Journal
NEUROLOGICAL SCIENCES
Volume 36, Issue 12, Pages 2177-2184Publisher
SPRINGER-VERLAG ITALIA SRL
DOI: 10.1007/s10072-015-2292-0
Keywords
Propofol; Ventrolateral preoptic; Locus coeruleus; General anesthesia; Consciousness
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Funding
- National Natural Science Foundation of China [81460219]
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The mechanisms underlying the unconsciousness of general anesthesia are not completely understood. Accumulating evidence indicates the ventrolateral preoptic nucleus (VLPO) in the endogenous sleep circuits may contribute to loss of consciousness (LOC) induced by GABA-enhancing anesthetics. However, there are few studies that look into distinct sleep pathway in the sleep-wake system. In the neural pathway from VLPO to the locus coeruleus (LC), we compared the inhibition effect of propofol on the LC activity before and after VLPO lesion in vivo rats. Systemic administration of propofol (20 mg/kg, i.p.) in normal rats caused a fast and obvious inhibition of LC neurons spontaneous firing (from 0.24 +/- A 0.06 to 0.12 +/- A 0.03 Hz). The LC neuronal firing rate of VLPO lesion rats only decreased to 0.18 +/- A 0.05 Hz (P = 0.021 vs. non-VLPO rats) after the propofol injection, and the time to reach the maximal inhibition level was also prolonged in VLPO lesion rats (2.3 +/- A 0.7 vs. 5.8 +/- A 1.2 min, P = 0.037). Microinjections of a selective GABA(A) receptor antagonist (SR95531) into the LC fully reversed the inhibitory effect of propofol on the LC neuronal activity, but did not significantly affect the latency to loss of righting reflex of rats after propofol administration (3.4 +/- A 0.9 vs. 3.7 +/- A 1.2 min, P = 0.639). Our results indicated that VLPO is necessary for the propofol-induced inhibition of LC activity, but the LC may not play an important role in the propofol-induced LOC.
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