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Abstract
Intracisternal (i.c.) administration of the glutamate-receptor antagonist kynurenate
to halothane-anesthetized rats (paralyzed, ventilated) produced an initial hypertension
associated with an increase in lumbar sympathetic nerve discharge. Kynurenate (i.c.)
blocked or greatly reduced all sympathetic reflexes investigated (somatosympathetic
70% reduction; vagal pressor and depressor responses, 100%; hypothalamic mixed responses,
90%; baroreflex, 100%) and increased the firing rate of reticulospinal sympathoexcitatory
cells of the rostral ventrolateral medulla (PGCL-SE neurons) by 33%. After i.c. kynurenate,
these cells exhibited a rhythmic, non-bursting firing pattern which could be reset
by spinal cord stimulation only when antidromic spikes were elicited. Cells with similar
characteristics were recorded in the nucleus paragigantocellularis lateralis (PGCL)
in an in vitro rat bulb preparation perfused through the basilar artery. Their 'pacemaker-like'
discharge pattern was observed even in the absence of kynurenate and was reset by
orthodromic activation. Cells with similar characteristics were also recorded within
the PGCL in 500-microns coronal slices in vitro. At 37 degrees C their discharge rate
was similar to that of PGCL-SE neurons recorded in vivo after i.c. kynurenate; it
was also pacemaker-like and was insensitive to glutamate receptor blockade. It is
suggested that the tonic discharge of PGCL-SE neurons is normally due to an intrinsic
pacemaker activity which is modulated in vivo by a variety of synaptic inputs.