Basolateral Amygdaloid Lesions Research Articles

Attenuated hippocampal long-term potentiation in basolateral amygdala-lesioned rats

Possible involvement of the amygdaloid input in long-term potentiation (LTP) in the medial perforant path-dentate gyrus granule cell synapses in vivo was investigated by evaluating the effects of lesions of the amygdaloid nucleus. The dentate gyrus synaptic potential evoked by low-frequency test stimulation did not change following lesions of the basolateral and central amygdala. However, when tetanic stimulation (30 pulses at 60 Hz) was applied 60 min after lesioning of the ipsilateral basolateral amygdala, the magnitude of LTP was significantly attenuated. Since lesions of the ipsilateral central amygdala and the contralateral basolateral amygdala did not affect the dentate gyrus LTP, the attenuation of the dentate gyrus LTP is a specific effect of acute lesions of the ipsilateral basolateral amygdala. The basolateral amygdaloid lesions significantly attenuated both LTP induced by weak (20 pulses at 60 Hz) and strong (100 pulses at 100 Hz) tetanus, indicating that the effect of the lesions does not depend on the strength of tetanus applied to induce LTP. When the ipsilateral basolateral amygdala was destroyed after application of tetanus, it did not affect the established LTP. The attenuation of LTP was also observed after the basolateral amygdala-lesioned rats were allowed a recovery period of 2 weeks. This is the first report providing evidence that the ipsilateral basolateral amygdala modulates hippocampal synaptic plasticity in vivo.

Involvement of cholinergic mechanisms in impairment of working memory in rats following basolateral amygdaloid lesions

In order to clarify the role of the amygdala in the working and reference memory of rats in the three-panel runway task, the effects of lesions of subnuclei of the amygdaloid complex on this behavior were studied. Rats that had been trained preoperatively, until they achieved the criterion of learning, were subjected to lesions of the amygdala. In the working memory task, lesions of the basolateral subdivision of the amygdala caused a significant increase in the number of errors (attempts to pass through two incorrect panels of the three panel-gates at four choice points), while lesions of the corticomedial amygdala had no effect on working memory errors. The increase in working errors, observed in basolateral amygdaloid-lesioned rats, declined gradually as retraining sessions were given once each day, reverting to control levels on and after the sixth session. In the reference memory task, the number of errors was not affected by lesions of the basolateral or corticomedial amygdala. The increase in working memory errors, induced by lesions of the basolateral amygdala was significantly reduced by intraperitoneal administration of the inhibitors of cholinesterase, tetrahydroaminoacridine (0.32–1.0 mg/kg) and physostigmine (0.032–0.1 mg/kg), and the muscarinic receptor agonist, oxotremorine (0.1 mg/kg), before the runway test. These findings suggest that the basolateral amygdala is selectively involved in working memory but not in reference memory and that the lowering of central cholinergic function may account for the impairment of working memory, induced by lesions of the basolateral amygdala.

Contrasting effects of centromedial and basolateral amygdaloid lesions on stress-related responses in the rat

The effects of lesions in the centromedial and basolateral amygdala were examined using three different tests sensitive to the following stress-related responses: exploratory behavior, pain reactivity, and immune responses. The most clear-cut results were found with exploratory behavior. Rats with lesions of the centromedial amygdala tended to explore a radial-arm maze more quickly and entered more novel arms of the maze than controls. Those with lesions of the basolateral amygdala were generally too hesitant to explore at all. No significant differences were found between groups on measurements of natural killer cell activity. In tests of pain perception, rats in the control group displayed an analgesic response on the hot plate following an injection of the anxiogenic drug, RO 15-1788, whereas rats with centromedial lesions tended to exhibit a blunted response. These findings provide modest support for the view that the central and lateral regions of the amygdala play complementary roles in aversively motivated behaviors and in stress-related response patterns.

Vomeronasal and olfactory pathways to the amygdala controlling male hamster sexual behavior: Autoradiographic and behavioral analyses

Previous studies suggest that the rostral corticomedial amygdala (CMA), particularly the medial nucleus, is an important site where vomeronasal and olfactory stimuli critical to male hamster copulatory behavior are processed. To test the possibility that mating deficits seen after lesions of the rostrally-placed medial nucleus may be due to the interruption of chemosensory afferents to more caudal areas, we injected tritiated amino acids into the accessory and main olfactory bulbs of male hamsters in which we had first produced bilateral electrolytic lesions or sham lesions in either the rostral CMA or basolateral amygdala, and then observed mating behavior. Autoradiographic analysis of ‘vomeronasal’ projections from the accessory olfactory bulb and ‘olfactory’ projections from the main bulb, revealed that rostral CMA lesions which damaged the medial nucleus and extended to the ventral surface of the brain (ventral lesions) interrupted vomeronasal input to the more caudally-placed posteromedial cortical nucleus, but spared olfactory inputs to adjacent caidal areas of the amygdala and piriform lobe. In contrast, lesions which damaged a major portion of the medial nucleus but left its ventral surface intact (dorsal lesions) spared both vomeronasal and olfactory inputs to more caudal areas. Animals with both dorsal and ventral lesions failed to mate posteperatively, whereas animals bearing sham lesions of basolateral amygdaloid lesions, which, like dorsal lesions, spared caudally-directed chemosensory afferents, continued to mate normally. We conclude that mating deficits seen after rostral CMA lesions are due primarily to destruction of the medial nucleus.

Behavioral changes induced by basolateral amygdala self-stimulation

Rats given continuous access to rewarding stimulation of the posterior hypothalamus are able to maintain normal food and water intake despite high rates of self-stimulation. However, access to rewarding stimulation of the basolateral amygdala produced suppression of feeding and drinking followed by dramatic increases in emotionality and subsequent decreases in self-stimulation. These findings are considered with regard to the existing literature on basolateral amygdaloid lesions and stimulation.

Differential effects of medial, central and basolateral amygdaloid lesions on four models of experimentally-induced aggression in rats

To clarify whether various nuclei of the amygdaloid complex play different roles in aggressive behavior including muricide, 4 types of aggression were experimentally induced in rats. These include olfactory bulbectomy (OB rats), midbrain raphe lesions (Raphe rats), administration of Δ 9-tetrahydrocannabinol (THC rats) and long-term isolation (Iso rats). Rats which exhibited muricide following these treatments were subjected to bilateral lesions of either the medial (AME), central (ACE) or basolateral (ABL) amygdaloid nuclei. Both muricide and hyperemotionality in the OB rat were markedly inhibited by AME lesions. Those of the Iso and THC rats were moderately inhibited. However, in the Raphe rat, aggressive behavior was not inhibited by AME lesions. Furthermore, ACE or ABL lesions caused no significant changes in all 4 models of aggression. These results suggest that the AME plays a facilitatory role in aggression of OB, Iso and THC rats, but aggression in Raphe rat is independent of amygdaloid activity.

Differential effects of amygdaloid lesions on conditioned taste aversion learning by rats

Rats with electrolytic lesions placed in either the basolateral or corticomedial divisions of the amygdala acquired a conditioned taste aversion to sucrose. Comparisons with a surgical control group indicated that damage to the corticomedial amygdala did not alter the animals' performance, while damage in the basolateral nuclei resulted in a small but significant attenuation of the aversion. Furthermore, these amygdaloid lesions did not alter the acceptability of two quinine hydrochloride solutions (0.01% and 0.001%). The daily drinking behavior of the rats with basolateral amygdaloid lesions appeared consistent with the hypothesis that this lesion affected the animals' appreciation of the novelty of the sucrose solution, and hence attenuated the subsequent aversion.

Effects of basolateral or corticomedial amygdaloid lesions on grooming, consummatory, and locomotor behaviours in rats

Grooming behaviour in rats was induced by limited water access and by water spray before and after corticomedial or basolateral amygdaloid lesions or control operations. Corticomedial lesions produced some attenuation of grooming induced by limited water access but increased grooming induced by water spray. Basolateral lesions did not consistently affect grooming. There was an increase in ambulation time following basolateral lesions and a relative decrease in feeding time following corticomedial lesions. There were no effects of either lesion on drinking or rearing. Detailed examination of both grooming and non-grooming behaviours provided little evidence for lesion induced disruption of response sequencing.

Effects of basolateral amygdaloid lesions on schedule induced and schedule dependent behavior

Rats were reduced to 80% body weight and were exposed to an FI-1 min food reinforcement schedule for 30 min 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 min 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.

7) - Differential effects of medial and basolateral amygdaloid lesions on three models of experimentally-induced aggression in rats

7) - Differential effects of medial and basolateral amygdaloid lesions on three models of experimentally-induced aggression in rats

Effects of delta9-tetrahydrocannabinol on active avoidance acquisition and passive avoidance retention in rats with amygdaloid lesions.

Delta9-Tetrahydrocannabinol was administered to rats with basolateral amygdaloid lesions, control rats, and normal rats in doses of 0.75, 1.5, and 3.0 mg/kg i.v. They were trained in a one-session two-way active avoidance task. Delta9-Tetrahydrocannabinol increased the percentage of avoidance and the intertrial crossing rates in all groups, regardless of lesion treatment. Rats with basolateral amygdaloid lesions were not different from controls on any measure. In a second experiment, delta9-tetrahydrocannabinol was administered to rats with basolateral amygdaloid lesions and control rats in doses of 0.75 and 3.0 mg/kg 24 h after learning of a one-trial passive avoidance task, and retention was measured. No differences were found as a function of drug treatment or lesion condition. It was concluded that the basolateral amygdala is not a necessary condition for the action of delta9-tetrahydrocannabinol on active avoidance acquisition, that the drug has no effect on passive avoidance retention, and the basolateral amygdala is not necessary for two-way active avoidance acquisition or passive avoidance retention. Active avoidance results are discussed in terms of a possible relationship between delta9-tetrahydrocannabinol, ACTH, and avoidance learning.

Food intake and spontaneous activity of rats with lesions in the amygdaloid nuclei.

Food intake and spontaneous activity of rats with lesions in the amygdaloid nuclei.