In a four-part study, we expand on our previous report that bulbospinal ser
otonin (5HT) neuronal activation occurs with 24 h of cold exposure. To char
acterize temporal aspects, rats were exposed to 3 degrees C or were maintai
ned at 22 degrees C for 2, 8, 48, or 96 h (experiment 1) or for 15, 30, or
60 min (experiment 2). To ensure that cold-induced changes in 5HT activity
were not due to disturbances in diurnal pattern, rats in experiment 3 were
exposed to cold (8 h) during the dark cycle. To explore the hypothesis that
cold-induced 5HT activation is part of a broad metabolic response that inc
ludes activation of the sympathetic nervous system, metabolically impaired
(hypothyroid) rats were exposed to 8 degrees C in experiment 4. Significant
increments in 5-hydroxyindoleacetic acid (5HIAA) concentration were eviden
t by 60 min of cold exposure and existed at all later time points measured.
These findings were most robust in spinal cord and rostral brainstem. Acti
vation in spinal cord was also found when rats were exposed to 8 h of cold
during the dark cycle, the active period for rats. In experiment 4, hypothy
roid rats exhibited significantly greater norepinephrine excretion compared
with control rats exposed to the same cold stimulus; this finding was acco
mpanied by significantly greater increments in 5HIAA concentration in rostr
al brainstem and spinal cord of hypothyroid rats. In addition, significant
elevations in tryptophan concentration were noted throughout the brainstem
and spinal cord of cold-exposed, hypothyroid rats relative to room temperat
ure, hypothyroid rats. This finding suggested that elevations in 5HIAA conc
entration in these rats were due to increases in precursor availability. Th
e implications of these findings relative to autonomic and metabolic contro
l are discussed.