Physiology & Behavior, Vol. 22, pp. 575--582.PergamonPress and Brain Research Publ., 1979.Printed in the U.S.A.
Effects of Basolateral Amygdaloid Lesions on Schedule Induced and Schedule Dependent Behavior C O S T A S C. L O U L L I S 2 A N D M A T T H E W J. W A Y N E R s
Brain R e s e a r c h Laboratory, Syracuse University, 601 University A v e n u e , Syracuse, N Y 13210 ( R e c e i v e d 12 O c t o b e r 1978) LOULLIS, C. C. AND M. J. WAYNER. Effects of basolateral amygdaloid lesions on schedule induced and schedule dependent behavior. PHYSIOL. BEHAV. 22(3) 575--582, 1979.mRats were reduced to 80% body weight and were exposed to an FI-1 rain food reinforcement schedule for 30 rain daily until lever presses, licks, and water consumption stabilized for at least 10 days. Bilateral lesions were then made in the basolateral amygdala of all animals. Animals were tested for 40 days following the lesions at 80% body weight, were permitted to recover body weight by increasing food rations, and were tested for an additional 15 days under ad lib feeding. Animals were then subjected to the following tests: food consumption following food deprivation, drinking following water deprivation, and salt arousal of drinking. In addition, consumption of 6.85% sucrose, 25% sucrose, 8% glucose, 21% glucose, and 0.125% Na saccharin on a FI-1 rain food reinforcement schedule and under home cage conditions were measured. On the basis of these data and lesion locus the 8 animals were divided into 2 groups, bilaterally symmetrical experimentals and asymmetrical controls. Although no effects were observed in licking, water consumption, and lever pressing, animals with bilateral symmetrical lesions of the basolateral amygdala displayed relatively permanent deficits in their responses to various taste stimuli. The effects of these lesions are evaluated and discussed in terms of the lateral hypothalamic involvement in schedule induced and schedule dependent behavior. Amygdaloid lesions Polydipsia Taste
Schedule dependent behavior Sapid solution intake
IN T H E RAT, the ventral amygdalofugal pathway does not appear to arise from the amygdala but from the periamygdaloid cortex. The stria terminalis (ST) arises from all of the amygdaloid nuclei . These two pathways provide most of the efferent and afferent connections between the hypothalamus and the amygdala [8, 14, 19, 31]. The involvement of the medial forebrain bundle (MFB) in these interconnections is well established in terms of both the ST and ventral arnygdalofugal pathways [8, 19, 31]. It has also been suggested  that the ventral amygdalofugal pathway "is essentially a laterally directed extension of the MFB and that the ST should be considered a dorsal component of this bundle which has become separated from the main part of the MFB by the development of the internal capsule." In addition to these afferent and efferent pathways to and from the hypothalamus and other structures, there appears to be a network of intra-amygdaloid interconnections between the different nuclei of the amygdala and very likely the periamygdaloid cortex [8,31]. There is considerable evidence that the amygdala modulates hypothalamic activity . For example, stimulation of the basolaterai amygdala inhibits spontaneous firing of rat
Schedule induced behavior
lateral hypothalamic (LH) neurons [26, 28, 43] and acetylcholine might be the inhibitory neurotransmitter involved . Single unit activity is altered in the anterior hypothalamus, ventromedial hypothalamic nucleus (VMH), and midbrain reticular formation following stimulation in the area of the basolateral amygdala . Amygdala stimulation also affects neural activity in the midbrain reticular formation. These data suggest a close relationship between the amygdala and the limbic forebrain and limbic midbrain system  which has important motor control functions in the production of ingestive behavior [39, 40, 41]. Results of stimulation and lesion experiments further support the close interaction of the amygdala and hypothalamus and their involvement in the production of ingestive behavior [10,12]. Bilateral electrical stimulation of the amygdala was shown to suppress food intake in deprived rats. Destruction of the VMH and severing of the ST prevented this suppression of eating . These data suggest that the amygdala exerts its effect via the ST and VMH to suppress activity in the LH which results in a reduction in food intake. Data from another study, where both the amygdala and the VMH were destroyed in the same animal, pro-
~This research was supported in part by NSF Grant No. BNS 76--18520. 2Present address: Department of Psychiatry, The Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, IN 46223. aSend reprint requests to Dr. M. J. Wayner, Brain Research Laboratory, Syracuse University, 601 University Avenue, Syracuse, NY 13210.
C o p y r i g h t © 1979 Brain R e s e a r c h Publications Inc.--0031-9384/79/030575-08502.00/0
L O U L L I S AND W A Y N E R
vide additional support for these effects . Lesions in the ventral amygdala produce increases in food and water intake in rats [12,13]. Larger and more posterior lesions produce more pronounced and long lasting increases. These results have been confirmed in other studies [3,6]. Hypophagia  or aphagia and adipsia have also been reported in rats with lesions in the dorsal aspect of the central amygdaloid nucleus  and the corticomedial nucleus [30, 32, 33]. Carbachoi stimulation of the amygdala indicates that the cortical amygdaloid nucleus has a modulatory influence on drinking behavior which is dependent on the level of activity in the L H . These data were in support of earlier observations  in which norepinephrine was injected into the ventral amygdala. It appears that the amygdaloid complex and, very likely, the peri-amygdaloid cortex exert both excitatory and inhibitory influences on ingestive behavior . In general, it seems that the facilitating influences originate primarily in the dorsal, anterior, and medial aspects of the amygdala; whereas, inhibitory influences arise largely from the ventral, posterior, and lateral regions. Such an explanation would be consistent with both facilitory and inhibitory effects on ingestive behavior which might explain reports where effects were not obtained , since destruction of both mechanisms would lead to essentially no effect. Such a hypothesis is further supported by the fact that the influences of the amygdala on ingestive behavior are largely indirect and via other structures such as the hypothalamus, hippocampus , and septum . Cells in the amygdala are responsive to stimulation of different sense modalities [10, 19, 25]. It has been demonstrated that amygdala lesions in rats result in sensorimotor deficits  similar to those observed following L H lesions . Decreased responsiveness to stimuli has also been demonstrated . Gustatory information is conveyed from the pontine taste area to the amygdaloid complex . Animals with large lesions in the amygdala show decreased licking of various concentrations of sucrose . Decreases were also shown in the consumption of 0.1% saccharin, 5% sucrose and 2% NaCI with different amygdaloid nuclei lesions . The most consistent and severe effects were seen with lesions in lateral ventral areas of the amygdala. Also basolateral amygdaloid lesions lead to an attenuation in taste aversion and reduced neophobia . The purpose of the present study was to determine the effects of amygdaloid lesions on schedule induced and schedule dependent behavior. In addition, the effects of these lesions were assessed in terms of several other measures such as deprivation induced drinking, deprivation induced eating, and salt arousal of drinking. Consumption of sapid solutions in the home cage and under schedule induced conditions was also measured. Results indicate no effects of bilateral symmetrical destruction of the basolateral amygdala on licking, water consumption, and lever pressing even though there were relatively permanent deficits in responses to various taste stimuli. METHOD
Eight male hooded rats with an average body weight of 281 +- 20 (SD) g were selected from our colony and allowed to adapt to individual home cages for 10 days. Procedure
Following adaptation to home cages, animals were han-
dled daily and records were kept of food and water intake and body weight. Body weight recorded on the tenth day was considered to be the 100% ad lib feeding weight for each animal. The group average was 393 -+ 16 (SD) g. Animals were gradually reduced to 80% of this weight over a 7 day period by restricting daily food rations. For the next 3 days, animals were trained in an experimental chamber to press a lever for 45 mg food pellets. Following the 3 days on continuous reinforcement, animals were placed on an F I 1 min reinforcement schedule for the duration of the experiment. All animals were tested daily for 30 min. The experimental chamber consisted of a standard LVE 1469 medium sized test cage and matching sound attenuating cubicle with a lever and pellet dispensing mechanism. A stainless steel ball point drinking spout was mounted in the center of the back wall of the chamber, 4.0 cm above the grid floor and protruded 1.5 cm into the cage. The drinking spout was attached to a graduated eudiometer tube for measuring water consumption. A standard food cup was mounted on the adjacent wall as close as possible to the back wall and 1.0 cm above the floor. The lever was mounted on the same wall as the food cup, 3.0 cm above the floor and 2.5 cm from the front of the cage. Licks were recorded by means of a contact resistance sensitive lickometer. During the experimental session, the number of licks and presses were recorded on individual counters and displayed on a cumulative recorder. When presses, licks and water intake appeared stable over a 10 day period, lesions were made in the basolateral amygdala immediately after the last preoperative session. Animals were anesthetized with a 3 cc/kg IP injection of Equi-Thesin followed by 0.2 cc IM injection of procaine penicillin G. Lesions were made with a Grass radio frequency lesion-maker Model LM3. For 22 sec, two megacycles sinewave AC current was passed between a tungsten electrode, size 10 rail, insulated except for the tip and an anal stainless steel electrode. The intensity dial on the lesion maker was set at 70. With the surface of the skull level, lesions were made by placing the electrode tip 3.8 mm posterior to bregma, 4.8 mm from the midline, and 9.2 mm ventral from bregma. All animals were maintained at 80% body weight for the following 40 days. Beginning with Day 41, all animals received increased food rations over the next 3-4 days until they were feeding ad lib on Day 46. Data were collected in the experimental chamber during the 10 day baseline condition, 40 days postoperative at 80% body weight, and for an additional 15 days during and after recovery of body weight on ad lib feeding. Animals were fed Purina lab chow blocks in the home cage and food and water intake and body weight were recorded daily. After testing in the experimental chamber was discontinued, a series of four home cage functional tests was performed on each animal. Because of the long duration of the pre-experimental baseline utilized in this experiment, functional tests were carried out only following the lesions. However, the functional tests are reliable and considerable data are available on normal animals under similar conditions from previous experiments [1, 17, 22, 24]. Animals were first deprived of food for 24 hr then permitted to eat for 3 hr and food consumption was measured. The second test consisted of 24 hr water deprivation followed by a 1 hr period of water consumption during which food was not present in the cage. The third test consisted of the water consumed in 1 hr following a 2 cc/kg body weight IP injection of 15% NaC1. Food was not present in the cage during this
AMYGDALOID LESIONS AND ADJUNCTIVE BEHAVIOR TABLE 1 COMPARISONOF AMYGDALOIDLESIONAND CONTROLANIMALS BASED ON 6.85% SUCROSE CONSUMPTION Number of Standard Deviations Away from Mean Intake of Intact Control Group; N=4 Mean = 394.5 _+ 85.8
G1 Control Lesion
V-23 V-25 V-31 V-32
Normal Normal Normal Normal
-1.0 -0.6 +0.3 -0.8
Gz Experimental Lesion
V-24 V-29 V-30 V-35
Reduced Reduced Reduced Reduced
-2.8 -2.1 -2.1 -2.1
577 where tissue damage was observed were outlined. The results of these tests and the histological data were utilized to classify animals into two groups. In addition to the eight animals already mentioned, a group of four rats were subjected to procedures identical to those described above. The average starting body weight for this group was 258 _+ 23 (SD) g. The 100% body weight for the day prior to reduction was 364 _+ 6 (SD) g. These animals were not subjected to any surgical procedures following stable baseline but continued to be tested in the operant boxes along with the other two groups. This intact group was used as an additional control group. Comparisons between this group and the lesion control group that are described below were made on all the measures used in this experiment. RESULTS
test. The f'mal test was the amount of 6.85% sucrose consumed in 48 hr in a two-tube preference test. The other tube was filled with water. Each test was separated by at least 2 days of free access to food and water in the home cage. Following these four home cage functional tests, animals were returned to the experimental chamber and tested daily for 30 min. After licks, lever presses and water consumption stabilized, the animals were presented with the following solutions, in a counterbalanced order, in place of water: 6.85% sucrose, 25% sucrose, 8% glucose, 21% glucose, and 0.125% sodium saccharin. All solutions were made weight by volume with distilled water. Each animal was exposed to each solution only once and each presentation was separated by 2 days of access to tap water during the experimental session. The animals were then returned to their home cages and testing in the experimental chamber was discontinued. Finally, the animals were presented with the same solutions as above in their home cages and 48 hr fluid consumption was recorded. Again, consecutive presentations of each solution were separated by 2 days of access to tap water. Consumption of distilled water for 48 hr was also recorded. Animals were then perfused intracardially with 0.9% NaC1 followed by 10% Formalin. The brain of each animal was removed, sectioned at 60 p.m, mounted and stained with cresyl violet. The extent and location of tissue damage was determined by projecting the stained slides onto copies of plates taken from the K6nig and Klippel atlas  and areas
Animals were assigned to two groups according to the results of the 6.85% sucrose solution home cage functional test and on the basis of lesion locus and extent of tissue damage. Results from this test for the nonlesion intact group of rats were used in the evaluation of all other animals. For the intact group, the mean amounts of 6.85% sucrose solution consumed over a 48 hr period, with water also available, were calculated. In addition, the standard deviation was computed. On the basis of the sucrose test and histological data, the 8 rats with lesions were divided into 2 groups of 4 animals each. The four animals with asymmetrical lesions are referred to as GI, the control lesion group. The four animals with symmetrical bilateral damage to the basolateral amygdaloid nuclei are referred to as G2, the experimental lesion group. Table I is a list of the data that were used in dividing the animals into groups. The amount of 6.85% sucrose consumed is expressed as the number of standard deviations above or below the control group mean. For example, the amount drunk by animal V-23 in 48 hr of 6.85% sucrose with water present was 1.0 standard deviation below the mean for the intact nonlesion control group. Values within -- 1.5 standard deviations of the control group mean were considered normal. Those values of 1.5 standard deviations or more below the control group mean were considered reduced and those above would have been considered increased. An examination of Table 1 reveals that the control lesion group G~ was normal in terms of these derived measures. Table 2 is a list of the means and standard deviations of
TABLE 2 GROUP MEANS AND STANDARDDEVIATIONSFOR HOME CAGE FUNCTIONALTESTS IN AMYGDALOID LESION ANIMALS
24 Hr Water Deprivation: 1 Hr Water Intake
24 Hr Food Deprivation: 3 Hr Food Intake
15% NaCI 2 cc/kg IP: 1 Hr Water Intake
6.85% Sucrose with Water Choice 48 Hr Intake
13.8 + 2.6
15.4 -+ 2.2
12.5 + 4.8
349.0 + 47.1
10.8 -+ 1.0
12.3 _+ 3.7
6.8 -+ 1.7
200.0 __ 32.0*
GI Control Lesion G~ Experimental Lesion
*Significantly different from control, p
LOULLIS AND WAYNER 800
600 ! e ~ 5OO
u 400 -
LICKS PRESSES HOH
DAYS S DAY MEANS
DAYS 5 DAY MEANS
FIG. 1. Mean number of lever presses, licks and water intake for the asymmetrical amygdaloid lesion control group GI before and after the lesion and during ad lib feeding as a function of 5 day periods for the 65 days of the 30 min dally testing.
both groups for the sucrose test and the three other home cage functional tests. Two-tailed t-tests were utilized to analyze comparisons between G1 and G~. Group G2 was significantly depressed in terms of 48 hr 6.85% sucrose consumption with water choice, t(6)=6.10, p<0.001. The two groups did not differ significantly in terms of 1 hr water intake in response to 2 cc/kg 15% NaCI, t(6)=2.26, p >0.05; 1 hr water intake following 24 hr water deprivation, t(6)= 2.14, p>0.05; or 3 hr food intake following 24 hr food deprivation, t(6) = 1.43, p >0.05. The data from the 65 days of daily testing in the experimental chamber were analyzed by means of a two-factor A N O V A with repeated measures, for presses, licks and water consumed during the 30 min daily test sessions. The factors were Days, 13 levels with repeated measures consisting of 5 day means for each animal over the 65 days of testing and Groups, 2 levels consisting of G1 and G2. The analysis of water intake indicated that the groups were not significantly different, F(1,6)=2.186, p >0.10. Days were significant, F(12,72)=22.957, p<0.01. The groups by days interaction was not significant, F(12,72)=0.444, p>0.25. The analysis of licks indicated that groups were not significantly different, F(1,6)=2.422, p>0.10. Days were significant, F(12,72)=12.629, p<0.01. The groups by days interaction was not significant, F(12,72)=0.409, p>0.10. Analysis of presses indicated that groups were not signifi-
FIG. 2. Mean number of lever presses, licks and water intake for the bilateral symmetrical amygdaloid lesion experimental group G~ before and after the lesion and during ad lib feeding as a function of 5 day periods for the 65 days of the 30 rain daily testing.
GLUCOSE GLUCOS£ SACCHARIN SOLUTIONS
FIG. 3. Mean intake in ml as a function of 6 different solutions presented to the amygdaloid lesion animals for 48 hr in the home cage. Consumption of each solution for the asymmetrical control group G, is indicated by open bars and that for the symmetrical group G~ is indicated by solid bars.
cantly different, F(1,6)=0.254, p>0.10. Days were significant, F(12,72)=6.450, p<0.01. The groups by days interaction was not significant, F(12,72)=0.287, p>0.10. Mean amounts of water consumed in ml, lever presses and licks for groups Gt and G2 are presented as a function of
AMYGDALOID LESIONS AND ADJUNCTIVE BEHAVIOR CONTROLSI--I LESIONS1
-- 1S E
Z 9 6
8Z 21Z 0.12SZ GLUCOSE GLUCOSE SACCHARIN SOLUTIONS
8g 21~ 0.125Z GLUCOSE GLUCOSE SACCHARIN SOLUTIONS
FIG. 4. Mean intake in ml as a function of 6 different solutions presented to the amygdaloid lesion animals during the 30 min test session in the experimental chamber under ad lib recovered body weight conditions. Consumption of each solution for the asymmetrical control group G] is indicated by open bars and that for the symmetrical group G~ is indicated by solid bars.
FIG. 5. Mean number of licks as a function of 6 different solutions presented to the amygdaloid lesion animals during the 30 min test session in the experimental chamber under ad lib recovered body weight conditions. Consumption of each solution for the asymmetrical control group Gt is indicated by open bars and that for the symmetrical group G2 is indicated by solid bars.
successive 5 day means in Figs. 1 and 2, respectively. The lesion which occurred on Day 11 is indicated by an arrow that appears between the 5 day means 10 and 15. The second arrow labeled AD LIB, which appears between the 5 day means 50 and 55, indicates the beginning of the 5 day periods during which the animals were tested while their body weight was increasing because the food rations were increased gradually during the first three days and then food was present ad lib. The data from the testing of various solutions in the home cage were analyzed by means of a two-factor ANOVA with repeated measures. The factors were Solutions, 6 levels consisting of 6.85% sucrose, 25% sucrose, 8% glucose, 21% glucose, 0.125% sodium saccharin and distilled water with repeated measures for each animal and Groups, 2 levels consisting of G~ and G2. The groups were significantly different, F(1,6)=17.983, p<0.01. Solutions were significant, F(5,30)=35.719,p<0.01. The groups by solutions interaction was significant, F(5,30)=6.233, p<0.01. A simple main effects analysis of solutions for each group indicated solutions at GE was significant, F(5,30)=35.82, p<0.01, and solutions at Gz was significant, F(5,30)=6.51, p<0.01. A Dunnett test was performed on the data for G~ and G2 using water as the control solution. For GE the consumption of all 5 solutions was significantly increased over distilled water: 6.85% sucrose, 8% glucose and 0.125% saccharin, p<0.01; 25% sucrose and 21% glucose, p<0.05. For G2 the consumption of 6.85% sucrose and 8% glucose was significantly increased over water, p<0.01, as was the consumption of 0.125% saccharin, p<0.05. The consumption of 25% sucrose and 21% glucose was not increased over water, p >0.05. Simple main effects analysis comparing the 2 groups at each solution indicated that Gz was significantly decreased in intake compared to G~ at 6.85% sucrose, F(2,27)=48.95, p<0.01; 8% glucose, F(2,27)=29.28, p<0.01; and 0.125% saccharin, F(2,27) =4.86, p<0.05. There were no significant differences between groups at 25% sucrose and 21% glucose, p>0.05. Figure 3 illustrates these effects where mean intake in ml is presented as a function of the six different solutions. For each solution, the mean intake for the control lesion group G~ is indicated by open bars and the mean intake for the experimental lesion group G2 is indicated by solid bars.
The data from the testing of all animals on the various solutions, when they were returned to the experimental chamber, were analyzed by means of a two-factor ANOVA with repeated measures, for presses, licks and fluid consumed in ml when offered the various solutions. The factors were Solutions, 6 levels consisting of 6.85% sucrose, 25% sucrose, 8% glucose, 21% glucose, 0.125% sodium saccharin and distilled water with repeated measures for each animal and Groups, 2 levels consisting of G1 and G2. Analysis of intake in ml indicated that the groups were significantly different, F(1,6)=29.495, p<0.01. Solutions were significant, F(5,30)=13.932, p<0.01. The groups by days interaction was not significant, F(5,30)=0.842, p >0.25. Figure 4 illustrates these effects where mean intake in ml is presented as a function of the six different solutions. For each solution, the mean intake of the control lesion group G~ is indicated by open bars and the mean intake for the experimental lesion group G2 is indicated by solid bars. Therefore, animals with bilaterally symmetrical basolateral amygdala lesions drank less of each solution including water. Analysis of licks indicated that groups were significantly different, F(1,6) =39.782, p <0.01. Solutions were significant, F(5,30)=9.739, p<0.01. The groups by solutions interaction was not significant, F(5,30)=0.472, p>0.25. Figure 5 illustrates these effects where mean number of licks is presented as a function of the six different solutions. For each solution, the mean number of licks for the control lesion group Gz is indicated by open bars and the mean number of licks for the experimental lesion group G2 is indicated by solid bars. Therefore, the animals with bilaterally symmetrical basolateral amygdala lesions licked less of each solution including water. Analysis of presses indicated that groups were not significantly different, F(1,6)=0.003, p>0.25. Solutions were significant, F(5,30)=9.968, p<0.01. The groups by solutions interaction was not significant, F(5,30)= 1.072, p>0.25. Figure 6 illustrates these effects where mean number of lever presses is presented as a function of the 6 different solutions. For each solution, the mean number of lever presses for the control lesion group G~ is indicated by open bars and the mean number of presses for the experimental lesion group G2 is indicated by solid bars. Therefore, lever pressing in the
L O U L L I S AND W A Y N E R
~, 75 60
FIG. 6. Mean number of lever presses as a function of 6 different solutions presented to the amygdaloid lesion animals during the 30 min test session in the experimental chamber under ad lib recovered body weight conditions. Consumption of each solution for the asymmetrical control group G, is indicated by open bars and that for the symmetrical group G2 is indicated by solid bars.
presence of sweetened solutions is less because animals are licking and drinking more; whereas, in the presence of water animals lick and drink less and consequently press more. Table 3 illustrates the results of the statistical analysis of the data from the testing of the various solutions in the home cage and operant chamber. The asterisks or daggers indicate decreases in 48 hr fluid intake in the home cage and 30 min fluid intake, number of licks, and number of lever presses in the operant chamber for experimental group G2 when compared to G~. Tabel 4 is the same as Table 3 except that comparisons are made within G, and G,, using water as the baseline measure. Examination of food and water intake and body weight data indicated no differences between the two groups on these measures. Diagrammatic reconstruction of a typical lesion for ani-
FIG. 7. Typical bilateral lesion in the symmetrical amygdaloid lesion experimental group G2. Rat V-35 is illustrated on Plates 35-40 of the Krnig and Klippel Atlas .
TABLE 3 RESULTS OF THE STATISTICALANALYSISOF THE EFFECTS OF THE VARIOUS SOLUTIONS ON DIFFERENT MEASURES FOR EXPERIMENTAL GROUP G2 WHEN COMPARED TO CONTROLGROUPG~ 6.85% Sucrose
48 Hr Intake Home Cage
0.5 Hr Intakes Operant Chamber
Licks$ Operant Chamber
Presses~ Operant Chamber
*Significantly different from control group, p<0.05. tSignificantly different from control group, p<0.01. NS Not significantly different from control group. SGroups by solutions interaction not significant, p<0.25; groups significant, p<0.01.
A M Y G D A L O I D L E S I O N S AND A D J U N C T I V E B E H A V I O R
TABLE 4 RESULTS OF THE STATISTICALANALYSISOF THE EFFECTS OF THE VARIOUSSOLUTIONSON DIFFERENT MEASURES FOR THE CONTROL AND EXPERMENTALGROUPS USING WATER AS A BASELINE Test
48 Hr Intake Home Cage
0.5 Hr Intake* Operant Chamber
Licks:~ Operant Chamber
Presses~ Operant Chamber
Control Experimental Control Experimental Control Experimental
*Significantly different from water baseline, p <0.05. TSignificantly different from water baseline, p<0.01. NS Not significantly different from water baseline. *Groups by solutions interaction not significant, p>0.05; therefore, within group comparisons were not possible.
mals in the experimental lesion group Gz is represented in Fig. 7 and illustrates the lesion of Animal V-35. Unlike the bilateral symmetrical destruction of the basolateral amygdala of all animals in G2, animals in G1 had asymmetrical damage or no damage at all in this area. The reconstruction is based upon Hates 35--40 of the Kfnig and Klippel atlas . There were no significant differences between the intact and lesion control group on any of the measures used. DISCUSSION Results demonstrate that bilateral symmetrical destruction of the basolateral amygdala does not produce any significant effects on schedule dependent lever pressing and schedule induced licking and drinking. However, these lesions produce a relatively permanent depression of the enhanced consumption under normal conditions of sapid solutions. The deficits observed in home cage consumption of various solutions due to amygdaloid lesions have been reported previously [3,15]. These results suggest a taste deficit which is further supported by the fact that taste pathways to the amygdala are well documented . In the present experiment, it is very likely that these pathways were at least
partially destroyed by basolateral amygdaloid lesions. However, the results from the testing of the various solutions in the operant chamber indicate that animals with basolateral amygdaloid lesions exhibit deficits which cannot be attributed to taste alone, since these animals showed depressed intake not only in the consumption of sapid solutions, but in water intake as well. These results are consistent with the results from an earlier study  which demonstrated that amygdaloid lesions produce sensorimotor deficits similar to those observed following L H lesions. The fact that deficits observed here were less severe might be attributed to the smaller lesions. Since there is considerable evidence that the amygdala modulates hypothalamic activity [26, 27, 28, 43] and considering the substantial amount of evidence implicating the LH in adjunctive and consummatory behavior [39, 40, 41, 42], these results are significant and substantiate the view that sensory inputs to the LH motor control system, involved in eating and drinking and the maintenance of schedule induced polydipsia, are partially destroyed by bilateral symmetrical ablation of the basolateral amygdala in the rat. The pathway and characteristics of these inputs have already been described [8, 10, 23].
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