Acoustic stress activates tuberoinfundibular peptide of 39 residues neurons in the rat brain.

Strong acoustic stimulation (105 dB SPL white noise) elicited c-fos expression in neurons in several acoustic system nuclei and in stress-sensitive hypothalamic nuclei and limbic areas in rats. In the present study, using this type of loud noise for 30 min, Fos-like immunoreactivity (Fos-ir) was investigated in neurons that synthesize tuberoinfundibular peptide of 39 residues (TIP39) in the rat brain: in the subparafascicular area of the thalamus, the posterior intralaminar complex of the thalamus and the medial paralemniscal nucleus in the lateral part of the pons. By double labeling, Fos-ir was shown in nearly 80% of TIP39-positive cells in the medial paralemniscal nucleus, 43% in the posterior intralaminar complex and 18.5% in the subparafascicular area 30 min after the end of a 30-min loud noise period. In control rats, only few neurons, including 0-4% of TIP39-positive neurons showed Fos-ir. While the majority of the Fos-ir neurons were TIP39-positive in the subparafascicular area and medial paralemniscal nucleus, a fairly high number of TIP39-immunonegative, chemically uncharacterized neurons expressed c-fos in the subparafascicular area and the posterior intralaminar complex of the thalamus. These observations clearly show that some TIP39 neurons in the so-called "acoustic thalamus" and the majority of TIP39 neurons in the medial paralemniscal nucleus are sensitive to loud noise and they may participate in the central organization of responses to acoustic stress. Furthermore, the present data suggest that non-TIP39-expressing neurons may play a prevalent role in the activity of the "acoustic thalamus".