Novel mutation in MYH7 gene associated with distal myopathy and cardiomyopathy.

A 25-year-old woman had childhood-onset muscle weakness and dilated cardiomyopathy. She exhibited predominantly distal weakness with early toe walking. Dilated cardiomyopathy required cardiac transplantation at age 15 years.

Kv1 channels selectively prevent dendritic hyperexcitability in rat Purkinje cells.

Purkinje cells, the sole output of the cerebellar cortex, encode the timing signals required for motor coordination in their firing rate and activity pattern. Dendrites of Purkinje cells express a high density of P/Q-type voltage-gated calcium channels and fire dendritic calcium spikes. Here we show that dendritic subthreshold Kv1.

The selective role of nitric oxide in opioid-mediated footshock stress antinociception in mice.

Different kinds of stress induce distinct antinociceptive properties that may be related or unrelated to the endogenous opioid system. Nitric oxide (NO) has been implicated in stress-activated mechanisms. NO also plays an important role in the modulation of nociceptive responses and has many functional interactions with opioidergic pathways.

Adrenoceptor mechanisms underlying imipramine-induced memory deficits in rats.

The post-training administration of tricyclic antidepressant imipramine impairs memory consolidation in the passive avoidance task. The present study investigated the effects of intrahippocampal (i.h.

Mediation of nitric oxide in inhibitory effect of morphine against electroshock-induced convulsions in mice.

Nitric oxide (NO) and morphine have been coupled in many physiological as well as pathological processes. The present study examined the involvement of the L-arginine/NO pathway in the anticonvulsant properties of systemic morphine (2-30 mg/kg) against electroshock seizures (ECS) in mice. Morphine decreased the intensity of maximal electroshock seizures (MES) and increased the threshold for ECS.

The effect of L-NAME and L-arginine on impairment of memory formation and state-dependent learning induced by morphine in mice.

Rationale: Morphine and nitric oxide (NO) have important functional interactions in different neural processes, and both modulate learning and memory although their interaction in cognitive performance has not been elucidated.

Objective: To examine the effect of the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) and NOS substrate L-arginine on morphine-induced impairment of memory formation and the state-dependent retrieval of a passive avoidance task learned under morphine influence.

Methods: All drugs were administered intraperitoneally, and a one-trial step-down paradigm was used for the assessment of memory in adult male NMRI mice.

The effects of adenosine receptor agonists and antagonists on morphine state-dependent memory of passive avoidance.

Pretraining administration of morphine (5 mg/kg, intraperitonically) in a step-down passive avoidance task led to state-dependent learning with impaired retrieval on the test day that was dose-dependently restored by pretest administration of morphine (0.5, 1, 3, and 5 mg/kg). This restoration was reversible by pretest naloxone administration.

The role of alpha-adrenoceptors in the amnestic effect of intracerebroventricular dexamethasone.

Corticosteroids exert dual enhancing or impairing effects on cognitive functions. While their memory-enhancing effects have been well investigated, the mechanisms involved in their amnestic effects are not completely understood. Thus, we examined the role of alpha-adrenoceptors on dexamethasone-induced amnesia using step-through passive avoidance test in rat.

The effect of cyclosporin A on morphine tolerance and dependence: involvement of L-arginine/nitric oxide pathway.

Cyclosporin A is known to decrease nitric oxide (NO) production in nervous tissues. The effects of systemic cyclosporine A on the induction and expression of morphine tolerance and dependence, acute morphine-induced antinociception, and the probable involvement of the L-arginine/nitric oxide pathway in these effects were assessed in mice. Cyclosporin A (20 mg/kg), N(G)-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg) and a combination of the two at lower and per se non-effective doses (5 and 3 mg/kg, respectively) showed a similar pattern of action, inhibiting the induction of tolerance to morphine-induced antinociception and increasing the antinociception threshold in the expression phase of morphine tolerance.

Dopamine receptor mechanism(s) and morphine tolerance in mice.

Based on our previous demonstration of the involvement of dopamine-2 (D2) dopamine receptors in morphine antinociception, we examined the role of D2 dopamine receptors in the expression and development of tolerance to morphine antinociception in mice. Tolerance to morphine antinociception was assessed by the tail-flick response after the administration of morphine (50 mg/kg) once daily for 3 days. The D2 dopamine receptor agonist, quinpirole (0.

The role of alpha2-adrenoceptors in the modulatory effects of morphine on seizure susceptibility in mice.

Purpose: To evaluate the effect of the alpha2-adrenoceptor agonist clonidine and the antagonist yohimbine on the dual modulation of seizure susceptibility induced by morphine and the anticonvulsant effect of acute stress in mice.

Methods: The thresholds for the clonic seizures induced after intravenous administration of pentylenetetrazole (PTZ) or bicuculline were assessed in mice weighing 23-30 g. Acute stress was induced by restraining mice for 2 h in a restrainer.

The role of nitric oxide in the proconvulsant effect of delta-opioid agonist SNC80 in mice.

The involvement of nitric oxide (NO) in modulation of seizure susceptibility by delta-opioid agonist (+)-4-((alpha R)-alpha-((2S, 5R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-methoxybenzyl)-N, N-diethyl-benzamide (SNC80) was examined in mice. Systemic administration of SNC80 (0.1-5 mg/kg, intraperitoneally (i.

The involvement of endogenous opioids and nitricoxidergic pathway in the anticonvulsant effects of foot-shock stress in mice.

The involvement of endogenous opioids and nitric oxide (NO) in the anticonvulsant effects of stress against pentylenetetrazole (PTZ)- or electroconvulsive shock-induced seizures was assessed in mice. The prolonged and intermittent foot-shock stress, which induced opioid-mediated analgesia, had significant protective effects against both seizure types which was reversible by naloxone (0.3, 1 or 2 mg/kg), while brief and continuous foot-shock did not alter the seizure susceptibility.

Anticonvulsant effects of cyclosporin A on pentylenetetrazole-induced seizure and kindling: modulation by nitricoxidergic system.

Cyclosporin A (CsA) is known to decrease nitric oxide (NO) release in the nervous system. The present study was aimed at investigating the effects of acute administration of CsA on pentylenetetrazole (PTZ)-induced seizure threshold and latency and probable modulation of these effects by NO synthesis substrate L-arginine, and NO synthesis inhibitors N(G)-nitro-L-arginine methyl ester (L-NAME) or aminoguanidine. Moreover, the effect of CsA per se or concomitant with L-arginine on the development of PTZ-induced kindling was assessed.

The involvement of nitric oxide in the antinociception induced by cyclosporin A in mice.

Cyclosporin A (CsA) and other immunophilin-binding agents are known to inactivate neuronal nitric oxide synthase (nNOS). Nitric oxide (NO) is involved in the nociception at the spinal level. We evaluated the effect of acute intraperitoneal (i.

The role of nitric oxide in anticonvulsant and proconvulsant effects of morphine in mice.

Acute subcutaneous administration of lower doses of morphine (0.5, 1 and 3 mg/kg) increase the threshold of seizures induced by pentylenetetrazole (PTZ) in mice, whereas higher doses of morphine (15, 30 and 60 mg/kg) have proconvulsant effects. The effect of systemic administration of nitric oxide synthase (NOS) inhibitors N(G)-nitro-L-arginine methyl ester (L-NAME) and N(G)-nitro-L-arginine (L-NNA) and nitric oxide synthase (NOS) L-arginine on biphasic effect of morphine was investigated.