Pharmacological evidence for the central serotonergic effects of monomethoxyamphetamines

The effects of three monomethoxyamphetamines, dl-para-methoxyamphetamine (dl-PMA), dl-meta-methoxyamphetamine (dl-MMA) and dl-ortho-methyoxyamphetamine (dl-OMA), and d-amphetamine (d-A) on the myoclonic twitch activity (MTA) of PMA, MMA and d-A were found to increase the MTA but OMA was ineffective. The increased MTA induced by d-A was not influenced by the blockade of 5-hydroxytryptamine (5-HT) receptor by methysergide or inhibition of 5-HT synthesis by para chlorophenylalamine (PCPA) but was reduced by haloperidol which blocked the dopamine receptor. On the other hand, the increased MTA produced by PMA was not influenced by haloperidol but was reduced by methysergide and PCPA. The increased MTA induced by MMA was not effectively blocked by either PCPA or haloperidol but was blocked by the combination of both PCPA and haloperidol. The results indicate that whereas the increased MTA produced by d-A is not dependent on the availability of 5-HT, PMA exerts by a release of 5-HT and that the MMA effect is due to a release of both 5-HT and dopamine. High doses of PMA and MMA increased the locomotor activity arevious biochemical findings that PMA releases 5-HT in brain tissue and suggests that PMA exerts its pharmacological effects by releasing 5-HT.     

5-HT2A/2C receptor agonists potentiate the discriminative cue of (+)-amphetamine in the rat

The possible effect of 5-HT2A/2C receptor agonists on an amphetamine-induced behavioral response was examined using the two-lever drug discrimination paradigm. The experiments were designed to investigate an interaction of the hallucinogenic 5-HT2A/2C agonists lysergic acid diethylamide (LSD) and 2,5-dimethoxy-4-iodoamphetamine (DOI), with the discriminative stimulus elicited by a relatively low dose of (+)-amphetamine (1.35 micromol/kg, 0.25 mg/kg, which produced approximately 50% selection of the drug lever). DOI and LSD did not produce amphetamine-like responding at any dose tested or time of administration. However, LSD alone was able to induce a drug-appropriate response in two of nine amphetamine-trained rats. Simultaneous administration of DOI or LSD with amphetamine was not significantly different from the response produced by amphetamine alone. Pre-administration of DOI (3 hr) or of LSD (2 hr) before amphetamine, however, evoked significant enhancement of the amphetamine cue. The results suggest that the enhanced behavioral response to amphetamine may be due either to an increased sensitivity of dopaminergic neurons in the mesolimbic area, or to an enhanced release of dopamine by amphetamine.     

Serotonin and fear retention in the rat.

Parachloramphetamine (PCA), which releases serotonin (5-hydroxytryptamine, 5-HT) stores in brain regions, injected (5 mg/kg, ip) into male Sprague-Dawley rats 30 min prior to the presentation of 4 inescapable shocks resulted in a profound fear-retention deficit as characterized by the total loss of the freezing and immobility posture that is normally the aftermath of shock presentation. The "PCA effect" on fear retention was found at the 2.5 mg/kg but not at the 1.25 mg/kg dose, and when PCA (5 mg/kg) had been injected at least 8 hrs before conditioning. The selective 5-HT uptake inhibitors zimelidine and fluoxetine, but not the noradrenaline (NA) uptake inhibitor desipramine, blocked the PCA effect, as did the 5-HT antagonist methergoline, but not the selective dopamine antagonist pimozide. A total retention impairment with a conditioning-testing delay of just 60 min was also evidenced, and the administration of PCA up to 2 hrs before fear-retention testing also produced the retention deficit, suggesting a "retrieval failure." The 5-HT specificity of the PCA effect on fear retention was established by the demonstration that 5-HT-depleted Ss, but not NA-depleted Ss, showed a nearly complete blockade of the fear-retention deficit. These experiments describe a role for 5-HT in both memory storage and retrieval processes. (72 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Vesicular and juxtavesicular serotonin: effects of lysergic acid diethylamide and reserpine

An extensive analysis of subcellular serotonin (5-HT) compartmentation with and without reserpine was undertaken in order to localize further the effect of LSD on rat brain 5-HT. Modification of the subfractionation procedure resulted in an increase in purity of fractions and a decrease in variability of 5-HT content. With the modified procedure, the administration of LSD produced a significant increase in 5-HT in the nerve-ending fraction prepared from rat whole brain. LSD caused a 50% increase in 5-HT in the vesicular fraction which was recovered after osmotic disruption of nerve-endings. The increase of 5-HT in the vesicular fraction after LSD was not demonstrable in rats treated with reserpine for as long as 2 weeks postreserpine. Instead, with reserpine pretreatment the LSD-induced increase in 5-HT was localized to the intrasynaptosomally derived "end supernatant" as early as 48 hours postreserpine. Thus, an unanticipated "juxtavesicular" site capable of 5-HT retention or binding was detected. In crude subcellular fractions, by contrast, significant increase in 5-HT were not observed with LSD administration until 4 days after reserpine, at which time at least a 50% 5-HT repletion had occurred. This study of drug interactions suggests a juxtavesicular compartment that may be of functional importance in presynaptic binding or transport of 5-HT.     

Role of glucocorticoids in an abnormal grooming behavior in cats with pontile or frontal neocortical lesions.

Cats with pontile or frontal neocortical lesions display a tactually elicited dissociation of appetitive and consummatory grooming behaviors. In the present study with 75 adult male cats, systemic administration of glucocorticoids abolished the abnormal grooming behavior in cats with lesions, even when the stimulatory effect of glucocorticoids on serotonin metabolism was blocked by administration of para-chlorophenylalanine (PCPA). Microinjections of glucocorticoids into the superior colliculi also significantly decreased the abnormal grooming behavior. Adrenalectomized Ss did not display the abnormal grooming behavior, but the abnormal behavior did occur in PCPA-treated adrenalectomized Ss. Administration of either glucocorticoids or 5-hydroxytryptophan abolished the abnormal behavior in PCPA-treated adrenalectomized Ss. Thus, it appears that the pontile and frontal neocortical lesions produce deficits in both glucocorticoids and serotonin, and these deficits are necessary and sufficient conditions for inducing the abnormal grooming behavior. (31 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Drugs and placebos: The effects of instructions upon performance and mood under amphetamine sulfate and chloral hydrate.

The experiment reports the effects of appropriate and inappropriate instructions and 2 drugs (.5 g chloral hydrate and 10 mg racemic amphetamine sulphate) on motor performance and mood measures. The Ss were 90 older men randomly assigned to 9 experimental groups. The design used was expansion of a model design involving Drug Disguised groups, Placebo groups (300 mg lactose), an Untreated group, and Amphetamine, Chloral Hydrate, and Neutral instructions. The drugs and placebos were given to the Ss in capsules, and all Ss received orange juice, which was also the vehicle for the disguise. The Untreated group received orange juice only. Instructions alone affected performance, but had little or no effect on mood. Instructions appropriate to the presumed drug effects produced performance deterioration on the simple motor tasks used. Instructions inappropriate to the presumed drug effects counteracted much of the drug produced decrement. A slight decrement in performance was found in the Placebo group which received Amphetamine instruction. Amphetamine treated Ss produced reports of greater comfort on the mood index than did chloral hydrate. On the other hand, the chloral hydrate instructions resulted in greater comfort than the Amphetamine instructions. There was no interaction between drug effects and instructional effects. The 2 Placebo groups did not differ significantly on the mood index. The effects of instructions on mood were found only when the drug was present. Several suggestions are offered for further research. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cholinergic influences in habituation of exploratory activity in mice.

Injected 30 male mice, chosen from a random-bred strain (ICR), with either saline, scopolamine, or methscopolamine. Ss were then allowed to explore a chamber, and locomotor activity was monitored every 7.5 min by photocells. Ss treated with saline and methscopolamine displayed a significant decrement in activity over the course of an exposure session, but Ss injected with scopolamine did not show this decrement. The decline in activity over time was considered to reflect habituation of exploratory responses in a novel environment. Results are interpreted in terms of the disruptive effects of scopolamine on habituation. It is concluded that activity of brain acetylcholine is critical to the process of habituation of locomotor activity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Changes in the central and peripheral serotonergic system in rats exposed to water-immersion restrained stress and nicotine administration

The effects of water-immersion restraint stress (WS) on chronically nicotine-administered rats were studied in the blood and various regions of the brain. Serotonin (5-HT) levels increased in the hypothalamus, hippocampus, cortex and cerebellum following the administration of nicotine. 5-HT levels increased in all the brain regions following stress. Nicotine decreased stress-induced increased levels of 5-HT in the hippocampus and cerebellum. Nicotine administration alone increased 5-hydroxyindole acetic acid (5-HIAA) levels in the hippocampus and cerebellum. Stress alone also increased 5-HIAA levels in all the brain regions. In the cortex, 5-HT and 5-HIAA levels further increased following the administration of a combination of stress and nicotine compared to rats given stress alone. In the blood as well as in all the brain regions, except the cerebellum, stress or nicotine administration did not affect tryptophan levels. Stress given to nicotine-administered rats resulted in a decrease in tryptophan levels in the blood and plasma. Although 5-HT and 5-HIAA levels were not influenced by stress and/or nicotine administration, the 5-HIAA/5-HT ratio increased in the blood and plasma of rats administered with nicotine and exposed to stress. The effects of nicotine on the serotonergic system depend upon the kind of stress given together with the organs and brain regions involved.     

The effect of infant colic on maternal self-perceptions and mother-infant attachment

The 5-HT2A and 5-HT2C antagonists MDL 100,907 and SER-082 were tested with the 5-HT2A/C agonist DOI and the 5-HT1A/2A/2C agonist LSD in the Behavioral Pattern Monitor, which provides multiple measures of locomotor and investigatory activity. Previous investigations have shown that these measures load onto three independent behavioral factors: amount of activity, exploratory behavior, and behavioral organization. Rats pretreated with saline, MDL 100,907 (0.25-2.0 mg/kg), or SER-082 (0.5-1.0 mg/kg) were treated with saline, 0.25 mg/kg DOI, or 60 micrograms/kg LSD. All effects of DOI were blocked by all doses of MDL 100,907, but only by the highest dose of SER-082. While the effects of LSD on activity and exploratory behavior were largely unaffected, either pretreatment antagonized the effects of LSD on behavioral organization. Thus, all of these effects of DOI were attributable to 5-HT2A receptors, whereas the effect of LSD on behavioral organization was influenced by both 5-HT2A and 5-HT2C receptors.     

Chronic administration of serotonergic antidepressants attenuates the subjective effects of LSD in humans

This study investigates the possible interactions of antidepressant agents and hallucinogens in humans through structured interviews using a standardized questionnaire. Volunteer subjects recruited through announcements placed on the Internet or other sources were asked to describe the somatic, hallucinatory, and psychological effects of self-administered LSD prior to and during chronic administration of an antidepressant. Twenty-eight out of 32 subjects (88%) who had taken an antidepressant with inhibitory effects on serotonin (5-HT) reuptake (fluoxetine, paroxetine, sertraline, trazodone) for over 3 weeks had a subjective decrease or virtual elimination of their responses to LSD. An additional subject who had taken fluoxetine for only 1 week had an increased response to LSD. These data are in contrast to our previous study that reported increased responses to LSD during chronic administration of tricyclic antidepressants or lithium. Possible mechanisms of action for the effects from serotonergic antidepressants involve 5-HT2 and 5-HT1A receptors, changes in extracellular brain serotonin concentrations, and changes in brain catecholamine systems.     

A study of the interface between bone and acrylic cement by scanning electron microscopy

The influence of different pretreatments upon locomotor stimulation, induced by injection of ergometrine into the nucleus accumbens of rats, was investigated. The noradrenergic antagonists phenoxybenzamine and propranolol and the serotonin antagonist methysergide produced no clear changes. Reserpine, alone or in combination with alpha-MPT, considerably shortened the delay between injection of ergometrine and start of locomotor stimulation. Ro-DOPA, but not Ro-5-HTP, clearly antagonized the locomotor stimulation. The effect of ergometrine was strongly diminished following injection of haloperidol directly into the nucleus accumbens. A strong inhibition was also observedfollowing intracerebral administration of the imidazoline derivative (3,4-dihydroxy-phenylamino)-2-imidazoline (DPI), but not after injection of the structurally related compound clonidine. DPI by itself and also the ergot derivatives ergocornine, bromocryptine, LSD, dihydroergotamine and methysergide in doses 5--10 times as high as that of ergometrine failed to produce locomotor stimulation following injection into the nucleus accumbens. The results are discussed, especially with regard to the role of dopamine.     

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)     

Serotonin1A receptor activation by flesinoxan in humans. Body temperature and neuroendocrine responses

The effects of the selective 5-HT1A receptor agonist flesinoxan on neuroendocrine function, temperature, and behavior were assessed in male healthy volunteers using a double-blind, placebo-controlled crossover design. Flesinoxan (7 and 14 micrograms/kg), administered intravenously in 11 healthy volunteers, elicited a dose-related decrease in body temperature and increases in growth hormone, adrenocorticotropic hormone (ACTH), cortisol, and prolactin plasma levels. In a second independent study, 12 healthy volunteers were pretreated sequentially, at one-week intervals, with either the 5-HT1A antagonist pindolol (30 mg, PO), the nonselective 5-HT1/2 antagonist methysergide (4 mg, PO), or placebo, prior to being administered flesinoxan (1 mg, IV). The growth hormone response to flesinoxan was blocked by pindolol but not by methysergide, whereas the prolactin response was blocked by methysergide but not by pindolol. The ACTH and cortisol responses to flesinoxan were potentiated by methysergide. The flesinoxan-induced hypothermia was attenuated by both methysergide and pindolol, although the latter effects did not reach statistical significance. The present results suggest that the growth hormone response and the hypothermic response to the intravenous infusion of flesinoxan may serve as a valid index of 5-HT1A receptor function in humans.     

Modulation of central serotonergic neurotransmission by risperidone: underlying mechanism(s) and significance of action

1. The effects of risperidone on brain 5-hydroxytryptamine (5-HT) neuronal activity were investigated using microdialysis in the frontal cortex (FC) or the dorsal raphe nucleus (DRN) as well as single cell recording in the DRN. 2. Systemic administration of risperidone (0.6 and 2.0 mg/kg, s.c.) dose-dependently increased 5-HT output in both the FC and the DRN. 3. Local cortical administration of both risperidone or idazoxan enhanced the 5-HT efflux in the FC, whereas local raphe administration of risperidone but not idazoxan increased the output of 5-HT in the DRN. 4. Systemic administration of risperidone (200 micrograms/kg, i.v.) or the selective alpha 1 adrenoceptor antagonist prazosin (400 micrograms/kg, i.v.) decreased, whereas selective alpha 2 adrenoceptor antagonist idazoxan (20 micrograms/kg, i.v.) increased the 5-HT cell firing in the DRN. 5. Pretreatment with the selective 5-HT1A receptor antagonist WAY 100,635 (5.0 micrograms/kg, i.v.) effectively antagonized the inhibition of 5-HT cells induced by risperidone, but failed to prevent the prazosin-induced decrease in 5-HT cell firing in the DRN. 6. The inhibitory effect of risperidone on 5-HT cell firing in the DRN was significantly attenuated in rats pretreated with the 5-HT depletor PCPA (p-chlorophenylalanine; 300 mg/kg/day i.p. for 3 consecutive days) in comparison with drug naive animals. 7. Consequently, the risperidone-induced increase in 5-HT output in the FC may be related to its alpha 2 adrenoceptor antagonistic action, an effect probably executed at the nerve terminal level, whereas the reduction in 5-HT cell firing by risperidone appears to be associated with increased availability of 5-HT in the somatodendritic region of the neurones leading to an enhanced 5-HT1A autoreceptor activation and, in turn, to inhibition of cell firing.     

Antisense oligonucleotide-induced reduction in 5-hydroxytryptamine7 receptors in the rat hypothalamus without alteration in exploratory behaviour or neuroendocrine function

The effect of a 5-hydroxytryptamine7 (5-HT7) receptor-directed antisense oligonucleotide on rat behaviour and neuroendocrine function was investigated. Six days of intracerebroventricular 5-HT7 antisense oligonucleotide treatment significantly reduced [3H]5-HT binding to hypothalamic 5-HT7 receptors, whereas cortical 5-HT2C density remained unchanged. In rats on a food-restricted diet, both antisense and mismatch oligonucleotides reduced food intake and body weight compared with that in vehicle-treated controls by day 4 of administration. 5-HT7 antisense oligonucleotide administration did not affect exploratory or locomotor activity in photocell activity monitors on day 4 or elevated plus-maze behaviour on day 6 of intracerebroventricular treatment. 5-HT7 antisense oligonucleotide did not affect plasma corticosterone or prolactin levels or 5-HT turnover in either 5-HT cell body or terminal areas. These data demonstrate that intracerebroventricular 5-HT7 antisense oligonucleotide administration selectively reduced rat hypothalamic 5-HT7 receptor density without affecting any of the biochemical or behavioural measures. The results suggest that this antisense protocol could be a valuable tool to investigate central 5-HT7 receptor functions, and that this receptor is not critical for the control of neuroendocrine function or food intake.     

Operational characteristics of the 5-HT1-like receptors mediating external carotid vasoconstriction in vagosympathectomized dogs. Close resemblance to the 5-HT1D receptor subtype

It has recently been shown that the external carotid vasoconstrictor response to 5-HT in the dog is primarily mediated by sumatriptan-sensitive 5-HT1-like receptors; however, the fact that these receptors are not blocked by metergoline, a 5-HT1D ligand, raises questions about their possible correlation with the 5-HT1D receptor subtype. Since a number of drugs display high affinity for the 5-HT1D (GR127935) and 5-HT1F (e.g. methysergide and oxymetazoline) receptor subtypes, in this study we have used these drugs to determine whether the above vasoconstrictor 5-HT1-like receptors correlate with the 5-HT1D and/or 5-HT1F receptor subtypes. One-minute intracarotid infusions of 5-HT (0.3-30 micrograms/min), sumatriptan (1-30 micrograms/min), oxymetazoline (0.03-3 micrograms/min) and noradrenaline (0.3-3 micrograms/min) resulted in dose-dependent decreases in external carotid blood flow without changes in arterial blood pressure or heart rate. These vasoconstrictor responses remained unaltered after i.v. administration of physiological saline (0.015, 0.05 and 0.15 ml/kg; n = 4) or ritanserin (1 mg/kg; n = 5). In contrast, GR127935 (1, 3 and 10 micrograms/kg, n = 6) potently blocked the responses to 5-HT (unmasking a dose-dependent vasodilator component) and sumatriptan without affecting those to oxymetazoline or noradrenaline. Interestingly, methysergide (10, 30 and 100 micrograms/kg, n = 5) also blocked the vasoconstrictor responses to 5-HT and sumatriptan, but unlike GR127935, did not revert the vasoconstrictor response to 5-HT; the responses to oxymetazoline remained unaffected, but those to noradrenaline were apparently attenuated by the highest dose. Taken together, the above findings suggest that the sumatriptan-sensitive 5-HT1-like receptors mediating canine external carotid vasoconstriction resemble 5-HT1D receptors, probably of the 5-HT1D beta subtype on the basis of the resistance to blockade by ritanserin. The pharmacological profile of these receptors could be similar (bovine and human cerebral arteries, porcine carotid arteriovenous anastomoses and human coronary arteries) to other putative 5-HT1D receptors mediating vascular responses.     

Alpha 2-adrenoceptors in the guinea-pig uterus: heterogeneity in the circular and longitudinal smooth muscle layers

Experiments have been performed to determine whether the antisecretory (antidiarrhoeal) actions of difenoxin and loperamide are mediated by enteric neurones. An iso-osmotic perfusion solution was circulated around the lumen of the jejunum of anaesthetised rats. Vasoactive intestinal peptide was infused intra-arterially to induce net fluid secretion which was inhibited by difenoxin (ED50, 0.23 mg/kg) and loperamide (ED50, 0.5 mg/kg). However, neither were able to restore the fluid transport rate to the control level of absorption. The antisecretory effects of difenoxin (0.77 mg/kg) and loperamide (0.6 mg/kg) were blocked by the opiate receptor antagonist naloxone (2 mg/kg). Their effects were also abolished by pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA; 200 mg/kg; with desmethylimipramine given beforehand to protect noradrenergic nerves and enhance 5-HT depletion). The effect of difenoxin was blocked with methiothepin (1 mg/kg) and methysergide (30 micrograms/kg) but not ketanserin (30 micrograms/kg), ritanserin (30 mg/kg), ondansetron (10 micrograms/kg) or ICS 205-930 (3 mg/kg). None of the above 5-HT receptor antagonists modified the antisecretory effect of loperamide. The antisecretory effect of difenoxin but not loperamide was prevented by phentolamine (2 mg/kg) and by pretreatment with 6-hydroxy-dopamine (150 mg/kg total). It is concluded that both difenoxin and loperamide inhibit net fluid secretion by indirect mechanisms. It is proposed that the initial action is on enteric mu-opiate receptors and that this results in the release of 5-HT. In the case of difenoxin, the 5-HT may act on 5-HT1-like receptors to release noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of adrenal hormones in incubation behavior of male ring doves (Streptopelia risoria).

Injected 111 male ring doves intramuscularly with dexamethasone throughout a reproductive cycle in an attempt to suppress adrenocortical secretions. Ss were tested for initiation and maintenance of incubation behavior. Treated Ss showed normal initiation of sitting when observed in their cages, but when they were tested alone in novel cages initiation of incubation tended to be disrupted. Prolonged dexamethasone treatment interfered with maintenance of incubation behavior in both test situations. The deleterious effect of dexamethasone on maintenance of home cage sitting was alleviated by concurrent treatment with prolactin or ACTH. In conclusion, adrenal secretions do not seem to be necessary for onset of incubation in males, but there are hormonal requirements for maintenance of this behavior. (35 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Reinstatement of orienting behavior by d-amphetamine in rats with superior colliculus lesions.

Assessed the involvement of the nigrotectal pathway in the expression of visual orienting behavior by a combination of superior colliculus (SC) lesions and increased dopamine transmission produced by administration of dextroamphetamine (1 mg/kg, intraperitoneally [ip]), using 60 naive male Long-Evans rats. Orienting behavior elicited by apparently moving or stationary light displays, its habituation, and recovery were observed. In intact Ss, amphetamine injections had a small but reliable effect on the habituation of orienting behaviors. Ss with SC lesions did not orient to the lights. Amphetamine-injected Ss with SC lesions did orient, and the topography of their orienting behavior, rate of habituation, and recovery of orienting with changes in the light display were comparable to those of the intact S. Results suggest a view of SC-lesion-impaired orienting behavior as a disturbance of sensory attention and emphasize the interaction of the SC and other neural systems in processes mediating the direction of attention. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of visual experience on the habituation of orienting behavior.

Three experiments studied the orienting behavior (OB) at 30, 60, 90, or 120 days old of male Long-Evans rats, of whom 88 were light-reared (LR) and 84 dark-reared (DR). OB was assessed by examining S's ability to interrupt ongoing licking and perform appropriate head and postural adjustments when presented with apparently moving or stationary light displays or tones. When the lights were first presented to the LR and DR Ss, their OB did not differ at any of the ages. However, age and visual experience did influence habituation and recovery of orienting with changes in the light display. The older DR Ss habituated with fewer repeated presentations of the light displays than the LR Ss and did not recover orienting as effectively to all the subsequent changes of the light displays. The younger LR and DR Ss did not differ reliably. Results are discussed with regard to the nature of the habituation process for rodents and the relation between visual experience and habituation of attentional responses. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)