Repetitive Transcranial Magnetic Stimulation Alleviates Neurological Deficits After Cerebral Ischemia Through Interaction Between RACK1 and BDNF exon IV by the Phosphorylation-Dependent Factor MeCP2.

Repetitive transcranial magnetic stimulation (rTMS) is acknowledged as a form of neurostimulation, especially for functional recovery. The foundational knowledge of molecular mechanism is limited regarding its role in cerebral ischemia, for which the present study was designed. Primary neurons were treated with oxygen-glucose deprivation (OGD) and repetitive magnetic stimulation (rMS), in which brain-derived neurotrophic factor (BDNF) and transcription of BDNF exons were examined.

[Primary headache associated with sexual activity: 15 new cases and therapeutic outcomes].

Objective: To explore the clinical manifestations, diagnosis, treatment and prognostic features of primary headache associated with sexual activity (PHASA) .

Methods: Fifteen patients were prospectively analyzed over the past 7 years at our hospital. There were 11 males and 4 females with a mean age of (42 ± 11) (26-56) years.

Dopamine receptor 1 modulates the discharge activities of inspiratory and biphasic expiratory neurons via cAMP-dependent pathways.

Dopamine receptor 1 (D(1)R) plays an essential role in regulating respiratory activity in mammals, however, little is known about how this receptor acts to modulate the basic respiratory rhythmogenesis. Here, by simultaneously recording the discharge activities of biphasic expiratory (biphasic E) neurons/inspiratory (I) neurons and the XII nerve rootlets from brainstem slices, we found that the application of D(1)R agonist cis-(±)-1-(aminomethyl)-3,4-dihydro-3-phenyl-1H-2-benzopyran-5,6-diolhydrochloride (A68930, 5 μM), or forskolin, an intracellular cAMP-increasing agent, substantially decreased respiratory cycle and expiratory time of both types of neurons, and elevated the integral amplitude and frequency of XII nerve rootlets discharge. These changes were reversed by subsequent application of their antagonists SCH-23390 and Rp-Adenosine 3',5'-cyclic monophosphorothioate triethylammonium salt hydrate (Rp-cAMPS), respectively.

[Effects of basic fibroblast growth factor on rat models of Alzheimer disease].

Objective: To study the effects of basic fibroblast growth factor (bFGF) on the praxiology and cerebral acetylcholinesterase (AchE) fiber density of kainic acid-lesioned rat models of Alzheimer disease (AD).

Methods: AD models were induced in 30 normal adult rats by damaging the rat nucleus basalis of Meynert (NBM) with kainic acid, and the models were then assigned into 3 groups to receive cerebroventricular infusion with bFGF, saline or nothing for treatment, serving respectively as the treatment group at 30 min, 1, 3 and 7 d after the injury, sham treatment group or injury group. Another 10 rats were used as control group, which received saline injections into the NBM without further treatment.

[Inducible nitric oxide synthase induces beta-amyloid neurotoxicity in vivo].

Aim: To investigate the causative role of nitric oxide synthase (NOS) and nitric oxide (NO) in neurotoxicity of beta-amyloid (Abeta) and the pathogenesis of Alzheimer's disease (AD).

Methods: Using behavioral and neuropathological methods, we observed the effects of Abeta(1-40) injection into hippocampi on rats learning and memory in Y maze and on the neuropathology in hippocampi. The intervention by intraperitoneal administration of aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, and 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor, in the neurotoxicity of Abeta(1-40) was studied then.