Lesions Of Stria Terminalis Research Articles

Stria terminalis lesions attenuate the effects of posttraining naloxone and beta-endorphin on retention.

Stria terminalis lesions attenuate the effects of posttraining naloxone and beta-endorphin on retention.

Effects of lesions in the amygdala and periventricular hypothalamus on striatal somatostatin-like immunoreactivity

Somatostatin has been found in substantial amounts in the basal ganglia by radioimmunoassay and has been demonstrated in both neurons and nerve terminals. Since the levels of somatostatin have been shown to vary in Huntington's and Alzheimer's disease it was of interest to see whether such changes could be produced experimentally. Lesions of the periventricular nucleus of the hypothalamus and knife cuts adjacent to this nucleus had no effect on striatal somatostatin-like immunoreactivity (SLI). Similarly lesions of mediodorsal frontal cortex, and those isolating pyriform cortex or the olfactory bulb had no effect on striatal SLI. Removal of tge amygdala resulted in significant increases in SLI in the ipsilateral striatum and nucleus accumbens, suggesting loss of an inhibitory interaction. Stria terminalis lesions failed to reproduce this effect suggesting that it is mediated via amygdalo-striatal projections traveling in the dorsal longitudinal bundle. Other findings support a somatostatin projection to the amygdala from the bed nucleus of the stria terminalis and one from the amygdala to the ventromedial hypothalamus.

Lesions of the stria terminalis attenuate the amnestic effect of amygdaloid stimulation on avoidance responses

The present study investigated the involvement of two amygdala pathways, the stria terminalis (ST) and the ventral amygdalofugal pathway (VAF), in the effect of post-training electrical stimulation of the amygdala on retention. Rats with implanted amygdaloid electrodes and ST lesions, VAF transections or sham pathway operations, were trained on an inhibitory avoidance task and an active avoidance task. Electrical stimulation of the amygdala was given immediately after training and retention was tested 24 h later. In rats with sham ST lesions, post-training amygdaloid stimulation impaired retention in both tasks. Lesions of the ST did not significantly affect retention in the unstimulated rats. However, the ST lesions attenuated the amnestic effect of amygdaloid stimulation. In rats with sham VAF transections, stimulation of the amygdala impaired retention in the inhibitory avoidance task but enhanced retention in the active avoidance task. Transecting the VAF impaired retention performance of the unstimulated rats in the inhibitory avoidance task. However, the VAF transections did not alter the effect of amygdaloid stimulation: in both tasks, the retention performance of stimulated rats with VAF transections did not differ from that of stimulated rats with sham transections. These findings suggest that the ST may be involved in mediating the influences of the stimulated amygdala in modulating memory storage processing in the brain.

Lesions of the stria terminalis attenuate the enhancing effect of post-training epinephrine on retention of an inhibitory avoidance response

This study investigated the effect of the stria terminalis (ST) lesions on the retention facilitation produced by post-training epinephrine. Rats with sham or bilateral ST lesions were trained on a one-trial step-through inhibitory avoidance task and, immediately after training, received saline or one of 3 doses (0.01, 0.1 or 1.0 mg/kg, s.c.) of epinephrine. In the rats with sham ST lesions, all 3 doses of epinephrine significantly enhanced retention performance. Lesions of the ST did not affect retention significantly. However, the lesions attenuated the facilitating effect of epinephrine on retention. These findings suggest that the integrity of the ST, which connects the amygdala and other brain structures, is essential for the effect of epinephrine on memory processes. The possible involvement of the brain structures processing visceral information in the memory modulatory effect of epinephrine is discussed.

Evidence for a ventral non-strial pathway from the amygdala to the bed nucleus of the stria terminalis in the male golden hamster

Male hamsters in which the stria terminalis (ST) had been interrupted either by electrolytic lesions or knife cuts, or normal control males, received iontophoretic injections of horseradish peroxidase in either the bed nucleus of the stria terminalis (BNST) or the medial preoptic-anterior hypothalamic area (MPOAH). Comparison of intact and St-lesioned brains revealed the existence of a ventral non-striatal pathway, from cells in the medial amygdaloid nucleus (M) to the preoptic portion of the BNST but not to the MPOAH. Since bilateral lesions of M completely eliminate male hamster mating behavior, but ST lesions do not, we suggest that the ventral pathway to the BNST may be an important route by which M influences male copulatory behavior.

Stria terminalis lesions alter the temporal pattern of copulatory behavior in the male golden hamster

The mating behavior of a group of male golden hamsters was observed before and after bilateral electrolytic lesions or knife cuts interrupting the stria terminalis (ST). Whereas males with bilateral lesions of the medial nucleus of the amygdala had previously been observed to stop mating, a majority of hamsters with bilateral ST destruction, whether by electrolytic lesions or knife cuts, continued to display mounts, intromissions, and ejaculations during tests over a two month postoperative period. ST-lesioned males did, however, display a distinctly altered pattern of copulation over the course of postoperative testing, consisting of an increase in mount latency during the first week, an increase in the inter-intromission interval during the second week, and an increase in the number of intromissions preceding ejaculation during the third and subsequent weekly tests. Males with bilateral lesions of the caudal amygdala, which damaged the amygdaloid exit of the ST, displayed alterations in copulatory behavior similar to those seen after bilateral ST destruction at a more rostral level.

Amygdaloid inhibition of maternal behavior in the nulliparous female rat

In the first experiment, the effects of lesions of (1) the amygdala, (2) its major efferent projection system, the stria terminalis or (3) other non-limbic brain sites on the induction of maternal behavior in the nulliparous female rat were investigated. Animals sustaining lesions of either the amygdala or the stria terminalis became maternal more rapidly than did control animals. In the second study the effects of lesions to different portions of the amygdala on both maternal and fear responding were investigated. It was found that animals sustaining damage to the corticomedial amygdaloid nuclei became maternal more quickly than did animals sustaining either basolateral amygdaloid damage or no amygdaloid damage. Also in comparison to lesioned controls, animals with lesions of the amygdala showed reduced ‘fearfulness’ on a number of fear-mediated tasks. The third study attempted to interrelate fear responsiveness and maternal behavior by observing nulliparous animals with amygdaloid or stria terminalis lesions for their responses to unfamiliar foster pups placed daily into their preferred nesting quadrant. While control animals actively avoided pups placed into their nest sites (by moving their nest site to another quadrant of the cage), animals with amygdaloid lesions or lesions of the stria terminalis, did not. These results are interpreted to mean that nulliparous females generally do not respond maternally to pups because these females are, in general, more neophobic than parturient females and they tend to find pups and their novel odors, aversive. This aspect of their behavior is likely mediated by the amygdala. These data are discussed in terms of their relevance to the rapid maternal responsiveness normally shown by the female at parturition.

Inhibition of adrenocortical responses following olfactory stimulation in rats with stria terminalis lesions

Previous experiments using hypothalamic deafferentation and brain lesions in rats have demonstrated that while anterior hypothalamic deafferentation blocked the adrenocortical response to olfactory stimulation completely, bilateral lesions in the ventolateral medial forebrain bundle and gemini region had only a partial effect. In order to elucidate the pathways mediating this response, the adreno-cortical responses to olfactory stimulation as well as to ether stress, photic, acoustic and sciatic stimulation were studied in rats with bilateral stria terminalis or small basolateral or corticomedial amygdaloid lesions. The adrenocortical responses to all the above modalities were normal and the only response which was completely inhibited was that to olfactory stimulation in rats with stria terminalis lesions. This would indicate that the stria terminalis serves as the hypothalamic afferent pathway activating the pituitary-adrenal reaction to olfactory stimulation.

Forebrain lesions and food intake in pigeons

Thirty pigeons were randomly assigned to one of four groups: those receiving bilateral ablation of the archistriatum, the neostriatum, the nucleus stria terminalis, or those receiving a sham operation. All groups showed a non-significant temporary postoperative decrease in food intake, a non-specific effect attributed to the surgery. However, the duration of the hypophagia in the archistriatum- and nucleus stria terminalis-ablated groups was slightly longer (four weeks instead of three). A slight increase in body weight occurred in the nucleus stria terminalis-lesioned group, in spite of decreased food intake. These results, especially that there is no persistent hypophagia following archistriatum and nucleus stria terminalis lesions, are discussed in relation to the suspected role of several forebrain structures in feeding behavior.

Effects of lesions of the amygdala, pyriform cortex, and stria terminalis on two types of exploration by rats

Bilateral lesions were made in three groups of rats, selectively destroying the corticomedial amygdala, the pyriform cortex, or the dorsal stria terminalis. During Phase 1 of the experiment, the behavior of each rat was observed in an open-field apparatus for 4 consecutive days for 5 min per day. This phase permitted an evaluation of exploration that occurs when a rat is forced into contact with novelty. During Phase 2, a novel object was placed in the center of the open field and the procedure was repeated for 4 more days. This phase permitted an evaluation of the exploration that occurs when a rat can interact voluntarily with novelty. Lesions of the corticomedial amygdala increased contact with novelty during Phase 1 and increased eploration of the novel object during Phase 2. Stria terminalis lesions produced the same pattern, except that contact and exploration were decreased. Pyriform lesions decreased exploration only during Phase 2. These data show that the effect of lesions of the amygdala and related structures on exploration are different when different types of exploration are measured. The role of the amygdala and its afferent and efferent neural connections in mediating the two types of exploration studied is discussed.

Amygdaloid and pontine projections to the ventromedial nucleus of the hypothalamus.

AbstractAmygdaloid and pontine projections to the feline ventromedial nucleus of the hypothalamus (HVM) were studied with retrograde transport of horseradish peroxidase (HRP) and anterograde transport of tritiated amino acids. Following injections of HRP into HVM, amygdaloid neurons were labeled in the ipsilateral cortical and medial nuclei and the ventral portion of the parvocellular part of the basal nucleus. In experiments in which HRP was injected into the tuberal hypothalamus following stria terminalis lesions, it was determined that amygdaloid neurons projecting to HVM by way of the stria terminalis were located in the cortical and medial nuclei while those projecting through another route, presumably the ventral amygdalofugal pathway, were found in the rostral part of the medial nucleus and the parvocellular basal nucleus.Following HRP injection into lateral hypothalamus at the level of HVM, labeled neurons were seen in the magnocellular basal nucleus. After preoptic injections, neurons containing the HRP reaction product were in cortical and medial nuclei and magnocellular and parvocellular parts of the basal nucleus.In addition to cells in the amygdala, rostral pontine neurons were labeled after HRP injections into HVM. The cells were located ipsilateral to the injection, mostly in the dorsal nucleus of the lateral lemniscus, lateral and dorsolateral to the brachium conjunctivum. The pontine cells labeled following HVM injections of HRP were different from those labeled following lateral hypothalamic and preoptic region injections. The pontine projection to HVM was confirmed using axoplasmic transport autoradiography. A mixture of tritiated leucine and tritiated proline was injected into the lateral pontine region labeled after HRP injections into HVM. Labeled axons ascending in the medial forebrain bundle terminated throughout the rostro‐caudal extent of HVM.

Contrôle amygdalien de comportements d'agression chez le rat

The effect of lateral amygdala or stria terminalis lesions on two different kinds of aggressive behavior have been studied in the rat. The lateral amygdala lesion does not change the non-killing rat's behavior towards mice; but it markedly reduces the shock-induced intraspecific aggression, without changing the flinch and jump thresholds to the electric shocks. A bilateral interruption of the stria terminalis elicits aggressive reactions in previously non killing rats. This initiation of mouse killing behavior is clearly facilitated through a prior food deprivation for 3 days. The interruption of the stria terminalis changes neither the shock induced aggression, nor the response thresholds. As the stria is the main efferent pathway of the cortico-medial nuclei of the amygdala, these results are in accordance with previous conclusions that tentatively localized in this part of the amygdala an essential component of a mechanism which inhibits muricide behavior in the non killing rat, probably through interactions with the olfactory input. This system is largely independent of amygdaloid structures which facilitate shock-induced intraspecific aggression.

The involvement of dopaminergic systems with the stereotyped behaviour patterns induced by methylphenidate.

Abstract The electrolytic brain lesion technique was used to investigate the role of dopamine-containing areas and pathways in the rat for the mediation of methylphenidate stereotypy. Ablation of the dopaminergic pathways to the extrapyramidal areas at the level of the lateral hypothalamus or substantia nigra was without effect suggesting a postsynaptic site of action in the extrapyramidal nuclei. This site was shown to be the paleo- and not the neostriatum. Deafferentation of the mesolimbic nuclei abolished the weaker components of stereotypy in the acute phase. This effect was generally reflected by ablation of the tuberculum olfactorium but not by nucleus accumbens septi or nucleus interstitialis stria terminalis lesions. The action in the mesolimbic areas may, therefore, involve presynaptic mechanisms. Lesion of the nucleus amygdaloideus centralis abolished the intense components of stereotypy. The greater importance of extrapyramidal function for the action of methylphenidate would indicate a possible value for this agent in the treatment of Parkinson’s disease.

Influence of contingent amygdaloid stimulation on lateral hypothalamic medial forebrain bundle self-stimulation

Rats were trained to self-stimulation for lateral hypothalamic medial forebrain bundle self-stimulation. When simultaneous ipsilateral amygdaloid stimulation accompanied each bar-press, there was an increase in response rate and a decrease in threshold for lateral hypothalamic self-stimulation. The same effect was observed after bilateral lesion of stria terminalis (Experiment 1). The increase in excitability of the lateral hypothalamic rewarding neurons in response to the contingent amygdala stimulation was also demonstrated by the findings that incentive shifts, indicated by positive and negative contrast effects, appeared when amygdala stimulation was started or interrupted, respectively (Experiment 2). On the basis of experimental data and the related literature it is assumed that the amygdala cannot represent a primary or basic reinforcing mechanism, but it has a definite role in the neural mechanism of central processes of higher level, whose control on the basic neuronal mechanism of reward may only be important in the organization of more complex forms of adaptive behavior.

Agonistic behavior after stria terminalis lesions in the rat

Rats with anodal lesions centered in the bed nuclei of the stria terminalis were subjected to a pain-elicited fighting paradigm. A transient increase in agonistic behavior was observed in S pairs which were allowed a 6–7-day recovery period and in pairs which were run only 24 h postsurgery. The increase in reflexive fighting was accompanied by a heightened startle response, which was replaced by shock-elicited stereotyped gnawing behavior when the fighting responses decreased.