Deficient passive and one-way active avoidance acquisition following medial forebrain bundle lesions in rats.

In 3 experiments with 93 Long-Evans male hooded rats, cathodal electrolytic lesions of the medial forebrain bundle (MFB) at posterior hypothalamic levels produced a mild, transient hypodipsia and lowered jump thresholds to footshock. Lesions produced marked deficits in passive avoidance performance in a paradigm that paired discrete, linearly incrementing footshock intensities with contact of a water spout following 48 hrs of water deprivation. Injections of levo-dextro-5-hydroxytryptophan (75 mg g, ip), the immediate metabolic precursor of serotonin, had no effect on the passive avoidance performance of either experimental or operated control Ss. Lesions of the MFB also resulted in deficient acquisition in a 1-trial step-through passive avoidance paradigm not using motivation to drink and caused a severe acquisition deficit in a 1-way active avoidance task. Lesions of the septal nuclei produced lowered jump thresholds but did not affect acquisition in the 1st passive avoidance task. Results are interpreted as indicating a lesion-induced deficiency in fear learning, independent of the serotonergic functions of the MFB. (45 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Altered sensitivity to footshock after selective serotonin depletion: Comparison of electrolytic lesions and neurotoxin injections in the medial forebrain bundle of the rat.

Compared the changes in 183 male albino rats' jump threshold with changes in monoamine content of the telencephalon after damage to the lateral hypothalamus produced either by electrolytic lesions or by 6-hydroxydopamine (6-OHDA) and 5,7-dihydroxytryptamine (DHT). Electrolytic lesions produced significant decreases in jump threshold and in telencephalic content of serotonin, norepinephrine, and dopamine. Infusions of DHT, with or without pretreatment with desipramine, always reduced both jump thresholds and serotonin content, even when there was no effect on norepinephrine or dopamine. In contrast, 6-OHDA had no effect on jump thresholds or serotonin content, even though both norepinephrine and dopamine were greatly reduced. Results suggest that the increased sensitivity to footshock was solely due to the interruption of ascending serotonergic pathways within the lateral hypothalamus and was not a result of damage either to norepinephrine and dopamine pathways or to some other neural system. (26 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Intensity difference thresholds in pigeons after lesions of the tectofugal and thalamofugal visual pathways.

Obtained visual intensity difference thresholds from 11 White Carneaux pigeons before and after thalamic lesions. Ss with lesions in nucleus rotundus (the thalamic component of the tectofugal pathway) showed moderate postoperative threshold elevations. After extensive retraining the thresholds returned to the preoperative value. Ss with lesions in the nucleus opticus principalis thalami (OPT), the thalamic component of the thalamofugal pathway, had smaller postoperative threshold elevations than the nucleus rotundus cases, but the deficit did not diminish after extensive retraining. Ss with combined lesions of both pathways (OPT + rotundus) had severe postoperative threshold elevations, which declined with retraining to the level of the Ss with OPT lesions, but not to the preoperative level. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Lesions of the amygdala, but not of the cerebellum or red nucleus, block conditioned fear as measured with the potentiated startle paradigm.

In Exp I, 97 male Sprague-Dawley albino rats were given 10 light–shock pairings on 2 successive days. At 24–48 hrs following training, groups of Ss received bilateral transection of the cerebellar peduncles, bilateral lesions of the red nucleus (which receives most of the cerebellar efferents), or bilateral lesions of the central nucleus of the amygdala. Controls were sham operated. At 3–4 days after surgery, Ss were tested for potentiated startle (PS [increased acoustic startle in the presence of the light previously paired with shock]). PS was blocked by lesions of the central nucleus of the amygdala but not by transection of the cerebellar peduncles or lesions of the red nucleus. Exp II, in which a visual prepulse test was used with 14 Ss, indicated that the blockade of PS observed in Ss with amygdala lesions could not be attributed to optic tract damage. Exp III, with 20 Ss, demonstrated that the absence of potentiation in Ss with amygdala lesions was not simply due to a lowered startle level ceiling, because these Ss could show increased startle with increased stimulus intensity and with administration of intraperitoneal strychnine, (0.75 mg/kg), a drug that increases startle. Results are consistent with the hypothesis that the amygdala is involved in fear conditioning. (64 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Inhibition of acoustic startle in the rat by a footshock prestimulus: Effects of morphine and naloxone.

Investigated the ability of footshock to inhibit the rat's acoustic startle response. Based on the mean thresholds obtained from a flinch-jump test, 8 rats were tested in a startle inhibition procedure with prestimulus intensities of 0.1, 0.2, 0.4, and 0.8 mA. Ss were presented with a series of startle-eliciting noise bursts, preceded by a 300-ms footshock of one of the four intensities. Control trials consisting of the noise alone were also included. Startle amplitude was measured during the 100 ms immediately following the noise onset. Footshock reliably inhibited startle at all intensities; inhibition was near maximum at 0.2 mA. Morphine administration reliably interfered with the inhibition at all intensities, and this was reversed by naloxone administration. Data suggest that morphine may have a more general effect than is currently believed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of septal lesions on inter- and intraspecies aggression in rats.

Conducted 3 experiments with septally lesioned and sham-operated male Sprague-Dawley albino rats (n = 97). Septal lesions affected shock-induced fighting, mouse killing, and fighting in a dominance situation differentially, depending on situational and temporal variables. Immediately following the lesion, preoperatively dominant Ss became submissive in a food competition test, displayed increased fighting in response to electric shock, and killed mice. 15 days after surgery, these effects on fighting behavior were no longer present. If tested for the 1st time 10-15 days after the lesion, septal Ss maintained their dominance in the food competition test, did not show an increase in shock-elicited fighting, and did not turn into "killer" rats. The effects on the muricide response were not reversible once they had been induced. (32 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Habituation of the acoustic startle response in rats after lesions in the mesencephalic reticular formation or in the inferior colliculus.

Extensive damage to the mesencephalic reticular formation (MRF) in 24 male albino rats altered long-term habituation of the acoustic startle response without disrupting short-term habituation. The MRF lesions did not alter initial startle amplitudes, but the Ss with lesions were unable to attain as low a long-term asymptote of habituation as could 21 control Ss. Subsequent manipulation of stimulus intensity and interstimulus interval revealed no differences in short-term habituation between the 2 groups. Large lesions to the inferior colliculus (IC) of 22 Ss did not disrupt long-term habituation of the acoustic startle response, but these Ss were unable to suppress responding as much as controls to intense stimuli presented rapidly. The deficits in long-term habituation following MRF lesions suggest a disruption of an extrinsic, inhibitory mechanism of habituation. The deficits following IC lesions could have been due either to a disruption of a short-term habituation mechanism or to an increase in response sensitization produced by the lesions. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Lesions of the bed nucleus of the stria terminalis block sensitization of the acoustic startle reflex produced by repeated stress, but not fear-potentiated startle

1. The effects of lesions of the bed nucleus of the stria terminalis (BST) on the acquisition of conditioned fear were examined. In Experiment 1, BST lesions did not block acquisition of fear-potentiated startle to an explicit visual conditioned stimulus (CS) over 20 days of training. However, BST lesions blocked a gradual elevation in baseline startle also seen over the course of training. 2. The gradual increase in baseline startle was replicated in Experiment 2 without the presence of an explicit CS, using unoperated subjects. Experiment 2 showed that the elevation was due to repetitive exposure to shock, because unshocked control subjects did not show any elevation over sessions. 3. In Experiment 3, lesions of the BST did not disrupt rapid sensitization of the startle reflex by footshock, showing that different neural substrates underlie sensitization of startle by acute and chronic exposure to footshock. 4. These data indicate that the BST, despite its anatomical continuity with the amygdala, is not critically involved in the acquisition of conditioned fear to an explicit CS. Nevertheless, the BST is involved in mediating a stress-induced elevation in the startle reflex. This suggests that the BST and the CeA, which constitute part of the "extended amygdala" have complementary roles in responses to stress.     

Electrolytic lesions of the amygdala block acquisition and expression of fear-potentiated startle even with extensive training but do not prevent reacquisition.

Lesions of the amygdala have been shown to block the expression of fear-potentiated startle (increased acoustic startle in the presence of a cue previously paired with shock). In the present study, bilateral lesions of the central nucleus of the amygdala given after extensive training totally blocked the expression of fear-potentiated startle but did not prevent reacquisition. In contrast, when the lesions were made before any training, the lesioned rats did not show potentiated startle even with extensive training. Thus, the central nucleus of the amygdala normally seems to be required for the initial acquisition and expression of potentiated startle regardless of the degree of learning. However, reacquisition of potentiated startle can occur without the central nucleus, which implies the presence of a secondary brain system that can compensate for the loss of the central nucleus of the amygdala under some circumstances. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Augmentation of the rat's acoustic startle reflex by nonreflexogenic stimuli.

The size of the rat's acoustic startle reflex was augmented by brief acoustic clicks (which did not themselves elicit startle) presented several milliseconds before the reflex-eliciting stimulus (RS). The same clicks presented after the RS gave relatively weak augmentation that was present in the 1st, but not the 2nd, testing session. Brief footshocks set to 75% of each animal's flinch threshold augmented startle when presented both before and after the RS in both testing sessions. Augmentation by a leading footshock increased with shock intensity and also with the intensity of the RS. Augmentation by a trailing footshock increased with shock intensity and also with the intensity of the RS. Reflex size is not fixed at the time of reflex elicitation but can be augmented by a later nonreflexogenic stimulus. Reflex augmentation may be caused by the 2nd member of a stimulus pair discharging elements of the reflex pathway that were partially activated by the 1st. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cold water stress abolishes hyperactivity produced by cortical suction lesions without altering noradrenergic depletion.

Through the 30-day postoperative period following focal right hemisphere cortical suction lesions, lesioned and sham-operated control male Sprague-Dawley rats were placed in cold water for 5 min either 4 times at weekly intervals, once during the 1st postoperative week, or not at all. Results indicate different effects of the swim on lesioned and control Ss. Stress at weekly intervals produced hyperactivity in controls but weekly stress in lesioned Ss blocked the development of their expected hyperactivity. A single stress experience occurring 1 wk postoperatively was also sufficient to block the development of hyperactivity in lesioned Ss. Stress, although affecting behavior, did not alter the pattern of norepinephrine depletions in lesioned Ss. (19 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Failure to obtain sex differences in development of obesity following ventromedial hypothalamic lesions in rats.

Gave 24 male and 24 female albino Charles River rats either a high-fat or a ground-food diet following ventromedial hypothalamic or sham lesions. After 63 days on 1 diet, diets were reversed for 27 days. Over 63 days (a) lesioned Ss of both sexes showed a significant increase in weight over their controls, (b) Ss on high fat gained more weight than those on ground food, and (c) there was no difference between the sexes in weight gain. When diets were reversed, lesioned Ss now on ground food maintained about the same weight as before reversal, while Ss switched to the high-fat diet rapidly increased their body weight to a point near that of Ss originally on the high-fat diet. Data indicate that there is no sex difference in weight gain following ventromedial lesions. It is suggested that previously reported differences result from (a) insufficient periods of observation, (b) offering unpalatable diets, or (c) the use of random-bred strains which increases variability of animal size and lesion placement. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A neuroanatomical investigation of enhanced cutaneous and gustatory responsivity associated with septal forebrain injury.

Observed enhanced reactivity to cutaneous stimulation (handling and footshock) in 14 male Sprague-Dawley rats sustaining either large septal lesions or medial forebrain bundle ablations at the level of the septum. Cutaneously elicited hyperreactivity was not noted in 7 unoperated controls or 28 Ss with smaller septal lesions placed in the anterior, posterior, or dorsal septum or with lesions in the stria terminalis. All septal ablations but neither the medial forebrain bundle nor the stria terminalis lesions produced a gustatory hyperreactivity in the form of altered intakes of quinine and saccharin solutions. The gustatory hyperreactivity to quinine was clearly maximal in Ss with posterior ventral septal injury. Significantly, this lesion always extended into the medial preoptic nucleus. These results point to different neuroanatomical mechanisms in the septum underlying cutaneous- vs. gustatory-elicited behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

"Disruption of contextual freezing, but not contextual blocking of fear-potentiated startle, after lesions of the dorsal hippocampus": Correction to McNish et al (2000).

Reports an error in "Disruption of contextual freezing, but not contextual blocking of fear-potentiated startle, after lesions of the dorsal hippocampus" by Kenneth A. McNish, Jonathan C. Gewirtz and Michael Davis (Behavioral Neuroscience, 2000[Feb], Vol 114[1], 64-76). The captions for Figure 4 (p. 70) and Figure 5 (p. 72) were printed incorrectly. The caption used for Figure 4 should appear under Figure 5, and the caption used for Figure 5 should appear under Figure 4. (The following abstract of the original article appeared in record 2000-13470-005.) The role of the dorsal hippocampus in contextual fear conditioning was investigated with a contextual blocking paradigm. In Experiment 1, rats were given pairings of a light conditioned stimulus (CS) and footshock after preexposure either to footshock or to the context alone. The group preexposed to footshock showed poorer fear conditioning to the light CS, as measured by the fear-potentiated startle reflex. In Experiment 2, a group preexposed to footshock in the same context showed poorer fear conditioning to the light CS than did a group preexposed to footshock in a different context, indicating contextual blocking of fear-potentiated startle. In Experiment 3, lesions of the dorsal hippocampus had no effect on contextual blocking, even though contextual freezing was disrupted. The sparing of contextual blocking indicated that contextual memory was intact following hippocampal lesions, despite the disruption of contextual freezing. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Startle amplitude and fear in an acoustic startle paradigm: Lesions to the brachium of the inferior colliculus or the lateral tegmental tract.

In 2 Experiments, startle amplitude and startle stimulus-induced freezing (an index of fear) were measured in an acoustic startle response (ASR) paradigm in rats. Lesions to lateral tegmental tract (LTG), a pathway medial to brachium of the inferior colllciulus (BIC), significantly decreased freezing and produced a persistent 5-fold increase in ASR amplitude compared with sham-operated controls. Lesions to BIC increased both ASR amplitude (2-fold) and freezing. Neither BIC not LTG lesions affected startle amplitude when startle was elicited by a brief footshock stimulus. Characteristics of the lesion effects were tested with manipulations of interstimulus interval, stimulus intensity, and prepulse inhibition. The data suggest (a) an ascending pathway medial to BIC that carries the fear-inducing dimensions of an acoustic stimulus and (b) a descending pathway that provides tonic inhibition of the sensory input to the ASR circuitry. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The effects of two cognitive strategies on pain threshold.

While 1 arm was immersed in ice water, each of 48 female student nurses were asked either to imagine a situation that, if real, would be inconsistent with pain (relevant strategy) or imagine a situation unrelated to pain (irrelevant strategy), or they were not given special instructions (control group). Ss were further divided into those with high and low pain thresholds based on a pretest. The use of strategies (relevant or irrelevant) did not alter the pain thresholds for Ss with low thresholds. Among those Ss with high thresholds, use of a relevant strategy led to a greater increase in threshold than an irrelevant strategy, which, in turn, led to a greater increase than the control condition. Ss who were highly involved in their imaginings showed greater increases in pain threshold than those who were not. (25 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Differential behavioral effects of lesions of the medial or dorsal raphe nuclei in rats: Open field and pain-elicited aggression.

Electrolytic lesions were placed in either the dorsal or median raphe nuclei of 32 male adult Sprague-Dawley rats. Both lesions produced significant reductions in forebrain serotonin levels. Lesions of the dorsal nucleus produced a long-lasting increase in pain-elicited aggression, whereas median lesions were without effect. By contrast, lesions of the median nucleus produced significant increases in open-field activity, which began immediately and lasted for at least 3 mo, whereas lesions of the dorsal nucleus had no such effect. Similarly, when 22 Ss with dorsal or sham lesions were tested in an open field and then given a brief noncontingent footshock, their open-field activity was markedly reduced on the following day. Median Ss, however, showed little or no decrease in open-field activity on the day after footshock. Results suggest that the serotonin-containing neurons of the median raphe nucleus may exert an influence over the emotional responsivity of the rat. Overall results extend previous reports that lesions specific to the dorsal nucleus produce markedly different behavioral effects than lesions confined to the median nucleus. They also challenge the utility of manipulations that fail to take this into account. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cortical cholinergic impairment and behavioral deficits produced by kainic acid lesions of rat magnocellular basal forebrain.

The rat magnocellular basal forebrain (MNBF) is homologous to the human nucleus basalis of Meynert, a structure implicated in the cholinergic hypothesis of cognitive impairment in Alzheimer's disease (AD). In the present study, 18 male Sprague-Dawley rats with kainic acid lesions in the MNBF were compared with 6 unoperated controls, 10 sham-operated controls, and 6 controls injected with kainic acid in the cortical area directly above the MNBF. MNBF lesions depleted choline acetyltransferase in cortex but not in striatum or hippocampus. Cortical dopamine levels were unchanged; serotonin levels were unchanged in hippocampus and parietal cortex but decreased in frontal cortex. Compared with controls, MNBF-lesioned Ss were impaired in 24-hr retention, but not acquisition, of a passive avoidance task with escapable footshock. The groups did not differ in mean number of daily avoidances on a barpress active avoidance task, although learning was slower in MNBF-lesioned Ss. In a serial spatial discrimination reversal test, MNBF-lesioned Ss performed significantly worse than controls. This model may be useful for studying the role of the cholinergic system in memory and possibly for developing treatment strategies to alleviate the cognitive dysfunction of AD. (63 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sensitization of the acoustic startle reflex by footshock.

Administration of footshock (500-ms duration, 0.2–2.4 mA) increased the amplitude of the startle reflex for a long time after its presentation. The effect occurred with a single footshock, although its magnitude and consistency across animals were greater with 5 or 10 footshocks presented 1/s. The facilitatory effect came on within 2–4 min with a 0.6-mA shock, peaking in about 10 min and then dissipating over the next 40 min. Stronger shocks also increased startle, but with a more delayed onset of facilitation (8–20 min). Footshocks increased startle in rats not previously given startle-eliciting stimuli, indicating sensitization rather than dishabituation. The facilitatory effect may not be attributable to a rapid conditioning to the experimental context, because a change in lighting conditions from shock presentation to testing did not attenuate shock sensitization. This excitatory effect of shock on startle may represent the unconditioned effect of shock that can become associated with a neutral stimulus to support classical fear conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of mesencephalic reticular formation lesions on habituation of startle and lick suppression responses in the rat.

In 2 experiments with 43 male albino Holtzman rats, extensive damage to the mesencephalic reticular formation (MRF) altered long-term habituation of the acoustic startle response without disrupting short-term habituation. Ss with MRF lesions, although initially neither more nor less responsive than controls, could not attain as low a long-term asymptote of habituation as could control Ss with repeated presentations of an auditory stimulus. Changing the quality of the auditory stimulus abolished the asymptotic difference in responsiveness. With repeated presentations of the 2nd auditory stimulus, control Ss again reached a significantly lower long-term habituation asymptote than did Ss with MRF lesions. The course of long-term habituation for the 2 groups suggested a disruption of an extrinsic, inhibitory habituation process by the lesions. The effects of MRF lesions were specific to the acoustic startle response. Control Ss and those with lesions showed comparable response levels, short-term habituation, and long-term habituation of the lick suppression response. Responsiveness and habituation to tactile stimuli were comparable for the 2 groups on both lick suppression and startle response measures. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)