摘要
Spreading depression (SD) can be elicited in the brainstem of rats younger than 13 days when excitability is enhanced by acetate superfusion [F. Richter, S. Rupprecht, A. Lehmenkc;hler, H.-G. Schaible, Spreading depression can be elicited in brain stem in immature but not adult rats, J. Neurophysiol. 90 (2003) 2163–2170]. To investigate whether voltage-gated calcium channels (VGCCs) modify initiation and propagation of SD in this type of tissue, we applied specific blockers to L-, T-, P/Q-, and N-type VGCCs locally or systemically. SD-related d.c. potentials and concomitant increases in extracellular potassium concentration ([K+]e) were unaffected by the L- and T-type VGCC blocker flunarizine that was applied either systemically (up to 2 mg/kg body weight) or by superfusion onto the brainstem (40 ;c;M). In addition, local application of the P/Q-type VGCC blocker c9;-agatoxin (1 ;c;M) or of the N-type VGCC blocker c9;-conotoxin (1 ;c;M) to the brainstem surface did not influence SD. The results indicate that VGCCs do not modify the generation or propagation of SDs in the brainstem of the immature rat. Blockade of N-type VGCCs disturbed the normal breathing rhythm. Application of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) (250–1000 ;c;M) that elicited SD in the immature cortex, failed to elicit SD in the immature brainstem. In summary, it is likely that K+ initiates and propagates brainstem SDs.