Anesthesia and Surgery Induce a Functional Decrease Selectively in Excitatory Synaptic Transmission in Mouse Prefrontal Cortex Neurons

Postoperative delirium (POD), a syndrome of confusion and inattention, frequently occurs after anesthesia and surgery. However, the neuropathogenesis of POD remains mostly unknown. The prefrontal cortex (PFC) plays an essential role in cognitive processes. We therefore investigated how anesthesia and surgery induce neurofunctional changes in the PFC, and assessed whether intraoperative administration of dexmedetomidine, an alpha-2 agonist, could prevent the functional changes in the PFC. Laparotomy was performed in mice under isoflurane anesthesia. After a battery of behavioral tests measuring natural behaviors and learning and anxiety levels, PFC neuronal activities were recorded using whole-cell patch-clamp recordings. Effects of intraoperative dexmedetomidine were also examined. In the anesthesia/surgery group, the frequency of excitatory synaptic responses in PFC pyramidal neurons was decreased after the surgery without any changes in the response kinetics. On the other hand, neuronal intrinsic properties and inhibitory synaptic responses were not changed. Intraoperative dexmedetomidine or glutamate receptor antagonists, prevented the excitatory synaptic dysfunction induced by anesthesia and surgery. These findings suggest that anesthesia and surgery induce functional reductions selectively in excitatory synaptic responses in PFC pyramidal neurons, and intraoperative dexmedetomidine inhibits the plastic change in the PFC synaptic transmission.

Thermodynamic Interpretation on the Rheology of Aqueous Bentonite Suspensions

Since their exceptional rheological behavior, bentonite suspensions are widely used in engineering, industrial, agricultural, and drilling applications. So, the aim of the present study is to investigate the rheological properties of three types aqueous suspensions prepared with calcium bentonite (CaB), sodium bentonite (NaB) obtained from that by Na2CO3 activation, and NaB with the excess soda. The CaB taken from Giresun/Turkey region contains calcium smectite (CaxS) as clay mineral and opal CT (SiO2.nH2O) as impurity which is paracrystalline silica. Soda content by the activation and bentonite content in the suspension were changed in the interval of 2.5-15.0% and 5-20% by mass, respectively. CaxS completely converted to sodium smectite (Na2xS) by the activation with the soda content of 2.5% and then Na2xS+Na2CO3 mixtures formed. Rheological properties of these aqueous suspensions were measured using a Fann Viscometer. These properties reached their maxima by the most thixotropic Na2xS suspensions and greatly increased with the increasing of smectite content. Rheological plots drawn of the shear rate vs. shear stress in the interval of 170-1020 s-1 showed that the suspensions flow as a Bingham Plastic. Change in rheological properties depending on the smectite type and content as well as excess soda content was explained thermodynamically based on the chemical potential gradient between interlayer and dispenser waters.

Learning-induced plasticity in the barrel cortex is disrupted by inhibition of layer 4 somatostatin-containing interneurons

ABSTRACTLearning-related plasticity in the cerebral cortex is linked to the action of disinhibitory circuits of interneurons. Pavlovian conditioning, in which stimulation of the vibrissae is used as conditioned stimulus, induces plastic enlargement of the cortical functional representation of vibrissae activated during conditioning, visualized with [14C]-2-deoxyglucose (2DG). Using layer-specific, cell-selective DREADD transductions, we examined the involvement of somatostatin- (SOM-INs) and vasoactive intestinal peptide (VIP-INs)-containing interneurons in the development of learning-related plastic changes. We injected DREADD-expressing vectors into layer IV (L4) barrels or layer II/III (L2/3) areas corresponding to activated vibrissae. The activity of interneurons was modulated during training, and 2DG maps were obtained 24 h later. In mice with L4 but not L2/3 SOM-INs suppressed during conditioning, the plastic change of whisker representation and the conditioned reaction were absent. No effect of inhibiting VIP-INs was found. We report that the activity of L4 SOM-INs is indispensable for learning-induced plastic change.

Elimination of the error signal in the superior colliculus impairs saccade motor learning

When movements become dysmetric, the resultant motor error induces a plastic change in the cerebellum to correct the movement, i.e., motor adaptation. Current evidence suggests that the error signal to the cerebellum is delivered by complex spikes originating in the inferior olive (IO). To prove a causal link between the IO error signal and motor adaptation, several studies blocked the IO, which, unfortunately, affected not only the adaptation but also the movement itself. We avoided this confound by inactivating the source of an error signal to the IO. Several studies implicate the superior colliculus (SC) as the source of the error signal to the IO for saccade adaptation. When we inactivated the SC, the metrics of the saccade to be adapted were unchanged, but saccade adaptation was impaired. Thus, an intact rostral SC is necessary for saccade adaptation. Our data provide experimental evidence for the cerebellar learning theory that requires an error signal to drive motor adaptation.

Plastic Change along the Intact Crossed Pathway in Acute Phase of Cerebral Ischemia Revealed by Optical Intrinsic Signal Imaging

The intact crossed pathway via which the contralesional hemisphere responds to the ipsilesional somatosensory input has shown to be affected by unilateral stroke. The aim of this study was to investigate the plasticity of the intact crossed pathway in response to different intensities of stimulation in a rodent photothrombotic stroke model. Using optical intrinsic signal imaging, an overall increase of the contralesional cortical response was observed in the acute phase (≤48 hours) after stroke. In particular, the contralesional hyperactivation is more prominent under weak stimulations, while a strong stimulation would even elicit a depressed response. The results suggest a distinct stimulation-response pattern along the intact crossed pathway after stroke. We speculate that the contralesional hyperactivation under weak stimulations was due to the reorganization for compensatory response to the weak ipsilateral somatosensory input.

Plastic Change in the Auditory Minimum Threshold Induced by Intercollicular Effects in Mice

In the auditory pathway, the commissure of the inferior colliculus (IC) interconnects the two ICs on both sides of the dorsal midbrain. This interconnection could mediate an interaction between the two ICs during sound signal processing. The intercollicular effects evoked by focal electric stimulation for 30 min could inhibit or facilitate auditory responses and induce plastic changes in the response minimum threshold (MT) of IC neurons. Changes in MT are dependent on the best frequency (BF) and MT difference. The MT shift is larger in IC neurons with BF differences ≤2 kHz than in those with BF differences >2 kHz. Moreover, MTs that shift toward electrically stimulated IC neurons increase with the increasing MT difference between the two ICs. The shift in MT lasts for a certain period of time and then returns to previous levels within ~150 min. The collicular interactions are either reciprocal or unilateral under alternate stimulating and recording conditions in both ICs. Our results suggest that intercollicular effects may be involved in the acoustic experience-dependent plasticity of the MT of IC neurons.