Search

1. Neurons in the amygdala are implicated in mediating hedonic appreciation, emotional expression, and conditioning, particularly as these relate to feeding. The amygdala receives projections from the primary taste cortex in monkeys, offering a route by which it could gain access to the gustatory information required to guide feeding behavior. We recorded the activity of 35 neurons in the amygdala of alert rhesus macaques in response to a range of gustatory intensities and qualities to characterize taste-evoked activity in this area. 2. The stimulus array comprised 26 chemicals, including four concentrations of each of the four basic taste stimuli, a series of other sugars, salts, and acids, monosodium glutamate, and orange juice. 3. Neurons responsive to taste stimulation could be found in a 76-mm3 region of the amygdala, centered 9.1 mm lateral to the midline, 14.9 mm anterior to the interaural line, and 25.7 mm below the surface of the dura. They composed 7.2% (35/484) of the cells tested for gustatory sensitivity in the amygdala. 4. The mean spontaneous activity of taste cells was 8.2 +/- 2.3 (SE) spikes per second. This rather high level provided an opportunity for reductions from spontaneous rate that was used regularly in the amygdala. When these negative response rates were included, the mean breadth-of-tuning coefficient of this sample of taste cells was 0.82. There was no strong evidence for gustatory neuron types, nor were functionally similar cells located together in a chemotopic arrangement. 5. Responses across 1.5 log units of stimulus concentration were nearly flat, with increasing excitation in some neurons largely offset by increasing inhibition in others. Taking the absolute value of the evoked activity, concentration-response functions rose monotonically to all basic stimuli except HCl, but were not sufficiently steep to account for human psychophysical data. The neural response to HCl did not rise with stimulus concentration within the range used. 6. Neural patterns representing the taste qualities of the basic stimuli were less sharply separated in the amygdala than at lower-order gustatory relays. Glucose elicited activity patterns that were most distinct from those of the nonsweet chemicals; those associated with NaCl were next most distinct. There was no clear separation between the patterns generated by chemicals that humans describe as sour and bitter. Monosodium glutamate evoked responses that did not correlate well with those of any basic stimulus, implying that its quality cannot be subsumed under the four basic tastes.(ABSTRACT TRUNCATED AT 400 WORDS)

On the basis of their responsiveness to electrophoretically applied glucose, neurons in the lateral hypothalamic area (LHA) have been characterized as either glucose sensitive or glucose nonsensitive. Glucose-sensitive neurons are important in feeding control (4, 36-38, 44, 54). The aim of this study was to increase understanding of the neurophysiological mechanisms involved in the disturbance of feeding by pain. Radiant heating of the scrotum, strong tail pinch, and immersion of the tail in hot water were used as noxious stimuli. In order to correlate the responses of LHA neurons to noxious inputs with possible local release of endogenous opiates, effects of electrophoretically applied morphine and naloxone were also tested. The effects of glucose, morphine, and noxious stimulation were studied in a total of 165 neurons recorded from 75 adult male urethane-chloralose-anesthetized rats. Of 52 neurons determined to be glucose sensitive, 36 (69%) were inhibited by both noxious stimulation and morphine. A majority of the glucose-nonsensitive neurons did not respond to either morphine or noxious stimulation (87/113, 74%). The relation of glucose sensitivity to inhibition by pain and/or morphine was statistically significant (Fisher's exact probability test, P less than 0.01). Naloxone attenuated the inhibitory effects of both pain and morphine, thus suggesting mediation of both by the same neuronal mechanism. From this evidence we conclude that LHA glucose-sensitive neurons are involved in the suppression of feeding by noxious stimulation.

1. The aim of this study was investigation of neuronal mechanisms underlying inputs from the fastigial nucleus (FN) to the lateral hypothalamic area (LHA). 2. In male anesthetized rats, 295 extracellular and 82 intracellular recordings of LHA responses to electrical stimulation of the FN, which elicited stimulus-locked pressor responses, were examined. 3. Contralateral FN stimulation evoked three types of responses in 48% of spontaneously firing LHA neurons: inhibition with 11 +/- 6 (SD) ms latency followed by excitation (30%), excitation with 15 +/- 12.5 ms latency (14%), and excitation followed by inhibition with 6 +/- 4 ms latency (4%). 4. Contralateral FN stimulation after transection of the inferior cerebellar peduncle (ICP), which resulted in a substantial fall of the fastigial pressor response, also evoked the three types of responses. These responses were unaffected by transection of the ICP. 5. Neuronal activity was recorded intracellularly from 82 LHA neurons, of which 36 (44%) responded to FN stimulation. Of the 36 neurons, 24 showed inhibitory postsynaptic potentials (IPSPs) with a mean latency of 7.5 +/- 2 ms. Of the 24 neurons, 16 were checked for change in IPSP latency with stimulus intensity, and 11 were considered to be monosynaptically connected since their latencies were constant when FN stimulation intensity was changed. The remaining 12 exhibited excitatory postsynaptic potentials (EPSPs) with a longer latency of 10.5 +/- 3 ms, which indicated polysynaptic conduction. The reversal potentials of the IPSP and EPSP were estimated to be about -77 mV and -13 mV, respectively. 6. Most glucose-sensitive neurons (78%), which were identified by their inhibition in response to electrophoretically applied glucose, were inhibited by FN stimulation, whereas only 7% of the glucose-insensitive neurons responded to such stimulation. 7. From the results, it was concluded that LHA neurons receive inhibitory monosynaptic and excitatory polysynaptic inputs from the FN via the superior cerebellar peduncle. These connections may contribute to hypothalamic modulation of feeding behavior.

Neuronal activity was studied in the behaving active monkey to elucidate the functional significance of catecholamines (CA) in the amygdala during reward-related behavior, and the effects of noradrenaline (NA), dopamine (DA), and their antagonists, electrophoretically applied, were examined using multibarreled electrode techniques. The operant food intake task had four phases: 1) cue light on to signal the start of bar pressing, 2) execution of high fixed-ratio bar pressing (FR 20), 3) short cue tone triggered by the last bar press to signal the presentation of food, and 4) ingestion, reward. More than half of the 292 cells tested (198, 68%) changed activity during the task. Most changes occurred during the bar press and/or reward periods (164/198, 83%), the former affecting neuronal activity more (127/198, 64%) than the latter (70/198, 35%). Phasic responses to the cue light and cue tone were observed in 62 cells (31%) and 19 cells (10%), respectively. The effects of NA and DA were studied in 199 and 177 cells, respectively. Of these, 90 cells (46%) responded to NA, 87 (97%) with a decrease of firing, and only 3 (3%) with an increase, whereas 40 (26%) responded to DA by increasing (28 cells, 70%) or decreasing (18 cells, 30%) activity. The inhibitory effect of NA was blocked by alpha- and/or beta-adrenoceptive antagonists. Task-related activity changes occurred significantly more often among DA sensitive cells than among DA insensitive cells. CA sensitivity and task-related neuronal activity were functionally correlated only in the reward period. Activity of NA sensitive cells decreased in this period more frequently than insensitive cells, and DA sensitive cells increased more often than insensitive cells. Application of a beta-adrenoceptive antagonist or a DA antagonist attenuated the activity changes during the reward period. Application of a alpha-adrenoceptive antagonist had no effect on the reward-related neuronal activity changes. When grouped according to recording site, centromedial cells had a significantly higher occurrence of task-related activity changes than those in the basolateral parts of the amygdala. The bar-press responsive and reward-related cells, the firing of which decreased, were found more often in the centromedial than in the basolateral division, although the numbers of cells that responded to sensory cues were not different in the two parts. Catecholaminergic involvement in the task-related activity changes was also different.(ABSTRACT TRUNCATED AT 400 WORDS)

1. The effects of dorsal raphe (DR) stimulation on neural activity in the rat lateral hypothalamic area (LHA), including specific glucose-sensitive neurons, were investigated by extracellular and intracellular recording in vivo, and the neurotransmitters involved were determined. 2. In 67 adult male anesthetized rats, 287 extracellular and 49 intracellular recordings of LHA responses to electrical stimulation of the DR were examined. 3. To determine neurotransmitter candidates, the effects of serotonin and the serotonin antagonists methysergide, lisuride, and (-)-propranolol were investigated by systemic administration and microelectrophoresis. 4. Of 287 spontaneously firing LHA neurons tested by DR stimulation, 157 (55%) were inhibited. Among these, 51% were glucose sensitive. The serotonin 1 receptor antagonists, lisuride and (-)-propranolol, attenuated the inhibitory responses to both DR stimulation and electrophoretic serotonin application. 5. Seventy-three (25%) were excited by DR stimulation, and 71% of these were glucose insensitive. Methysergide attenuated the excitatory responses to DR stimulation and the inhibitory response to electrophoretic serotonin application, but (-)-propranolol did not attenuate the excitation. 6. Intracellular recordings of LHA neurons during DR stimulation showed monosynaptic excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs) with 3.8 and 3.0 ms latency, respectively. The reversal potential for the former was approximately -17 and for the latter, -94 mV. 7. From the results we concluded that 75% of LHA glucose-sensitive neurons receive inhibitory serotonin inputs from the DR through serotonin 1 receptors, and 20% of glucose-insensitive neurons receive excitatory inputs from the DR through serotonin 2 receptors though 41% of these receive inhibitory inputs through serotonin 1 receptor.