ADRENOCORTICAL RESPONSES TO OLFACTORY STIMULATION IN RATS WITH HYPOTHALAMIC ISLANDS
S. FELDMAN
AND
N. CONFORTI
Department ofNeurology, Hadassah University Hospital, Jerusalem, Israel
(Received 27 October 1975) There exists both anatomical and electrophysiological evidence that olfactory pathways project to the hypothalamus (Scott & Pfaffmann, 1967; Scott & Chafin, 1975). Hypothalamic island preparations were used to differentiate between 'systemic' stresses which produced normal adrenocortical responses and 'neurogenic' stresses which caused a reduced adrenal discharge (Feldman, Conforti, Chowers & Davidson, 1970; Feldman, Conforti & Chowers, 1975). This paper describes the role of the hypothalamic neural connexions in the mediation of the adrenocortical response following olfactory stimulation. Experiments were performed on male albino rats of the Hebrew University strain weighing approximately 250 g. Adrenocortical responses to ether stress and to olfactory stimulation, as determined by changes in plasma corticosterone levels (Click, von Redlich & Levine, 1964), were studied in 33 intact animals and in 33 rats with hypothalamic islands (Halasz & Pupp, 1965). The protocol consisted of submitting intact rats to olfactory stimulation, and hypo¬ thalamic deafferentation was performed after 1 week only in those animals which showed an adequate adrenocortical response. Ten to fourteen days later the animals were exposed to ether stress and 1 week after this, those rats which showed a normal response were submitted to a repeated olfactory stimulation. This stimulus consisted of placing rats, anaesthetized 15 min earlier with pentobarbitone (35 mg/kg, i.p.), in a box into which compressed air was delivered through a bottle containing concentrated amyl acetate, at a rate of 8 litres/min, for a period of 30min. Blood was then withdrawn from ajugularvein for corticosterone determina¬ tion, when the animals were still asleep. The ether stress consisted of exposing the animals to ether vapour for 2 min. Fifteen minutes later a skin incision was made under ether anaesthesia and a blood sample removed for corticosterone determination. The stressing stimuli were applied between 08.00 and 12.00h. The basal corticosterone levels 15 min after pento¬ barbitone administration were determined in intact and deafferentated rats. All data were analysed by Student's f-test. The brains were examined h istologie ally to confirm the complete¬ ness of the hypothalamic island. It extended from behind the optic chiasma to the mammillary region and 1-2-1-3 mm laterally. The ether stress produced similar adrenocortical responses in intact and hypothalamic deafferentated rats. However, while olfactory stimulation in intact animals produced an adrenocortical discharge equal to that observed after ether stress, the response in rats with hypothalamic islands was reduced by 36-3 % compared with that of the intact animals (
S. FELDMAN
AND
N. CONFORTI
Department ofNeurology, Hadassah University Hospital, Jerusalem, Israel
(Received 27 October 1975) There exists both anatomical and electrophysiological evidence that olfactory pathways project to the hypothalamus (Scott & Pfaffmann, 1967; Scott & Chafin, 1975). Hypothalamic island preparations were used to differentiate between 'systemic' stresses which produced normal adrenocortical responses and 'neurogenic' stresses which caused a reduced adrenal discharge (Feldman, Conforti, Chowers & Davidson, 1970; Feldman, Conforti & Chowers, 1975). This paper describes the role of the hypothalamic neural connexions in the mediation of the adrenocortical response following olfactory stimulation. Experiments were performed on male albino rats of the Hebrew University strain weighing approximately 250 g. Adrenocortical responses to ether stress and to olfactory stimulation, as determined by changes in plasma corticosterone levels (Click, von Redlich & Levine, 1964), were studied in 33 intact animals and in 33 rats with hypothalamic islands (Halasz & Pupp, 1965). The protocol consisted of submitting intact rats to olfactory stimulation, and hypo¬ thalamic deafferentation was performed after 1 week only in those animals which showed an adequate adrenocortical response. Ten to fourteen days later the animals were exposed to ether stress and 1 week after this, those rats which showed a normal response were submitted to a repeated olfactory stimulation. This stimulus consisted of placing rats, anaesthetized 15 min earlier with pentobarbitone (35 mg/kg, i.p.), in a box into which compressed air was delivered through a bottle containing concentrated amyl acetate, at a rate of 8 litres/min, for a period of 30min. Blood was then withdrawn from ajugularvein for corticosterone determina¬ tion, when the animals were still asleep. The ether stress consisted of exposing the animals to ether vapour for 2 min. Fifteen minutes later a skin incision was made under ether anaesthesia and a blood sample removed for corticosterone determination. The stressing stimuli were applied between 08.00 and 12.00h. The basal corticosterone levels 15 min after pento¬ barbitone administration were determined in intact and deafferentated rats. All data were analysed by Student's f-test. The brains were examined h istologie ally to confirm the complete¬ ness of the hypothalamic island. It extended from behind the optic chiasma to the mammillary region and 1-2-1-3 mm laterally. The ether stress produced similar adrenocortical responses in intact and hypothalamic deafferentated rats. However, while olfactory stimulation in intact animals produced an adrenocortical discharge equal to that observed after ether stress, the response in rats with hypothalamic islands was reduced by 36-3 % compared with that of the intact animals (
