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Response of the lateral hypothalamic neurons to preoptic thermal stimulation in rats
Neuroscience Letters, 22 (1981) 257-262
257
© Elsevier/North-Holland Scientific Publishers Ltd.
RESPONSE OF THE LATERAL HYPOTHALAMIC NEURONS TO PREOPTIC THERMAL STIMULATION IN RATS
KOHJI YAMAMOTO, TERUO NAKAYAMA* and YOUZOU ISHIKAWA
Department of Physiology, Osaka University Medical School, Nakanoshima, Kita-ku, Osaka 530 (Japan) (Received December 18th, 1980; Accepted December 27th, 1980)
The effects of iontophoretic application of glucose and Na and responses to preoptic thermal stimulation were observed on lateral hypothalamic neurons in rats. Twenty-two neurons out of 54 were inhibited by glucose but not by Na. Twelve neurons out of 22 were facilitated by preoptic cooling, 4 were facilitated by warming and 6 were not influenced. Out of 17 neurons which did not respond to glucose and Na, 12 were not influenced by thermal stimulation. The main result is that neurons inhibited by glucose in the feeding center are facilitated by a fall in preoptic temperature.
Accumulated evidence has indicated the relationship between temperature and food intake, i.e. food consumption rises in cold environments and falls below normal levels in hot environments. According to the thermostat theory proposed by Brobeck [4], a decrease in body temperature would activate the feeding center in the lateral hypothalamus and depress the satiety center in the ventromedial hypothalamus. The opposite result is caused by increased body temperature. An emphasis was put on the specific dynamic action of food which increases heat production and leads to satiety. The theory was supported by Andersson and Larsson [3] who showed that local cooling of the preoptic area (PO) and rostral hypothalamus induced eating in the fed goat, while warming the same brain area inhibited eating in the hungry animal. Neuronal activities of the satiety center and the feeding center, however, were not influenced directly by changes in local brain temperature [1]. These results suggest the possibility that the thermosensitive neurons located in PO [5] may influence the hypothalamic structures involved in the control of food intake. In this study, responses to glucose and to preoptic thermal stimulation were observed on single neuron activities of the lateral hypothalamus in rats. Male Wistar rats weighing 230-400 g were used under anesthesia of 0.8 g/kg urethane and 60 mg/kg chloralose injected intraperitoneally. Subsequent maintenance doses were injected if necessary. The rats were mounted stereotaxically *To whom correspondence should be addressed.
258 with the heads fixed according to the Pellegrino and Cushman coordinate system. A stainless steel tube (o.d. 0.9 mm) was implanted in the right half of the brain at a location 2.0 m m lateral (L) to the midline, 8.0 m m anterior (A) and inserted to a depth (H) of - 3 . 0 m m from the stereotaxic zero point, as a water perfusing thermode for conductive warming or cooling of the brain tissue. Three-barrelled glass micropipettes glued to a recording electrode were used as previously described by O o m u r a et al. [7]. Each barrel was filled with one of the following materials: 2 M monosodium-L-glutamate (pH 8.0), 1 M glucose (in 0.9% sodium chloride) and 0.9% sodium chloride. The recording microelectrode was filled with 2% Pontamine sky blue with 0.5 M sodium acetate. The DC resistances of the pipettes ranged from 50 to 150 Mfl, and those of the recording electrodes were 10-30 Mfl. A direct electric current of the order of nA flowing through the pipette caused electrophoretic application of ionized chemicals (glutamate- and Na +) or electro-osmotic application of non-ionized chemicals (glucose). The temperature o f the left preoptic area was estimated indirectly by a thermocouple placed at A: 8.0 m m , L: 5.0 m m and H: - 3.0 m m . In our preliminary experiment we observed that thermocouples placed 3.0 m m to the right and left of the thermode always gave the same temperature. The brain temperature was altered by thermal stimulation not only in the preoptic area but also in the lateral hypothalamus, but to a lesser extent. The temperature change in the lateral hypothalamus (A: 6.0 mm, L: 2.0 m m and H: - 2 . 0 mm) was 0.4°C when the preoptic temperature was changed 1.0°C. Usual experimental procedures were as follows. When a unit discharge was obtained, the response to glutamate was examined in a sense to check the whole experimental apparatus, including the neuron subjected, the iontophoretic pipette and the recording electrode. Neurons facilitated by glutamate were used for further studies to see the responses to glucose and Na. Subsequently, preoptic temperature was changed between 32 and 43°C to observe the thermal response of the neuron. Rectal temperature was monitored by a thermistor-thermometer and maintained at 37-38.5°C by intermittent radiation of an infra-red lamp. All experiments were performed at a room temperature of 23-27°C. In order to verify electrode positions, the Pontamine sky blue marking technique was used. With the tip as a cathode, currents of 2 - 1 0 ~A were passed for 2 - 6 min. Following each experiment, the rat was perfused with saline, followed by 10% formalin. Frozen sections of the brain were cut at 50 ~m to confirm placement of the electrode. The present findings are based on the observation of 54 lateral hypothalamic neurons, of which 22 decreased discharge frequency in response to glucose, 13 were inhibited by Na, 2 were facilitated by Na and 17 were not influenced either by glucose or by Na (Table I). In 12 neurons out of 22 inhibited by glucose, the firing rates were decreased by a rise in preoptic temperature. One of these responses is shown in Fig. 1A. The application of glucose with + 2 0 nA decreased the discharge rates from 13
259
TABLE I RESPONSES OF LATERAL H Y P O T H A L A M I C NEURONS IN RATS Neuronal response to glucose and Na
Response to preoptic thermal stimulation
Total
Facilitated by warming
Facilitated by cooling
No response
No. inhibited by glucose No. inhibited by glucose and Na No. facilitated by Na No response
4 2 1 2
12 4 0 3
6 7 1 12
22 13 2 17
Total
9
19
26
54
Control
A_l+,J
Jt
JJ.
I L
[J t t J , , l l
l i p ' frl~ i[
_O_ Control
.2~t 1_1/ I i
i
irlrr ',+T
Glu"l-20nAr T • - ':" ;
(41%) (24%) (4%) (31%)
A
,
IlJt.ll
Jl ] , ] i t '
[l',llJ:l I[•[ lr j i l l o
Na+20nA
Contro,
o
'--LJ'j'~ J ' ~ J L ± l J I l , ~ l , J
[
ITIll I i r i]ii!iJl[i:
,-
35.5"(:;
I1,tltT[IF]I II
,t, I t I I J itlhil
,I ~ I J
T[i[[ []T[III[I[;i :11
rrll I L ]J
I]11
I.-39,9"(:; i
Glu +20
Na +20
1 sec
i
B
~1o o c~
f
-I E
~ 40
Tpo
35 Fig. 1. Response of a lateral hypothalamic neuron in rat to iontophoretic application of glucose (Glu) and Na with + 20 nA and to preoptic temperature (Tpo).
impulses/sec to 4 within 3 sec. The inhibitory effect persisted for 4 sec after termination of the iontophoretic current. The control discharge frequency was not changed by application of Na. The lower 2 traces show the effect of preoptic temperature. The discharge rates were 17 and 6 impulses/sec when the preoptic temperature was 35.5 and 39.9°C, respectively. Fig. 1B shows the ink-writer recording o f the discharge rate o f another neuron which showed the same type of responses. The application of glucose with + 2 0 nA produced a decrease in the
260 discharge frequency with a latency of 2 sec. The application of Na with + 20 nA produced no change. Subsequently, the preoptic temperature was changed. The discharge rates were decreased to 2 impulses/sec by preoptic warming to 39.7°C, were increased to 6 impulses/sec by cooling to 34.8°C and were decreased again by warming. Four neurons out o f 22 responded to increased preoptic temperature with increased firing rates. In one neuron, the spontaneous activity was 2 impulses/sec at a preoptic temperature of 35.8°C. The application of glucose with +25 nA produced complete suppression of activity with a latency o f 3 sec. Full recovery took place 6 sec after current termination. The application o f Na had no effect. Six neurons out of 22 did not respond to changes in preoptic temperature. In one of these neurons, the application o f glutamate with - 10 nA produced an increase of activity with a latency of 1 sec. The discharge frequency was decreased by the application o f glucose with + 20 nA within 3 sec. The application of Na had no effect. The discharge rate was not influenced by changes in preoptic temperature between 34.8 and 39.9°C. Thirteen neurons out of 54 were inhibited both by glucose and Na to a same extent, so that the inhibitory effects were attributed to the action of Na of the solvent. In 2 neurons out of 13 inhibited by Na, the firing rates were increased by a rise in preoptic temperature. Four neurons out o f 13 responded to decreased preoptic temperature with increased firing rates. Seven neurons out of 13 did not respond to changes in preoptic temperature. Two neurons were facilitated by Na. One of them was facilitated by glucose and by preoptic warming, while the other did not respond either to glucose or to thermal stimulation. Out of 17 neurons which did not respond to glucose and Na, 2 neurons increased their firing rates by a rise in preoptic temperature. Three neurons responded to increased preoptic temperature with decreased firing rates and the rest did not respond to changes in preoptic temperature. The lateral hypothalamic neurons inhibited by glucose are most likely to be involved in an activation of feeding behavior [7]. The present study indicated that the spontaneous activities of lateral hypothalamic neurons are influenced by PO thermal stimulation. The most frequent observation was that the neurons inhibited by glucose were facilitated by PO cooling. Changes in brain temperature are detected by the thermosensitive neurons in the P O A H and then the temperature information seems to be conveyed to the lateral hypothalamus. It is not clear whether the facilitation of glucose inhibitory neurons in the lateral hypothalamus is brought about by decreased activities of warm-sensitive neurons a n d / o r by increased activities of cold-sensitive neurons in the P O A H . In our preliminary experiment, thermal stimulation which caused a 1 °C change in P O A H produced 0.4°C change in the lateral hypothalamus. According to Anand et al. [1], the lateral hypothalamic neurons were not influenced by local temperature.
261
From these observations, it is less likely that the glucose inhibitory neurons themselves are directly influenced by brain temperature. The fact that the activities o f glucose inhibitory neurons are facilitated by PO cooling supports Brobeck's 'thermostatic theory' [4]. Spector et al. [8] reported that the effect of PO thermal stimulation on food intake was variable according to the environmental temperature. The firing rate o f PO thermosensitive neurons is not only controlled by local brain temperature, but also modified by peripheral thermal afferents [6]. Thus the various temperature signals of the living body are integrated in the PO, which in turn may influence food intake even when the PO temperature is unchanged. Neurons inhibited by injection of hypertonic NaC1 were found in the ventromedial nuclei but not in the lateral hypothalamus [9]. O o m u r a et al. [7] reported that 3~/0 o f neurons tested in the lateral hypothalamus were inhibited by Na applied by iontophoretic current. In the present study, 13 out of 54 tested in the lateral hypothalamus were inhibited both by glucose and by Na. At present, there is no explanation for the difference of the results mentioned above and it is not known whether neurons are sensitive to osmotic pressure or to concentration of Na. Neurons facilitated by Na are regarded to detect osmotic pressure and participate in drinking behavior. O o m u r a showed that 20°/o of the lateral hypothalamic neurons were facilitated by Na [7]. In this study only 2 neurons out of 54 were facilitated by Na. As PO heating increased water intake in goats [2], it is suspected that the neurons facilitated by Na might receive afferents from the PO thermo-sensitive neurons. This will be the subject for future studies. The function of 17 neurons which were not influenced either by glucose or by Na is not clear. Our results indicate that 12 neurons o f this type did not respond to thermal stimulation. It can be said that few thermal signals are conducted to the non-responsive neurons of the lateral hypothalamus. The effects of PO thermal stimulation on neurons o f the ventromedial nuclei will be expected to throw more light on the functional relation between temperature and food intake. Experiments on this line are now under way in our laboratory.
1 Anand, B.K., Banerjee, M.G. and Chhina, G.S., Single neurone activity of hypothalamic feeding centres: effect of local heating, Brain Res., 1 (1966) 269-278. 2 Andersson, B., Gale, C.C. and Sundsten, J.W., Preoptic influences on water intake. In M.J. Wayner (Ed.), Thirst, Pergamon Press, Oxford, 1964, pp. 361-379. 3 Andersson, B. and Larsson, B., Influence of local temperature changes in the preoptic area and rostral hypothalamus on the regulation of food and water intake, Acta physiol, scand., 52 (1961) 75-89. 4 Brobeck, J.R., Food intake as a mechanism of temperature regulation, Yale J. Biol. Med., 20 (1948) 545-552. 5 Nakayama, T., Hammel, H.T., Hardy, J.D. and Eisenman, J.S., Thermal stimulation of electrical activity of single units of the preoptic region, Amer. J. Physiol., 204 (1963) 1122-1126.
262 6 7 8 9
Nakayama, T., lshikawa, Y. and Tsurutani, T., Projection of scrotal thermal afferents to lhe preoptic and hypothalamic neurons in rats, Pflfigers Arch., 380 (1979) 59 64. Oomura, Y., Ono, T., Ooyama, H. and Wayner, M.J., Glucose and osmosensitive neurones of the rat hypothalamus, Nature (Lond.), 222 (1969) 282-284. Spector, N.H., Brobeck, J.R. and Hamilton, C.L., Feeding and core temperature in albino rats: Changes induced by preoptic heating and cooling, Science, 161 (1968) 286 288. Wayner, M.J. and Kahan, S.A., Central pathways involved during the salt arousal of drinking, Ann. N.Y. Acad. Sci., 157 (1969) 701 722.
257
© Elsevier/North-Holland Scientific Publishers Ltd.
RESPONSE OF THE LATERAL HYPOTHALAMIC NEURONS TO PREOPTIC THERMAL STIMULATION IN RATS
KOHJI YAMAMOTO, TERUO NAKAYAMA* and YOUZOU ISHIKAWA
Department of Physiology, Osaka University Medical School, Nakanoshima, Kita-ku, Osaka 530 (Japan) (Received December 18th, 1980; Accepted December 27th, 1980)
The effects of iontophoretic application of glucose and Na and responses to preoptic thermal stimulation were observed on lateral hypothalamic neurons in rats. Twenty-two neurons out of 54 were inhibited by glucose but not by Na. Twelve neurons out of 22 were facilitated by preoptic cooling, 4 were facilitated by warming and 6 were not influenced. Out of 17 neurons which did not respond to glucose and Na, 12 were not influenced by thermal stimulation. The main result is that neurons inhibited by glucose in the feeding center are facilitated by a fall in preoptic temperature.
Accumulated evidence has indicated the relationship between temperature and food intake, i.e. food consumption rises in cold environments and falls below normal levels in hot environments. According to the thermostat theory proposed by Brobeck [4], a decrease in body temperature would activate the feeding center in the lateral hypothalamus and depress the satiety center in the ventromedial hypothalamus. The opposite result is caused by increased body temperature. An emphasis was put on the specific dynamic action of food which increases heat production and leads to satiety. The theory was supported by Andersson and Larsson [3] who showed that local cooling of the preoptic area (PO) and rostral hypothalamus induced eating in the fed goat, while warming the same brain area inhibited eating in the hungry animal. Neuronal activities of the satiety center and the feeding center, however, were not influenced directly by changes in local brain temperature [1]. These results suggest the possibility that the thermosensitive neurons located in PO [5] may influence the hypothalamic structures involved in the control of food intake. In this study, responses to glucose and to preoptic thermal stimulation were observed on single neuron activities of the lateral hypothalamus in rats. Male Wistar rats weighing 230-400 g were used under anesthesia of 0.8 g/kg urethane and 60 mg/kg chloralose injected intraperitoneally. Subsequent maintenance doses were injected if necessary. The rats were mounted stereotaxically *To whom correspondence should be addressed.
258 with the heads fixed according to the Pellegrino and Cushman coordinate system. A stainless steel tube (o.d. 0.9 mm) was implanted in the right half of the brain at a location 2.0 m m lateral (L) to the midline, 8.0 m m anterior (A) and inserted to a depth (H) of - 3 . 0 m m from the stereotaxic zero point, as a water perfusing thermode for conductive warming or cooling of the brain tissue. Three-barrelled glass micropipettes glued to a recording electrode were used as previously described by O o m u r a et al. [7]. Each barrel was filled with one of the following materials: 2 M monosodium-L-glutamate (pH 8.0), 1 M glucose (in 0.9% sodium chloride) and 0.9% sodium chloride. The recording microelectrode was filled with 2% Pontamine sky blue with 0.5 M sodium acetate. The DC resistances of the pipettes ranged from 50 to 150 Mfl, and those of the recording electrodes were 10-30 Mfl. A direct electric current of the order of nA flowing through the pipette caused electrophoretic application of ionized chemicals (glutamate- and Na +) or electro-osmotic application of non-ionized chemicals (glucose). The temperature o f the left preoptic area was estimated indirectly by a thermocouple placed at A: 8.0 m m , L: 5.0 m m and H: - 3.0 m m . In our preliminary experiment we observed that thermocouples placed 3.0 m m to the right and left of the thermode always gave the same temperature. The brain temperature was altered by thermal stimulation not only in the preoptic area but also in the lateral hypothalamus, but to a lesser extent. The temperature change in the lateral hypothalamus (A: 6.0 mm, L: 2.0 m m and H: - 2 . 0 mm) was 0.4°C when the preoptic temperature was changed 1.0°C. Usual experimental procedures were as follows. When a unit discharge was obtained, the response to glutamate was examined in a sense to check the whole experimental apparatus, including the neuron subjected, the iontophoretic pipette and the recording electrode. Neurons facilitated by glutamate were used for further studies to see the responses to glucose and Na. Subsequently, preoptic temperature was changed between 32 and 43°C to observe the thermal response of the neuron. Rectal temperature was monitored by a thermistor-thermometer and maintained at 37-38.5°C by intermittent radiation of an infra-red lamp. All experiments were performed at a room temperature of 23-27°C. In order to verify electrode positions, the Pontamine sky blue marking technique was used. With the tip as a cathode, currents of 2 - 1 0 ~A were passed for 2 - 6 min. Following each experiment, the rat was perfused with saline, followed by 10% formalin. Frozen sections of the brain were cut at 50 ~m to confirm placement of the electrode. The present findings are based on the observation of 54 lateral hypothalamic neurons, of which 22 decreased discharge frequency in response to glucose, 13 were inhibited by Na, 2 were facilitated by Na and 17 were not influenced either by glucose or by Na (Table I). In 12 neurons out of 22 inhibited by glucose, the firing rates were decreased by a rise in preoptic temperature. One of these responses is shown in Fig. 1A. The application of glucose with + 2 0 nA decreased the discharge rates from 13
259
TABLE I RESPONSES OF LATERAL H Y P O T H A L A M I C NEURONS IN RATS Neuronal response to glucose and Na
Response to preoptic thermal stimulation
Total
Facilitated by warming
Facilitated by cooling
No response
No. inhibited by glucose No. inhibited by glucose and Na No. facilitated by Na No response
4 2 1 2
12 4 0 3
6 7 1 12
22 13 2 17
Total
9
19
26
54
Control
A_l+,J
Jt
JJ.
I L
[J t t J , , l l
l i p ' frl~ i[
_O_ Control
.2~t 1_1/ I i
i
irlrr ',+T
Glu"l-20nAr T • - ':" ;
(41%) (24%) (4%) (31%)
A
,
IlJt.ll
Jl ] , ] i t '
[l',llJ:l I[•[ lr j i l l o
Na+20nA
Contro,
o
'--LJ'j'~ J ' ~ J L ± l J I l , ~ l , J
[
ITIll I i r i]ii!iJl[i:
,-
35.5"(:;
I1,tltT[IF]I II
,t, I t I I J itlhil
,I ~ I J
T[i[[ []T[III[I[;i :11
rrll I L ]J
I]11
I.-39,9"(:; i
Glu +20
Na +20
1 sec
i
B
~1o o c~
f
-I E
~ 40
Tpo
35 Fig. 1. Response of a lateral hypothalamic neuron in rat to iontophoretic application of glucose (Glu) and Na with + 20 nA and to preoptic temperature (Tpo).
impulses/sec to 4 within 3 sec. The inhibitory effect persisted for 4 sec after termination of the iontophoretic current. The control discharge frequency was not changed by application of Na. The lower 2 traces show the effect of preoptic temperature. The discharge rates were 17 and 6 impulses/sec when the preoptic temperature was 35.5 and 39.9°C, respectively. Fig. 1B shows the ink-writer recording o f the discharge rate o f another neuron which showed the same type of responses. The application of glucose with + 2 0 nA produced a decrease in the
260 discharge frequency with a latency of 2 sec. The application of Na with + 20 nA produced no change. Subsequently, the preoptic temperature was changed. The discharge rates were decreased to 2 impulses/sec by preoptic warming to 39.7°C, were increased to 6 impulses/sec by cooling to 34.8°C and were decreased again by warming. Four neurons out o f 22 responded to increased preoptic temperature with increased firing rates. In one neuron, the spontaneous activity was 2 impulses/sec at a preoptic temperature of 35.8°C. The application of glucose with +25 nA produced complete suppression of activity with a latency o f 3 sec. Full recovery took place 6 sec after current termination. The application o f Na had no effect. Six neurons out of 22 did not respond to changes in preoptic temperature. In one of these neurons, the application o f glutamate with - 10 nA produced an increase of activity with a latency of 1 sec. The discharge frequency was decreased by the application o f glucose with + 20 nA within 3 sec. The application of Na had no effect. The discharge rate was not influenced by changes in preoptic temperature between 34.8 and 39.9°C. Thirteen neurons out of 54 were inhibited both by glucose and Na to a same extent, so that the inhibitory effects were attributed to the action of Na of the solvent. In 2 neurons out of 13 inhibited by Na, the firing rates were increased by a rise in preoptic temperature. Four neurons out o f 13 responded to decreased preoptic temperature with increased firing rates. Seven neurons out of 13 did not respond to changes in preoptic temperature. Two neurons were facilitated by Na. One of them was facilitated by glucose and by preoptic warming, while the other did not respond either to glucose or to thermal stimulation. Out of 17 neurons which did not respond to glucose and Na, 2 neurons increased their firing rates by a rise in preoptic temperature. Three neurons responded to increased preoptic temperature with decreased firing rates and the rest did not respond to changes in preoptic temperature. The lateral hypothalamic neurons inhibited by glucose are most likely to be involved in an activation of feeding behavior [7]. The present study indicated that the spontaneous activities of lateral hypothalamic neurons are influenced by PO thermal stimulation. The most frequent observation was that the neurons inhibited by glucose were facilitated by PO cooling. Changes in brain temperature are detected by the thermosensitive neurons in the P O A H and then the temperature information seems to be conveyed to the lateral hypothalamus. It is not clear whether the facilitation of glucose inhibitory neurons in the lateral hypothalamus is brought about by decreased activities of warm-sensitive neurons a n d / o r by increased activities of cold-sensitive neurons in the P O A H . In our preliminary experiment, thermal stimulation which caused a 1 °C change in P O A H produced 0.4°C change in the lateral hypothalamus. According to Anand et al. [1], the lateral hypothalamic neurons were not influenced by local temperature.
261
From these observations, it is less likely that the glucose inhibitory neurons themselves are directly influenced by brain temperature. The fact that the activities o f glucose inhibitory neurons are facilitated by PO cooling supports Brobeck's 'thermostatic theory' [4]. Spector et al. [8] reported that the effect of PO thermal stimulation on food intake was variable according to the environmental temperature. The firing rate o f PO thermosensitive neurons is not only controlled by local brain temperature, but also modified by peripheral thermal afferents [6]. Thus the various temperature signals of the living body are integrated in the PO, which in turn may influence food intake even when the PO temperature is unchanged. Neurons inhibited by injection of hypertonic NaC1 were found in the ventromedial nuclei but not in the lateral hypothalamus [9]. O o m u r a et al. [7] reported that 3~/0 o f neurons tested in the lateral hypothalamus were inhibited by Na applied by iontophoretic current. In the present study, 13 out of 54 tested in the lateral hypothalamus were inhibited both by glucose and by Na. At present, there is no explanation for the difference of the results mentioned above and it is not known whether neurons are sensitive to osmotic pressure or to concentration of Na. Neurons facilitated by Na are regarded to detect osmotic pressure and participate in drinking behavior. O o m u r a showed that 20°/o of the lateral hypothalamic neurons were facilitated by Na [7]. In this study only 2 neurons out of 54 were facilitated by Na. As PO heating increased water intake in goats [2], it is suspected that the neurons facilitated by Na might receive afferents from the PO thermo-sensitive neurons. This will be the subject for future studies. The function of 17 neurons which were not influenced either by glucose or by Na is not clear. Our results indicate that 12 neurons o f this type did not respond to thermal stimulation. It can be said that few thermal signals are conducted to the non-responsive neurons of the lateral hypothalamus. The effects of PO thermal stimulation on neurons o f the ventromedial nuclei will be expected to throw more light on the functional relation between temperature and food intake. Experiments on this line are now under way in our laboratory.
1 Anand, B.K., Banerjee, M.G. and Chhina, G.S., Single neurone activity of hypothalamic feeding centres: effect of local heating, Brain Res., 1 (1966) 269-278. 2 Andersson, B., Gale, C.C. and Sundsten, J.W., Preoptic influences on water intake. In M.J. Wayner (Ed.), Thirst, Pergamon Press, Oxford, 1964, pp. 361-379. 3 Andersson, B. and Larsson, B., Influence of local temperature changes in the preoptic area and rostral hypothalamus on the regulation of food and water intake, Acta physiol, scand., 52 (1961) 75-89. 4 Brobeck, J.R., Food intake as a mechanism of temperature regulation, Yale J. Biol. Med., 20 (1948) 545-552. 5 Nakayama, T., Hammel, H.T., Hardy, J.D. and Eisenman, J.S., Thermal stimulation of electrical activity of single units of the preoptic region, Amer. J. Physiol., 204 (1963) 1122-1126.
262 6 7 8 9
Nakayama, T., lshikawa, Y. and Tsurutani, T., Projection of scrotal thermal afferents to lhe preoptic and hypothalamic neurons in rats, Pflfigers Arch., 380 (1979) 59 64. Oomura, Y., Ono, T., Ooyama, H. and Wayner, M.J., Glucose and osmosensitive neurones of the rat hypothalamus, Nature (Lond.), 222 (1969) 282-284. Spector, N.H., Brobeck, J.R. and Hamilton, C.L., Feeding and core temperature in albino rats: Changes induced by preoptic heating and cooling, Science, 161 (1968) 286 288. Wayner, M.J. and Kahan, S.A., Central pathways involved during the salt arousal of drinking, Ann. N.Y. Acad. Sci., 157 (1969) 701 722.