsible for dopaminergic homeostasis. At the same time, it is known that nicotinic cholinergic receptors (nAChRs) mediate the excitatory influence of pontine-nigral projection. However, the effect of PPN injury on the expression of transcription factors that modulate dopaminergic neurotransmission in the adult brain as well as the α7 nAChRs gene expression has not been studied. The main objective of the present work was the study of the effects of the unilateral neurotoxic lesion of PPN in nuclear receptor-related factor 1 (Nurr1), paired-like homeodomain transcription factor 3 (Pitx3), and α7 nAChRs mRNA expression in nigral tissue. Materials and Methods: The molecular biology studies were performed by means of RT-PCR. The following experimental groups were organized: Non-treated rats, N-methyl-D-aspartate (NMDA)-lesioned rats, and Sham operated rats. Experimental subjects were sacrificed 24 h, 48 h and seven days after PPN lesion. Results: Nurr1 mRNA expression, showed a significant increase both 24 h (p < 0.001) and 48 h (p < 0.01) after PPN injury. Pitx3 mRNA expression evidenced a significant increase 24 h (p < 0.001) followed by a significant decrease 48 h and seven days after PPN lesion (p < 0.01). Finally, the α7 nAChRs nigral mRNA expression remained significantly diminished 24 h, 48 h (p < 0.001), and 7 days (p < 0.01) after PPN neurotoxic injury. Conclusion: Taking together these modifications could represent early warning signals and could be the preamble to nigral neurodegeneration events.