caa a22 4500 463157842 CHVBK 20180406164739.0 cr unu---uuuuu 170326e20070201xx s 000 0 eng 10.1007/s10286-006-0394-8 doi (NATIONALLICENCE)springer-10.1007/s10286-006-0394-8 McLachlan Elspeth Spinal Injuries Research Centre, Prince of Wales Medical Research Institute, Gate 1 Barker Street, 2031, Randwick, NSW, Australia aut Diversity of sympathetic vasoconstrictor pathways and their plasticity after spinal cord injury [Elektronische Daten] [Elspeth McLachlan] Sympathetic vasoconstrictor pathways pass through paravertebral ganglia carrying ongoing and reflex activity arising within the central nervous system to their vascular targets. The pattern of reflex activity is selective for particular vascular beds and appropriate for the physiological outcome (vasoconstriction or vasodilation). The preganglionic signals are distributed to most postganglionic neurones in ganglia via synapses that are always suprathreshold for action potential initiation (like skeletal neuromuscular junctions). Most postganglionic neurones receive only one of these "strong” inputs, other preganglionic connections being ineffective. Pre- and postganglionic neurones discharge normally at frequencies of 0.5-1Hz and maximally in short bursts at <10Hz. Animal experiments have revealed unexpected changes in these pathways following spinal cord injury. (1) After destruction of preganglionic neurones or axons, surviving terminals in ganglia sprout and rapidly re-establish strong connections, probably even to inappropriate postganglionic neurones. This could explain aberrant reflexes after spinal cord injury. (2) Cutaneous (tail) and splanchnic (mesenteric) arteries taken from below a spinal transection show dramatically enhanced responses in vitro to norepinephrine released from perivascular nerves. However the mechanisms that are modified differ between the two vessels, being mostly postjunctional in the tail artery and mostly prejunctional in the mesenteric artery. The changes are mimicked when postganglionic neurones are silenced by removal of their preganglionic input. Whether or not other arteries are also hyperresponsive to reflex activation, these observations suggest that the greatest contribution to raised peripheral resistance in autonomic dysreflexia follows the modifications of neurovascular transmission. Steinkopff Verlag Darmstadt, 2007 sympathetic nervous system nationallicence sympathetic ganglia nationallicence autonomic dysreflexia nationallicence vasoconstriction nationallicence norepineph- rine nationallicence autonomic nervous system nationallicence Clinical Autonomic Research Steinkopff-Verlag; www.steinkopff.springer.de 17/1(2007-02-01), 6-12 0959-9851 17:1<6 2007 17 10286 https://doi.org/10.1007/s10286-006-0394-8 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s10286-006-0394-8 text/html Onlinezugriff via DOI NATIONALLICENCE 100 1- McLachlan Elspeth Spinal Injuries Research Centre, Prince of Wales Medical Research Institute, Gate 1 Barker Street, 2031, Randwick, NSW, Australia aut NATIONALLICENCE 773 0- Clinical Autonomic Research Steinkopff-Verlag; www.steinkopff.springer.de 17/1(2007-02-01), 6-12 0959-9851 17:1<6 2007 17 10286 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer