RESUMEN
Despite extensive characterization of sex differences in the medial preoptic area (mPOA) of the hypothalamus, we know surprisingly little about whether or how male and female mPOA neurons differ electrophysiologically, especially in terms of neuronal firing and behavioral pattern generation. In this study, by performing whole-cell patch clamp recordings of the mPOA, we investigated the influences of sex, cell type, and gonadal hormones on the electrophysiological properties of mPOA neurons. Notably, we uncovered significant sex differences in input resistance (male > female) and in the percentage of neurons that displayed post-inhibitory rebound (male > female). Furthermore, we found that the current mediated by the T-type Ca
RESUMEN
The thalamus is a brain structure known to modulate sensory information before relaying to the cortex. The unique ability of a thalamocortical (TC) neuron to switch between the high frequency burst firing and single spike tonic firing has been implicated to have a key role in sensory modulation including pain. Of the two firing modes, burst firing, especially maintaining certain burst firing properties, was suggested to be critical in controlling nociceptive behaviors. Therefore, understanding the factors that influence burst firing properties would offer important insight into understanding sensory modulation. Using computational modeling, we investigated how the balance of excitatory and inhibitory inputs into a TC neuron influence TC bursting properties. We found that intensity of inhibitory inputs and the timing of excitatory input delivery control the dynamics of bursting properties. Then, to reflect a more realistic model, excitatory inputs delivered at different dendritic locations—proximal, intermediate, or distal—of a TC neuron were also investigated. Interestingly, excitatory input delivered into a distal dendrite, despite the furthest distance, had the strongest influence in shaping burst firing properties, suggesting that not all inputs equally contribute to modulating TC bursting properties. Overall, the results provide computational insights in understanding the detailed mechanism of the factors influencing temporal pattern of thalamic bursts.
Asunto(s)
Encéfalo , Canales de Calcio Tipo T , Biología Computacional , Dendritas , Incendios , Neuronas , Filtrado Sensorial , TálamoRESUMEN
AIM:To observe the effect of thyroxine on the expression of T-type calcium channels Cav3. 1, Cav3. 2 and Cav3. 3 in rat myocardium, and to explore the possible biological mechanism between the changes of the ex-pression of T-type calcium channels and the arrhythmia in hyperthyroid heart disease. METHODS:Healthy SD rats (n=20) were randomly divided into normal control group (n=10) and hyperthyroid heart disease group (n=10). The animal model was established by intraperitoneal injection of levothyroxine for 35 d. The contents of T3 and T4 in serum, the heart-to-body weight ratio, the diameter of cardiac myocytes and electrocardiograph were measured to evaluate hyperthyroid heart disease. Moreover, the mRNA and protein expression levels of T-type calcium channels in the myocardium were measured by RT-PCR, immunohistochemistry and Western blot. RESULTS:After intraperitoneal injection of levothyroxine for 35 d, compared with the normal control group, the serum contents of T3 and T4, the heart-to-body weight ratio and the diameter of cardiac myocytes were significantly increased in hyperthyroid heart disease group (P<0.05), and arrhythmia occurred in hyperthyroid heart disease group. By immunohistochemistry and Western blot, the protein expression of Cav3. 1 in-creased significantly (P<0.05), while the protein expression of Cav3.2 decreased significantly (P<0.01). However, no change of the Cav3. 3 protein was observed. The results of RT-PCR were the same as immunohistochemistry and Western blot. CONCLUSION:Thyroxine promotes the expression of Cav3. 1 in the myocardium but inhibits the expression of Cav3. 2 at mRNA and protein levels, which might be involved in arrhythmia in hyperthyroid heart disease.
RESUMEN
T-type calcium channels are expressed in various tis-sues and play key roles in physiology and pathophysiology,inclu-ding neuronal firing,hormone secretion,pain,and cancer,etc. Hence,it is critical to understand the molecular mechanisms un-derlying the regulation of T-type channels.Substantial literature suggests many G protein-coupled receptors (GPCRs)and related second messengers can modulate T-type channel in some extent. Here,this review focuses on the modulation of T-type calcium channels by GPCRs and related second messengers.
RESUMEN
Aim To investigate the effects of T-and L-type calcium channel blockers on isolated thoracic aorta from thyroxine-induced hypertensive rats.Methods Hyperthyroidism was induced by administering L-thyroxine (T4,0.5 mg·kg~(-1),sc) daily for 16 days.Sham-treated euthyroid control rats were only received vehicle saline for 16 days. Experiments were performed in isolated thoracic aorta rings from euthyroid and hyperthyroid rats. Mibefradil and diltiazem were used to inhibit T-and L-type calcium channels,respectively.Results Thyroid hormone excess for 16 days induced characteristic changes in body weight,heart rate and systolic blood pressure in rats. The body weight was significantly decreased,heart rate and systolic blood pressure were increased in T4-treated rats. Thoracic aorta morphology was altered in T4-treated rats. The thickness of adventitia was increased with hypertrophy and hyperplasia of the smooth musle cells in T4-treated rats. Vasorelaxant effect of T-and L-type calcium channel blockers were accentuated in aortic rings from T4-treated rats.Conclusion These data suggest that T-and L-type calcium channels are functionally upregulated in isolated thoracic aorta from hyperthyroid rats and they,may be a therapeutic target in thyroxine-induced hypertension.