Molecular basis of R-type calcium channels in central amygdala neurons of the mouse.

نویسندگان

  • Seung-Chan Lee
  • Sukwoo Choi
  • Taehoon Lee
  • Hyung-Lae Kim
  • Hemin Chin
  • Hee-Sup Shin
چکیده

R-type Ca2+ channels play a critical role in coupling excitability to dendritic Ca2+ influx and neuronal secretion. Unlike other types of voltage-sensitive Ca2+ channels (L, N, P/Q, and T type), the molecular basis for the R-type Ca2+ channel is still unclear, thereby limiting further detailed analyses of R-type Ca2+ channel physiology. The prevailing hypothesis is that alpha(1E) (Ca(V)2.3) gene encodes for R-type Ca2+ channels, but the dearth of critical evidence has rendered this hypothesis controversial. Here we generated alpha1E-deficient mice (alpha1E-/-) and examined the status of voltage-sensitive Ca2+ currents in central amygdala (CeA) neurons that exhibit abundant alpha1E expression and R-type Ca2+ currents. The majority of R-type currents in CeA neurons were eliminated in alpha1E-/- mice whereas other Ca2+ channel types were unaffected. These data clearly indicate that the expression of alpha1E gene underlies R-type Ca2+ channels in CeA neurons. Furthermore, the alpha1E-/- sign mice exhibited signs of enhanced fear as evidenced by their vigorous escaping behavior and aversion to open-field conditions. These latter findings imply a possible role of alpha1E-based R-type Ca2+ currents in amygdala physiology associated with fear.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

P19: Long-Term Potentiation

The term synaptic plasticity points to a series of persistent changes related to the activity of synapses. Long-term potentiation (LTP) is a reflection of synaptic plasticity that has an important role in learning and memory. LTP is a long-lasting increase of synaptic activity due to enhancement of excitatory synaptic transmission after a high-frequency train of electrical stimulations. Differe...

متن کامل

P30: Effects of Hemin on Ca2+Influx in Neurons of C57BL/6 Mouse Brain

Excitotoxicity results in a significant increase in Ca2+ influx; essentially from open N-Methyl-D-aspartate receptors (NMDARs) channels that cause a secondary rise in the intracellular Ca2+ concentration. It is correlated with neuronal death induced by Ca2+ overload. Dysfunction of NMDARs is associated with excitotoxic neuronal death in neurodegenerative disorders. In this study, the effects of...

متن کامل

Involvement of voltage-dependent calcium channels in synaptic plasticity of the rat visual cortex

In this study, involvement ofvoltage-dependent calcium channels in LTP of responses of rat visual cortex slices was analyzed. Field potentials including EPSP1 and EPSP2 from layers II/III were recorded through stimulation of layer IV. Whereas nifedipine, a L-type calcium channel blocker (L-VDCC), did not considerably affect the LTP of responses, but Ni2+, a relatively selective blocker of T-typ...

متن کامل

Involvement of voltage-dependent calcium channels in synaptic plasticity of the rat visual cortex

In this study, involvement ofvoltage-dependent calcium channels in LTP of responses of rat visual cortex slices was analyzed. Field potentials including EPSP1 and EPSP2 from layers II/III were recorded through stimulation of layer IV. Whereas nifedipine, a L-type calcium channel blocker (L-VDCC), did not considerably affect the LTP of responses, but Ni2+, a relatively selective blocker of T-typ...

متن کامل

Activation of inwardly-rectifying k+ channels in hypothalamic POMC neurons: role in integrating synaptic and metabolic input

Hypothalamic proopiomelanocortin (POMC) neurons are critical for controlling homeostatic functions in mammals. We used a transgenic mouse model in which the POMC neurons were labeled with enhanced-green fluorescent protein (EGFP) to perform visualized, whole-cell patch recordings from pre-pubertal female hypothalamic slices. The mouse POMC-EGFP neurons expressed the same endogenous conductance ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Proceedings of the National Academy of Sciences of the United States of America

دوره 99 5  شماره 

صفحات  -

تاریخ انتشار 2002