Dissociation of tactile and acoustic components in air puff startle

Tactile (air puff) or acoustic startle stimuli elicit behavioral (motor) and complex cardiovascular responses which include pressor as well as cardiac decelerative and accelerative responses. An acoustic component of the air puff stimulus (12.5 psi) was identified. Studies were conducted to separate the contributions of both stimulus modalities to the observed responses. The acoustic component was approximated with a wide-spectrum 97-dB white-noise stimulus. This acoustic stimulus failed to evoke heart rate responses but did yield motor and pressor responses. In a second approach, tympanic membrane rupture (TMR) was used to interrupt acoustic sensory stimuli. TMR fully abolished the motor and pressor responses to acoustic startle. With air puff startle, while TMR severely attenuated the motor response it only decreased slightly the pressor and cardiac accelerative responses and failed to influence the cardiac decelerative component. Our results indicate that air puff startle contains both tactile and acoustic modalities. Further, the motor response is largely driven by the acoustic modality since TMR abolished this response elicited by either acoustic or tactile stimulation. More importantly, motor and cardiovascular responses to startle may be separated through discrimination of afferent stimuli suggesting either differences in neural pathways for acoustic and tactile stimuli or a differential dependency of the various responses on stimulus characteristics.     

Evidence for a dissociation between cardiovascular and behavioral reactivity in the spontaneously hypertensive rat

Spontaneously hypertensive rats of the Okamoto strain (SHR) were compared with normotensive rats of the Wistar-Kyoto strain (WKY) on the acoustic startle response in rats prepared for simultaneous blood pressure recordings. Blood pressure was continuously recorded by means of an indwelling cannula in the caudal tail artery. The presentation of the startle stimulus caused a blood pressure response in both strains consisting of an initial increase in blood pressure followed by a decrease and after that a longer lasting, but less pronounced second increase in pressure. The startle-elicited increase in blood pressure was significantly elevated in SHRs and at the same time the acoustic startle response was depressed as compared to WKY rats. These data indicate a dissociation between cardiovascular and behavioral reactivity in the SHR.     

Differential cardiovascular responses to stressors in hypertensive and normotensive rats

The aim of this study was to determine to what extent stress-induced cardiovascular responses depend upon rat strain and/or stressor. Spontaneously hypertensive rats (SHRs), Wistar-Kyoto rats (WKYs) and Sprague-Dawley (SD) rats were implanted with telemetry probes in order to measure heart rate and blood pressure changes when exposed to a stressor. The stress protocols employed included handling, air-jet and restraint, where each stressor was repeated over 10 consecutive days. In addition, a heterologous protocol was established whereby the experimental groups having experienced 10 days of air-jet stress were then immediately exposed to 10 consecutive days of restraint. Each stressor caused graded tachycardic and pressor responses in all strains. For all strains, the magnitude and duration of heart rate and blood pressure increases were greatest in the restraint-based protocols while handling and air-jet caused submaximal changes. A comparison between strains indicated that SHRs exhibited prolonged pressor responses to each of the stressor types tested as compared to the normotensive strains. In addition, repeated exposure over 10 days to handling and air-jet in SHRs caused tachycardic and/or pressor responses to adapt to 'normotensive-like' levels. Heterologous restraint stress caused sensitization of cardiovascular responses upon first exposure, predominantly in normotensive strains. Collectively these data show that the magnitude and duration of the tachycardia and pressor responses evoked by the stressors were different within the strains and were also modified by prior experience. In addition, the cardiovascular profiles presented in this study demonstrate that, within each strain, the heart rate response during stress is graded according to the type of stressor encountered.     

Influence of neonatal handling on blood pressure,locomotor activity,and preweanling heart rate in spontaneously hypertensive and Wistar Kyoto rats

This experiment tested the hypothesis that increased stimulation early in development would (a) alter developmental changes in heart rate and behavioral reactivity and (b) affect the level at which blood pressure was regulated in adulthood. For this purpose, the effects of daily handling and maternal separation (3 min per day) on both behavioral and cardiovascular measures were examined in spontaneously hypertensive (SHR) and normotensive control Wistar Kyoto (WKY) rats. Prior to weaning, elevated heart rates in pups handled during the first postnatal week were most pronounced among 4-week-old prehypertensive SHR pups. Early handling affected behavior observed during openfield testing similarly in young adult rats of the SHR and WKY strains (e.g., increased locomotor activity on the first day of testing). In female rats of the WKY strain, early handling resulted in a lower baseline blood pressure; the blood pressure; the blood pressure of SHR rats was not affected by increased stimulation in infancy. Examination of longitudinal data yielded no support for a direct association between behavioral reactivity or preweaning heart rate and high blood pressure. These findings demonstrate the influence of both early environmental conditions and genetic factors on maturation within the cardiovascular system and suggest that genetic models of pathological conditions may provide a productive means of examining environmentally shaped aspects of individual differences in physiological regulation.     

Cochlear and trigeminal systems contributing to the startle reflex in rats.

The startle reflex is evoked by strong acoustic or tactile stimuli, or by electrical stimulation of acoustic or tactile pathways. To dissociate the contributions of acoustic and tactile pathways, stimulating electrodes were placed in adjacent cochlear and trigeminal nuclei. The currents needed to evoke startle-like responses were an order of magnitude lower in ventral trigeminal sites (12-80 microA for a 0.1-ms pulse) than in cochlear nucleus sites (150-800 microA). At low threshold sites in both areas, brief acoustic stimuli were followed 0-4 ms later by a single electrical pulse and the current required to evoke startle was measured at several interstimulus intervals. Summation between the acoustic and electrical stimuli for startle was strong in both cochlear and trigeminal sites. Collision effects were found in the anteroventral cochlear nucleus when the electrical stimulus followed the ipsilateral acoustic stimulus by 2.0 ms, suggesting that acoustic startle is mediated by axons in the anteroventral cochlear nucleus. Collision effects were found at 4.0 ms if the electrical stimulus was presented in the contralateral pontine reticular formation, suggesting that acoustic signals mediating startle mainly cross to the pontine reticular formation. Collision effects were not found in medial or posterior sites in the cochlear nucleus, or trigeminal sites, suggesting that the neurons that mediate startle in these sites do not mediate acoustic startle. Therefore, acoustic startle is mediated through high threshold cochlear nucleus sites, while low threshold sites are non-acoustic, probably as a result of trigeminal or vestibular stimulation.     

Experimental dissociation of behavioral and cardiovascular outcome in the borderline hypertensive rat

F1 Offspring of hypertensive and normotensive rats (BHR) were reared with either hypertensive (SHR) or normotensive (WKY) cagemates, and observations were conducted at two developmental periods to assess the effects of rearing condition on the social environment and the behavior of BHR subjects. SHR displayed significantly more agonistic behavior during development than WKY, and BHR subjects reared with SHR were the targets of significantly more agonistic behavior than BHR subjects reared with WKY cagemates. BHR reared with SHR initiated twice as much agonistic behavior as BHR reared with WKY. When heart rate and blood pressure were assessed at 75-80 days of age, however, neither the alterations in developmental social environment nor the alterations in the behavioral characteristics of BHR were associated with differences in cardiovascular variables. The results do not support a causal connection between behavioral characteristics and cardiovascular outcome.     

Renal vascular resistance and reactivity in the spontaneously hypertensive rat.

Renal vascular resistance is elevated in spontaneously hypertensive rats (SHR) when compared to normotensive control Wistar-Kyoto rats (WKY). The present study examined possible determinants of this raised vascular resistance in in situ autoperfused kidneys of pentobarbital-anesthetized, 12- to 16-wk-old SHR and WKY. Over a wide range of arterial pressures (30--100 mmHg) renal blood flow was consistently higher in WKY than in SHR. This relative flow difference was unchanged by acute renal denervation, with renal vascular resistance decreasing approximately 20% in both strains. Changes in renal vascular resistance to renal nerve stimulation and the administration of intra-arterial vasoactive hormones also were assessed. Vascular responses to renal nerve stimulation, tyramine, angiotensin II, and acetylcholine were similar in kidneys of the two strains, but reactivity to norepinephrine was significantly less in kidneys of SHR. It was concluded that elevated renal vascular resistance in the SHR does not result from an excessive neurogenic influence on the renal vasculature or from vascular hyperreactivity to norepinephrine or angiotensin II.     

Long-lasting cardiovascular depressor response to somatic stimulation in spontaneously hypertensive rats.

It has been known that a short-lasting stimulation of the somatic afferent nerves elicits either a depressor or a pressor response depending on the stimulus parameters (Johansson 1962). In the present study cardiovascular responses were observed during and after a long-lasting sciatic nerve stimulation in conscious spontaneously hypertensive rats (SHR) and their normotensive controls, the Wistar Kyoto rats (WKR).     

Differences in response to an acoustic startle stimulus among forty-six rat strains

The startle response to intense environmental stimuli is found in most, if not all, animal species. Previous studies have shown that selected rodent strains differ in startle response to an acoustic stimulus, suggesting genetic variability. The current experiment was designed to extend these differences to a wider range of rat strains. Forty-six inbred and outbred rat strains were studied. These strains exhibited differences in both the mean amplitude of the startle response and the rate of habituation to startle stimuli over repeated trials. In addition, there was a significant relationship between these measures. These results suggest that robust phenotypic differences in startle response exist among rat strains. As previous investigations have demonstrated a direct relationship between the startle response and other behavioral end points, the use of strain differences in startle response may be an effective way to determine genetic contributions to specific behavioral responses.     

Kynurenate in the pontine reticular formation inhibits acoustic and trigeminal nucleus-evoked startle, but not vestibular nucleus-evoked startle

The startle reflex is elicited by acoustic, trigeminal or vestibular stimulation, or by combinations of these stimuli. Acoustic startle is mediated largely by ibotenate-sensitive neurons in the ventrocaudal pontine reticular formation (PnC). In these studies we tested whether startle elicited by stimulation of different modalities is affected by infusion of the non-selective glutamate antagonist, kynurenate, into the PnC. In awake rats, startle responses evoked by either acoustic or spinal trigeminal nucleus stimulation were inhibited by kynurenate, but not saline, infusions, with the most effective placements nearest PnC. In chloral hydrate-anesthetized rats, kynurenate in the PnC reduced trigeminal nucleus-evoked hindlimb EMG responses, but not vestibular nucleus-evoked startle. Kynurenate in the vestibular nucleus had no effect on trigeminal nucleus-evoked startle. These results indicate that trigeminal nucleus stimulation evokes startle largely through glutamate receptors in the PnC, similarly to acoustic startle, but vestibular nucleus-evoked startle is mediated through other pathways, such as the vestibulospinal tract.     

Interaction between "mental stress" and baroreceptor reflexes concerning effects on heart rate, mean arterial pressure and renal sympathetic activity in conscious spontaneously hypertensive rats

Spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared concerning the interactions between cortico-hypothalamic alerting responses and baroreflex influences on neurogenic cardiovascular control. For this purpose mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were continuously recorded during night time in conscious, otherwise undisturbed rats. Baroreceptor sensitivity was assessed as percentage HR and RSNA reductions per mmHg MAP elevation when a standardized phenylephrine infusion was performed. A state of acute "mental stress" could be induced by a likewise standardized sudden blowing of air. These two opposing influences on neurogenic cardiovascular control were also experimentally superimposed in various ways and the effects on MAP, HR and RSNA followed. During "rest" RSNA was higher in SHR than in WKY and it also increased more during "mental stress". The baroreflex sensitivity was clearly reduced in SHR and WKY concerning HR reduction (0.44 +/- 0.06 vs. 0.78 +/- 0.08%/mmHg; p less than 0.01) but not so concerning RSNA, which was similar in SHR and WKY (2.6 +/- 0.2 vs. 2.9 +/- 0.4%/mmHg). If expressed (HR + 1 +/- 3%; p less than 0.025 vs. SHR and RSNA + 11% +/- 10, p less than 0.01 vs. SHR). These results) (0.10 +/- 0.02 vs. 0.06 +/- 0.01 microV/mmHg; p less than 0.12). Also single fibre recordings in anaesthetized rats showed the same principle difference between SHR and WKY.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sensitivity of pressor responses to central hypertonic saline is greatly enhanced even in pre-hypertensive spontaneously hypertensive rats

It has been suggested that intracerebroventricular injection of hypertonic saline mimics the effects of a high salt diet in spontaneously hypertensive rats (SHR), a genetic model of hypertension. Intracerebroventricular injection of hypertonic saline produces an increase in blood pressure and the pressor response to hypertonic saline is enhanced in adult hypertensive SHR. In this study, we examined whether the intracerebroventricular hypertonic saline-induced pressor response is enhanced even in pre-hypertensive SHR. The basal mean blood pressure was almost the same in 4-week-old SHR and age-matched Wistar Kyoto rats (WKY), whereas it was greater in 15-16-week-old SHR than in age-matched WKY. Intracerebroventricular injection of hypertonic saline (10 microl of 230 mM NaCl) produced an increase in blood pressure in both 4-week-old and 15-16-week-old SHR, whereas it did not affect blood pressure in both age-matched WKY. Intracerebroventricular injection of hypertonic saline (10 microl of 260 mM NaCl) produced an increase in blood pressure in all rats but the pressor response was greater in both 4-week-old and 15-16-week-old SHR than in respective age-matched WKY. Intracerebroventricular injection of Phe-Met-Arg-Phe amide (FMRF), an FMRF-inducible sodium channel activator, produced an increase in blood pressure in all rats but the pressor response was greater in SHR than in WKY at both ages. These findings indicate that the sensitivities of pressor responses to intracerebroventricular hypertonic saline and FMRF are enhanced not only in hypertensive but also in pre-hypertensive SHR.     

Contributions of the vestibular nucleus and vestibulospinal tract to the startle reflex.

The startle reflex is elicited by strong and sudden acoustic, vestibular or trigeminal stimuli. The caudal pontine reticular nucleus, which mediates acoustic startle via the reticulospinal tract, receives further anatomical connections from vestibular and trigeminal nuclei, and can be activated by vestibular and tactile stimuli, suggesting that this pontine reticular structure could mediate vestibular and trigeminal startle. The vestibular nucleus, however, also projects to the spinal cord directly via the vestibulospinal tracts, and therefore may mediate vestibular startle via additional faster routes without a synaptic relay in the hindbrain. In the present study, the timing properties of the vestibular efferent pathways mediating startle-like responses were examined in rats using electrical stimulation techniques.Transient single- or twin-pulse electrical stimulation of the vestibular nucleus evoked bilateral, startle-like responses with short refractory periods. In chloral hydrate-anesthetized rats, hindlimb electromyogram latencies recorded from the anterior biceps femoris muscle were shorter than those for stimulation of the trigeminal nucleus, and similar to those for stimulation of the caudal pontine reticular nucleus or ventromedial medulla. In awake rats, combining vestibular nucleus stimulation with either acoustic stimulation or trigeminal nucleus stimulation enhanced the whole-body startle-like responses and led to strong cross-modal summation without collision effects. In both chloral hydrate-anesthetized and awake rats, combining vestibular nucleus stimulation with ventromedial medulla stimulation produced a symmetrical collision effect, i.e. a loss of summation at the same positive and negative stimulus intervals, indicating a continuous connection between the vestibular nucleus and ventromedial medulla in mediating vestibular startle. By contrast, combining trigeminal nucleus stimulation with ventromedial medulla stimulation resulted in an asymmetric collision effect when the trigeminal nucleus stimulation preceded ventromedial medulla stimulation by 0.5 ms, suggesting that a monosynaptic connection between the trigeminal nucleus and ventromedial medulla mediates trigeminal startle.We propose that the vestibulospinal tracts participate strongly in mediating startle produced by activation of the vestibular nucleus. The convergence of the vestibulospinal tracts with the reticulospinal tract within the spinal cord therefore provides the neural basis of cross-modal summation of startling stimuli.     

Effects of Cross Fostering on Open-Field Behavior, Acoustic Startle, Lipopolysaccharide-Induced Corticosterone Release, and Body Weight in Lewis and Fischer Rats

Lewis (LEW/N) and Fischer (F344/N) rats differ on a myriad of behavioral and physiological endpoints, some of which have been reported to be affected by maternal experience in outbred rats and other strains. To assess whether epigenetic factors contribute to the differential behavioral responses to stress and pro-inflammatory challenges in these strains, the effects of cross fostering on open-field, acoustic startle, and glucocorticoid reactivity to lipopolysaccharide (LPS) were examined in the present experiment. In the open-field test, although in-fostered female LEW/N and F344/N strains did not differ, female LEW/N rats displayed significantly greater activity than female F344/N rats in the cross-fostered condition. Differences between males of the two strains were increased by cross fostering, with the LEW/N strain displaying greater total activity. In acoustic startle, there was little strain difference between in-fostered or cross-fostered female rats. On the other hand, in-fostered male LEW/N rats had a significantly greater startle response than in-fostered male F344/N rats, an effect that was dramatically reduced by cross fostering. In-fostered female LEW/N rats displayed a blunted corticosterone response relative to in-fostered female F344/N rats, an effect that was reduced by cross fostering. Conversely, although there was no strain difference between male in-fostered rats, cross-fostered male F344/N rats displayed a significantly greater corticosterone response to LPS than cross-fostered male LEW/N rats. Finally, body weight differences between in-fostered LEW/N and F344/N rats were reduced by cross fostering. Together, these data illustrate that maternal factors play a role in the behavioral and physiological responses to stress between the two strains.     

Sympathetic-adrenal medullary response to stress in hyperactive and hypertensive rats

Sympathetic-adrenal medullary hyperreactivity to acute stress, measured as an exaggerated elevation of plasma epinephrine and norepinephrine levels in response to footshock, was examined in four genetically related, inbred rat strains, all derived from the Wistar-Kyoto rat (WKY). These four strains are endowed with the traits of hypertension and behavioral hyperactivity, expressed either together (in SHR), or separately in two new strains (Wistar-Kyoto hyperactive rats, WK-HA, and Wistar-Kyoto hypertensive rats, WK-HT), or not at all (in WKY). Male rats of the SHR, WKY, WK-HA and WK-HT strains were subjected to acute footshock stress in order to determine whether the previously reported hyperreactivity of the SHR is attributable to the hypertensive trait, or to the behavioral hyperactivity trait, both of which are characteristic of the SHR. Plasma catecholamine levels were determined prior to, immediately following, and 5 min following acute footshock stress. We report here that the WK-HA strain (hyperactive but not hypertensive) exhibited the hyperreactivity characteristic of SHRs, and not the WK-HT strain (hypertensive but not hyperactive). We conclude that the exaggerated sympathetic-adrenal medullary response to acute stress is associated with the hyperactivity trait and not with hypertension among these congenic rat strains.     

Attenuation of conducted vasodilatation in rat mesenteric arteries during hypertension: role of inwardly rectifying potassium channels

The present study was designed to elucidate whether the conduction of vasomotor responses mediated by endothelium-derived hyperpolarizing factor (EDHF) in rat mesenteric arteries is altered during hypertension. Iontophoresed acetylcholine (ACh; 500 ms) caused EDHF-mediated hyperpolarization and vasodilatation at the local site and these responses spread through the endothelium to remote sites in 12-week-old Wistar-Kyoto rats (WKY). Conducted responses were significantly attenuated in age-matched spontaneously hypertensive rats (SHR) although the rate of decay with distance did not change. Inhibition of inwardly rectifying potassium (Kir) channels (30 μ m barium) eliminated the difference between WKY and SHR by attenuating conducted responses in WKY but not SHR. At the local site, barium (30 μ m ) significantly reduced the duration but not the amplitude of ACh-induced hyperpolarization in WKY only. Barium had no effect when the iontophoretic stimulus was reduced to 350 ms. After blockade of EDHF in SHR, ACh elicited a depolarization which our indirect data suggest spreads along the vessel in the endothelium. Messenger RNA expression of Kir2.0 genes did not differ between the strains nor did the amplitude of K⁺-induced hyperpolarization, which was abolished by disruption of the endothelium. Immunohistochemistry revealed a decrease in connexin (Cx)37 but not Cx40 or Cx43 protein in endothelial cells of SHR compared to WKY. Results suggest that conduction of EDHF-mediated responses in WKY, but not in SHR, is facilitated by activation of Kir channels at the site of ACh application and not by differences in endothelial connexin expression. Lack of Kir channel involvement in hypertension may result from reduction in the duration of the hyperpolarization due to the development of ACh-mediated depolarization, rather than to any difference in Kir subunit expression or function.     

Differences in striatal spiny neuron action potentials between the spontaneously hypertensive and Wistar-Kyoto rat strains

The spontaneously hypertensive rat (SHR) and the Wistar-Kyoto (WKY) inbred rat strains display behavioral differences characterized by relative increases and decreases in levels of activity. Both strains have subsequently been utilized as animal models of hyperactive and hypoactive behavioral traits. The etiology of these behavioral characteristics is poorly understood, but may stem from alterations in the physiology of selected neural circuits or catecholamine systems. This study investigated the cellular properties of neurons from three genetically related strains: the SHR; WKY; and Wistar (WI). In vivo intracellular recordings were made under urethane anesthesia from spiny projection neurons in the striatum, a brain area involved in behavioral activation. Results obtained from 71 spiny projection neurons indicate that most cellular properties of these neurons were very similar across the three strains. However, the amplitude and half-duration of both spontaneously occurring and current-evoked action potentials were found to be significantly different between the SHR and WKY strains with neurons from the SHR firing action potentials of relatively greater amplitude and shorter duration. Action potential parameters measured from the WI rats were intermediate between the two other strains. These differences in action potentials between two behaviorally distinct strains may reflect altered functioning of particular membrane conductances.     

Stimulus specificity in the habituation of the startle response in the rat

A series of experiments evaluated whether the habituation of the startle response of the rat to tactile and auditory cues is stimulus specific. Experiment 1 showed stimulus specificity of a short-term habituation effect, whereby the startle to the second of a pair of stimuli was significantly less when the initial stimulus involved the same rather than the different modality. Experiments 2 and 3 focused on the more persistent decrement in startle that is a result of repeated stimulation, and demonstrated that such long-term habituation to the tactile and auditory stimuli contained a stimulus specific component in addition to a generalized component. The generalized habituation observed between the tactile and auditory stimuli in the three experiments may be due to an auditory accompaniment of the tactile stimulus employed. Discussion emphasized the utility of investigating habituation in a preparation with robust specificity.     

Strain differences in Fos expression following airpuff startle in Spontaneously Hypertensive and Wistar Kyoto rats

The airpuff startle stimulus elicits both a behavioral and a concurrent sympathetic and parasympathetic activation, which have been shown to differ between inbred normotensive Wistar Kyoto and Spontaneously Hypertensive rat strains. Neither the brain sites responsible for the cardiovascular and motor responses, nor the origins of the strain differential responses, have yet been elucidated. The goals of the present study were (i) to define the neuronal pattern of immunoreactive Fos expression to the airpuff stimulus, and (ii) to determine whether this pattern of expression differed between the two contrasting inbred rat strains, thereby relating to observed differences in response. The airpuff stimulus induced Fos protein expression in discrete nuclei within the hypothalamus, thalamus, midbrain, pons and medulla of both strains, with strain-dependent differences evident in the hypothalamus (lateral, ventromedial and dorsomedial), pons (locus coeruleus) and medulla (rostroventrolateral medulla and solitary tract nuclei). To remove Fos expression arising from test chamber novelty, which was observed in both strains, a subset of animals was habituated to the test chamber for four days prior to testing. Habituation reduced Fos expression in several brain regions in the Wistar Kyoto, but failed to do so in the Spontaneously Hypertensive rat. The present results are the first to identify a set of brain regions likely to be responsible for the mediation of the cardiovascular and motor responses associated with the airpuff startle stimulus. Several of the identified areas contain neurotransmitters implicated by prior pharmacological studies. Further, these data identify differences in the degree of activation of specific neuronal structures that probably underlie strain differences in the cardiovascular response to the airpuff. Additionally, the results provide a cellular correlate to reported deficits in behavioral habituation by the Spontaneously Hypertensive rat and suggest a potentially profound difference between the ability of these two strains to adapt to repeated mild stress stimuli.     

Spontaneously hypertensive and Wistar Kyoto rats differ in delayed matching-to-place performance and response to dietary long-chain polyunsaturated fatty acids

Spontaneously hypertensive rats (SHR) were used as an animal model of attention deficit hyperactivity disorder (ADHD). This study investigated whether, in comparison with its progenitor strain, Wistar-Kyoto rats (WKY), SHR would show deficits in spatial short-term memory in the delayed-matching-to-place (DMP) version of the Morris water maze and be more distracted by exposure to a novel stimulus during recall trials. It also addressed whether dietary supplementation with long-chain polyunsaturated fatty acids (LCPUFA) during development would increase brain docosahexaenoic acid (DHA) and improve SHR behavioral performance. Beginning at weaning (21 days), male SHR and WKY were fed either a control or LCPUFA supplemented diet [0.5% arachidonic acid (AA) and 0.9% DHA], and behavioral testing began at 8 weeks. The first three tasks comprised a series of problems, each consisting of an initial search trial and subsequent recall trials. The intertrial interval (ITI) between the search and recall trial was either 60 s or 60 min. Surprisingly, in contrast to SHR, WKY did not appear to use a spatial short-term memory strategy to solve the problem. Notwithstanding, the performance of both strains was affected by the delay, such that they showed longer path lengths at the long compared with the short ITI. There was no effect of dietary supplementation on DMP performance. SHR fed the control diet were less responsive to a novel stimulus introduced on the first recall trial than WKY, and this tended to increase with supplementation. Analysis of brain fatty acid composition indicated that supplementation did increase DHA in the phosphatidylethanolamine fraction in WKY; however, in SHR, there was either no change (phosphatidylethanolamine) or paradoxical decreases (phosphatidylcholine and phosphatidyserine/phosphatidylinositol). Further research is needed to determine whether SHR are an appropriate model for studying a possible relationship between dietary LCPUFA and the behavioral symptoms of ADHD.