Brain research bulletin
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Brain research bulletin · Apr 2017
Overexpression of phosphodiesterase-4 subtypes involved in surgery-induced neuroinflammation and cognitive dysfunction in mice.
Postoperative cognitive dysfunction (POCD) is characterized by cognitive impairments in patients after surgery. Hippocampal neuroinflammation induced by surgery is highly associated with POCD. Phosphodiesterase-4 (PDE4) is an enzyme that specifically hydrolyses cyclic adenosine monophosphate (cAMP), which plays an important role during neuroinflammation and the process of learning and memory. ⋯ Meanwhile, rolipram attenuated the cognitive impairment and the elevation of pro-inflammatory cytokines induced by surgery. Moreover, rolipram reversed the reduction of p-CREB and PSD95. These results indicate that PDE4 subtype overexpression may be involved in the development of surgery-induced cognitive dysfunction in mice.
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Brain research bulletin · Mar 2017
ReviewGephyrin and the regulation of synaptic strength and dynamics at glycinergic inhibitory synapses.
Glycinergic synapses predominate in brainstem and spinal cord where they modulate motor and sensory processing. Their postsynaptic mechanisms have been considered rather simple because they lack a large variety of glycine receptor isoforms and have relatively simple postsynaptic densities at the ultrastructural level. However, this simplicity is misleading being their postsynaptic regions regulated by a variety of complex mechanisms controlling the efficacy of synaptic inhibition. ⋯ Many of these mechanisms are governed by converging excitatory activity and regulate gephyrin oligomerization and receptor binding, the architecture of the postsynaptic density (and by extension the whole synaptic complex), receptor retention and stability. These newly uncovered molecular mechanisms define the size and number of gephyrin postsynaptic regions and the numbers and proportions of glycine and GABAA receptors contained within. All together, they control the emergence of glycinergic synapses of different strength and temporal properties to best match the excitatory drive received by each individual neuron or local dendritic compartment.
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Brain research bulletin · Jan 2017
Effect of co-administration of memantine and sertraline on the antidepressant-like activity and brain-derived neurotrophic factor (BDNF) levels in the rat brain.
A developing body of data has drawn attention to the N-methyl-d-aspartate (NMDA) receptor antagonists as potential drugs for the treatment of major depressive disorder (MDD). We investigated the possibility of synergistic interactions between the antidepressant sertraline with the uncompetitive NMDA receptor antagonist, memantine. The present study was aimed to evaluate behavioural and molecular effects of the chronic treatment with memantine and sertraline alone or in combination in rats. ⋯ Our results indicate that co-administration of antidepressant memantine with sertraline may induce a more pronounced antidepressant activity than treatment with each antidepressant alone. Antidepressant properties using the combination of memantine and sertraline could be attributed to increased levels of BDNF. This finding may be of particular importance in the case of drug-resistant patients and could suggest a method of obtaining significant antidepressant actions whereas limiting side effects.
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Brain research bulletin · Oct 2016
Cordycepin attenuates traumatic brain injury-induced impairments of blood-brain barrier integrity in rats.
Loss of blood-brain barrier (BBB) integrity is a downstream event caused by traumatic brain injury (TBI). BBB integrity is affected by certain physiological conditions, including inflammation and oxidative stress. Cordycepin is a susbtance with anti-inflammatory and anti-oxidative effects. ⋯ Furthermore, cordycepin inhibited NADPH oxidase (NOX) expression and activity following TBI, probably through NOX1, but not NOX2 and NOX4. Cordycepin has protective effects against brain damages induced by TBI. The protection of cordycepin on BBB integrity was probably achieved through recovery of tight junction proteins, inhibition of local inflammation, and prevention of NOX activity.
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Brain research bulletin · Oct 2016
Postnatal changes in glutamatergic inputs of jaw-closing motoneuron dendrites.
Dendrites of masseter (jaw-closing) motoneurons (MMNs) are well developed and ramify extensively throughout the trigeminal motor nucleus and often extend into the adjacent reticular formation. It is possible that the dendrites have active properties, which are altered with the development of the orofacial musculoskeletal system. Thus, we examined the changes in somatic voltage responses evoked by photostimulation of the MMN dendrites by laser photolysis of caged glutamate from postnatal day (P) 2-5 and 9-12 rats. ⋯ In 75% of P2-5 MMNs, the step-like increase in amplitude, which was blocked by 20μM D(-)-2-amino-5-phosphonovaleric acid application, corresponded to the NMDA spikes/plateau potentials. In contrast, at P9-12 the responses became significantly smaller in amplitude and shorter in duration and only one neuron out of 12 MMNs showed NMDA spikes/plateau potentials. These results suggest that the glutamatergic responses evoked by photostimulation of the MMN dendrites change during the first two postnatal weeks, and these changes may be involved in the transition from suckling to chewing during postnatal development.