Primed-bursts induced long-term potentiation in rat visual cortex: effects of dark-rearing

Theta burst stimulation (TBS) and primed bursts (PBs) stimulation are among the effective tetanic stimulations for induction of long-term potentiation (LTP) in the hippocampus. Recent studies have indicated that TBS is effective in LTP induction of layer III synapses of neocortex, only if applied to layer IV. However, the possibility of neocortical LTP induction using PBs has not been investigated yet. Sensory deprivation greatly influences the development of neocortex. According to the effect of sensory deprivation on synaptic plasticity of developing neocortex, we studied the induction of LTP by PBs in visual cortical slices of control and dark-reared rats. The results showed that application of PBs to layer IV could effectively induce LTP of layer II/III field potentials. These potentials are consisted of two components: pEPSP1, (population excitatory postsynaptic potential 1) and pEPSP2. In control slices PBs led to selective potentiation of pEPSP2. Visual deprivation increased the incidence of LTP of pEPSP1 and decreased the amount of LTP of pEPSP2. These findings showed that PBs could be used as an effective tetanic stimulation to study the synaptic plasticity in neocortex. The effects of visual deprivation on PBs-induced LTP are consistent with its role in the development of excitatory system in neocortex.     

Primed-burst potentiation in adult rat visual cortex in vitro

The effectiveness of θ pattern primed-bursts (PBs) on development of PB potentiation was investigated in layer II/III of the adult rat visual cortex in vitro. Experiments were carried out in the visual cortical slices. Population excitatory postsynaptic potentials (pEPSPs) were evoked in layer II/III by stimulation of either white matter or layer IV. To induce long-term potentiation (LTP), eight episodes of PBs were delivered at 0.1 Hz. Regardless of stimulation site, field potential recorded in layer II/III consisted of two components: a short latency and high amplitude response called pEPSP1, and a long latency and low amplitude response called pEPSP2. The incidence of LTP produced by PBs of layer IV was higher than that of the white matter tetanization. In contrast, PBs of both layer IV and white matter reliably produced LTP of pEPSP2 in layer II/III. It is concluded that PBs, as a type of activity pattern, of either white matter or layer IV can gain access to the modifiable synapses that are related to pEPSP2 in layer II/III, but accessibility of the modifiable synapses that are related to pEPSP1 depends on tetanization site. Relevancy of the results to the plasticity gate hypothesis is also discussed.     

A new series of Schiff base derivatives bearing 1,2,3‐triazole: Design,synthesis, molecular docking,and α‐glucosidase inhibition

A series of new Schiff bases bearing 1,2,3‐triazole 12a ? o was designed, synthesized, and evaluated as α‐glucosidase inhibitors. All the synthesized compounds showed promising inhibition against α‐glucosidase and were more potent than the standard drug acarbose. The kinetic study on the most potent compound 12n showed that this compound acted as a competitive α‐glucosidase inhibitor. The docking study revealed that the synthesized compounds interacted with the important residues in the active site of α‐glucosidase.     

Longitudinal Tissue Velocity and Deformation Imaging in Inferobasal Left Ventricular Aneurysm

Background: Longitudinal myocardial tissue velocity imaging (TVI) and strain rate imaging (SRI) quantify regional myocardial function. We aimed to measure TVI and SRI indices for inferobasal aneurysmal segments by echocardiography at rest. Method: Sixteen patients with inferobasal left ventricular (LV) aneurysm, LV ejection fraction (EF) ≤50%, and 14 normal coronaries with normal echocardiography (control group) were studied. In SRI, peak systolic strain (ST), strain rate (SR), and pattern of strain curves and in TVI, peak systolic inward motion (Sm) were evaluated all at rest. Ascending curve means systolic expansion and descending means shortening. Results: LVEF was significantly lower in the patient group. Mean ST, SR, and Sm of inferobasal segment showed significant difference between patient and control groups; for ST: 1.45 ± 7.18% versus ?17.64 ± 7.45%, P < 0.0001; SR: ?0.25 ± 0.26 versus ?1.44 ± 0.64 sec^?1, P < 0.0001; and Sm: 3.85 ± 1.26 versus 5.56 ± 1.28 cm/sec, P = 0.006, respectively. All inferobasal aneurysmal segments had ascending curve while normal segments showed a descending curve. In patient group, aneurysmal segments had significantly reduced ST and SR compared to normal segments. Normal functioning segments of patients showed significant reduction of ST and SR compared to normal LV segments in control subjects. The range of SR and ST for inferobasal aneurysmal segments did not overlap with that of the normal segments (?0.60, 0.19 and ?3.00, ?0.80 sec^?1 for SR, and ?8.30, 23.30 and ?35.30, ?10.00% for ST, respectively). Conclusion: SRI indices were significantly reduced in inferobasal aneurysmal segment in comparison with either the same segment in normal subjects or normal functioning segments in the same patients. SR and ST may be superior to Sm in the evaluation of inferobasal aneurysmal segments. (Echocardiography 2010;27:803‐808)     

Contribution of ionotropic glutamate receptors and voltage-dependent calcium channels to the potentiation phenomenon induced by transient pentylenetetrazol in the CA1 region of rat hippocampal slices

The role of ionotropic glutamate receptors and voltage-dependent calcium channels (VDCCs) in potentiation phenomenon and epileptic activity induced by a transient pentylenetetrazol (PTZ) application in the CA1 region of rat hippocampal slices was investigated. Also we examined whether adenosine as an inhibitory neuromodulator would interact with expression of the long-lasting effect of transient PTZ. Population spikes (PS) were recorded in the CA1 cell body layer of the hippocampal slices following stratum radiatum stimulation. Changes in the PS amplitude potentiation and number of extra PS, which induced by transient PTZ were used as indices to quantify the effects of drugs. PS input-output curve was significantly increased 10 min after PTZ application and persisted at least for 60 min after PTZ washout. Polyspikes also appeared, but did not persist. Both ketamine and APV reduced the extent of potentiation of PS amplitude but had no effect on number of extra PS. The selective non-NMDA receptor antagonist CNQX prevented the amplitude potentiation and the generation of extra PS. The blocker of VDCCs, verapamil, prevented the amplitude potentiation and inhibited polyspike activity. Co-application of adenosine and PTZ produced a rapid and reversible decrease in the PS amplitude, but PTZ-induced potentiation phenomenon was observed after washout. It is concluded that ionotropic glutamate receptors as well as VDCCs involve in the PTZ-induced LTP of PS amplitude. PTZ-induced LTP is also insensitive to adenosine. The epileptiform activity induced by a transient PTZ application could be attributed to VDCCs. The polyspikes mediated by VDCCs are dependent on prior activation of AMPA receptors.     

Effect of transient hippocampal inhibition on amygdaloid kindled seizures and amygdaloid kindling rate

In this study the effect of transient inhibition of the CA1 region of the dorsal hippocampus by lidocaine on amygdala kindling rate and amygdaloid kindled seizures was investigated. In experiment 1, rats were divided into four groups. In group 1, animals were implanted only with a tripolar electrode into the amygdala but in groups 2-4, two guide cannulae were also implanted into the CA1 regions of the dorsal hippocampi. Animals were stimulated daily to be kindled. In groups 3 and 4, saline or 2% lidocaine (1 microl/2 min) was also injected respectively into the hippocampus, 5 min before each stimulation. Results obtained showed that amygdala kindling rate and the number of stimulations to receive from stage 4 to stage 5 seizure were significantly increased in group 4. In experiment 2, lidocaine (1% and 2%) was infused (1 microl/2 min) into the hippocampus of amygdala kindled rats bilaterally and animals were stimulated at 5, 15 and 30 min after drug injection. Twenty four h before lidocaine injection, saline was also infused (1 microl/2 min) into the hippocampus as control. Obtained results showed that afterdischarge duration was reduced 5 min after lidocaine (1% and 2%) injection. Stage 5 seizure duration was also decreased 5 and 15 min after 2% lidocaine. Thus, it may be suggested that in amygdala kindling, activation of the hippocampal CA1 region has a role in seizure acquisition and seizure severity so that inhibition of this region results in decreasing of seizure severity and retards amygdala kindling rate.     

Reversal of pentylenetetrazol-induced potentiation phenomenon by theta pulse stimulation in the CA1 region of rat hippocampal slices

The effect of theta pulse stimulation (TPS) on pentylenetetrazol (PTZ)-induced long-term potentiation of population spikes was studied in the CA1 region of rat hippocampal slices. The field excitatory postsynaptic potential (fEPSP) and population spikes (PS) were recorded from strata radiatum and pyramidale, respectively, following stimulation of Schaffer collaterals. A transient PTZ application produced a long-lasting enhancement of PS amplitude. A 3-min episode of TPS delivered at test-pulse intensity failed to reverse the PTZ potentiation. However, the same stimulation at a higher intensity produced complete reversal of the PTZ potentiation when delivered during the last minutes of PTZ application. Prior application of high-intensity TPS also decreased the amount of PTZ potentiation, whereas it had no long-lasting effect on baseline synaptic responses. High-intensity TPS induced reversal was blocked by adenosine A1 receptor antagonist and, furthermore, was reduced by protein phosphatase 1 inhibitor. The results suggest that mechanism of PTZ-induced LTP reversal involves activation of adenosine receptors and protein phosphatases.     

Caffeine increases paragigantocellularis neuronal firing rate and induces withdrawal signs in morphine-dependent rats

Using single unit recording in nucleus paragigantocellularis neurons located in the rostral ventrolateral medulla, and measuring the precipitated withdrawal syndrome, we investigated whether chronic morphine administration would produce adaptive changes in the adenosine system. Caffeine (50 mg/kg, i.p.) induced withdrawal signs (head shakes, tooth chattering, ejaculation, chewing, and irritability) in morphine-dependent rats 10-18 min after the injection. Only the tooth chattering and diarrhea were expressed following a direct paragigantocellularis injection of caffeine (200 microM, 0.5 microl). The spontaneous activity of paragigantocellularis neurons was significantly decreased by microinjection of both adenosine (10 nM) and an adenosine A1 receptor-selective agonist, cyclohexyladenosine (200 microM), into the paragigantocellularis nucleus of both control and morphine-dependent rats, but the decrease in firing rate of paragigantocellularis neurons of morphine-dependent rats was greater than that of control ones. There was also a significant enhancement of spontaneous activity of paragigantocellularis neurons 8-15 min after caffeine administration (50 mg/kg, i.p.) and 10-18 min after the injection of an adenosine A1 receptor-selective antagonist 8-phenyltheophylline (10 mg/kg, i.p.) in both control and morphine-dependent rats. However, the effect of the antagonists was greater in morphine-dependent rats than in control ones. These data suggest that there is an increase in the sensitivity of nucleus paragigantocellularis neurons to adenosine receptor ligands in morphine-dependent rats that may be associated with the ability of caffeine to produce withdrawal signs.