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PubMed1991

A quantitative autoradiographic study of serotonin1A receptor regulation. Effect of 5,7-dihydroxytryptamine and antidepressant treatments.

There have been few studies investigating the effect of treatments that alter serotonergic neurotransmission on the density of serotonin1A (5-hydroxytryptamine1A [5-HT1A]) receptors, even though lesioning serotonergic neurons has been reported to enhance certain responses thought to be due to activation of 5-HT1A receptors and repeated treatment of rats with different types of antidepressants can diminish 5-HT1A-mediated responses. Consequently, the binding of 3H-8-hydroxy-2-(di-n-propylamino)-tetralin (DPAT) to 5-HT1A receptors in serotonergic cell body and terminal field areas of rat brain was measured by quantitative autoradiography following either the lesioning of serotonergic neurons with 5,7-dihydroxytryptamine (5,7-DHT), or after chronic administration of monoamine oxidase inhibitors (MAOIs) (clorgyline, phenelzine, or tranylcypromine) or inhibitors of 5-HT uptake (citalopram or sertraline). Treatment of rats with 5,7-DHT did not cause any significant increase in binding of 3H-DPAT to 5-HT1A receptors in any area of the brain examined. There was no significant reduction in the binding of 3H-DPAT in terminal field areas of serotonergic innervation in rats treated with 5,7-DHT except in the CA2/CA3 region of the hippocampus (33% to 35% reduction). In the dorsal and median raphe nuclei, the specific binding of 3H-DPAT was reduced by treatment of rats with 5,7-DHT. In lesioned rats, the binding of 3H-cyanoimipramine (3H-CN-IMI) to uptake sites for serotonin was essentially eliminated in all terminal field areas examined, as well as in the dorsal and median raphe nuclei. Repeated administration of clorgyline, phenelzine, tranylcypromine, citalopram, or sertraline produced an attenuation of the hypothermic response of rats to acute subcutaneous injection of the 5-HT1A-receptor-agonist DPAT. In spite of this change in 5-HT1A responsivity, these treatments caused in the same animals no consistent change in the binding of 3H-DPAT in either serotonergic cell body or terminal field areas. Of the five drugs studied that diminished DPAT-induced hypothermia, only phenelzine and clorgyline significantly reduced the binding of 3H-DPAT, and even then in only a few of the 12 areas of brain measured. As a result of treatment of rats with tranylcypromine there was a significant increase in the binding of 3H-DPAT in the CA2/CA3 region of the hippocampus.(ABSTRACT TRUNCATED AT 400 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1990

Behavioral and neurochemical alterations following 5,6-dihydroxytryptamine administration into the median raphe nucleus in the cat.

The 5,6-dihydroxytryptamine administration into the median raphe nucleus in the cat resulted in an increase in the carbachol-induced emotional-defensive behavior and a decrease of 5-hydroxyindoleacetic acid and dopamine level in the hypothalamus, midbrain and amygdala. Lesions of median raphe nucleus resulted in similar, but more subtle alterations of post-carbachol emotional-defensive response similarly to dorsal raphe nucleus lesions, and they had also different biochemical effects in the "emotional regions" of the brain (hypothalamus, midbrain, amygdala). The absence of differentiated participation of both dorsal raphe nucleus and median raphe nucleus in the regulation of different aspect of the cat's behavior, and the role of both nuclei in the modulation of post-carbachol response is discussed.

5,6-Dihydroxytryptamine↗
PubMedDate not supplied

The influence of injection of 5,6-dihydroxytryptamine to the dorsal raphe nucleus on carbachol-induced defensive behavior and regional brain amine content in the cat.

The 5,6-dihydroxytryptamine-induced lesions of serotonergic neurons in the dorsal raphe nucleus of the cat resulted in an increase in the carbachol-induced growling response, a decrease in the concentrations of noradrenaline, serotonin and 5-hydroxyindoleacetic acid in the hypothalamus, midbrain and amygdala, and an increase in the hypothalamic dopamine level. Those changes were observed 6, but not 23, days after the lesion. The results suggest a close correlation between the state of the emotional-defensive arousal and neurochemical changes in the "emotional regions" of the brain. The role of the reduced activity of the serotonergic system in augmenting the emotional-defensive behavior was discussed.

5,6-Dihydroxytryptamine↗
PubMed1989

Basal cells of the frog's taste organ: fluorescence histochemistry with the serotonin analogue 5,7-dihydroxytryptamine in supravital conditions.

We utilized the fluorescent serotonin analogue 5,7-dihydroxytryptamine (5,7DHT) to visualize basal cells in the frog's taste organ in supravital conditions. In whole mounts of lingual mucosa, specifical and detailed morphological visualization of fluorescent basal cells was obtained in the peripheral and central region of the intact taste organ; similar results were obtained after mechanical dissociation. Preincubation with serotonin prevented any fluorescence in basal cells. Electron microscopy showed good preservation of the ultrastructural morphology of the taste disk after exposure to 5,7DHT. The advantages of the current method as compared with conventional ones are discussed. This simple, reliable procedure will be useful to further define the biology of neuroendocrine cells in taste as well as in other organs.

5,7-Dihydroxytryptamine↗
PubMed1987

Free amino acids in cytosol of rat brain after intraventricular administration of 5,6-dihydroxytryptamine and 6-hydroxydopamine.

Levels of 24 free amino acids were estimated in the brain after administration of 5,6-dihydroxytryptamine and 6-hydroxydopamine into the lateral brain ventricles of male Wistar rats. These neurotransmitters caused serotoninectomy and sympathectomy in the diencephalon, striatum, brain stem and medulla, thalamus and hypothalamus, cerebral cortex and cerebellum. The most abundant amino acids in these brain structures were: glutamic acid, serine, aspartic acid, cystine, gamma-aminobutyric acid, glycine, tryptophan and alanine. We detected and quantified changes in the levels of these and other amino acids in the investigated regions of the rat central nervous system, under the influence of these two neurotransmitters.

5,6-Dihydroxytryptamine↗
PubMed1981

Effects of 5,7-dihydroxytryptamine and 6-hydroxydopamine on fever response in conscious rats.

The effects of 5,7-dihydroxytryptamine (5,7-DHT) and 6-hydroxydopamine (6-OHDA) on the febrile response to E. coli lipopolysaccharide (LPS) of unanesthetized rats examined. Depleting serotonin (5-HT) in brain with 5,7-DHT produced an attenuation in fever response to LPS, while depleting noradrenaline (NA) content in the preoptic area with 6-OHDA produced an opposite effect. However, 6-OHDA when given intraventricularly (icv) was without any significant effect on fever response to LPS. Presented data indicate that alterations in both noradrenergic and serotoninergic system of the rat brain affect the febrile response response to bacterial pyrogen. Moreover, one might conclude that integrity of noradrenergic neurons in central nervous system (CNS) in the rat is not essential for appearance of pyrogen fever.

5,7-Dihydroxytryptamine↗
PubMed1995

The effects of neurotoxins 6-hydroxydopamine and 5,7-dihydroxytryptamine into the rat nucleus accumbens on the alcohol drinking behavior.

To elucidate the relationship between drinking behavior and brain monoamines in the brain rewarding system, the effects of injection of 6-hydroxydopamine (6-OHDA) and 5,7-dihydroxytryptamine (5,7-DHT) into the rat nucleus accumbens (ACC), which would affect dopamine- and indoleamine-containing neurons, respectively, on the rat alcohol preference score were examined. The 6-OHDA (4 micrograms/side)-treated rats showed a higher alcohol preference score for 2 weeks following the treatment, and a lowered dopamine (DA) level in the ACC and midbrain after ACC injection of 6-OHDA. On the other hand, although the serotonin (5-HT) and DA levels in the midbrain and 5-HT level in ACC were lowered after the injection of 5,7-DHT, the alcohol preference score was not significantly changed in the 5,7-DHT (4 micrograms/side)-treated rats. Taken together, these findings suggest that the alcohol drinking behavior is more influenced by the ACC DA activity than 5-HT activity. Changes in alcohol drinking behavior might be related to the compensatory mechanism for the rat to restore the original rewarding properties.

5,7-Dihydroxytryptamine↗
PubMed1994

Regeneration of serotonergic immunoreactive fibers in the brain of 5,6-dihydroxytryptamine treated rat.

After the intraventricular injection of 5,6-dihydroxytryptamine (5,6-DHT), the course of degeneration and regeneration of the serotonergic fibers in the rat brain was studied immunohistochemically by using serotonin antiserum. Three days after 5,6-DHT treatment, an extensive disappearance of serotonin immunoreactive fibers was observed throughout the brain. Degenerative serotonergic fibers characterized by droplet-like swelling and intense staining by serotonin antiserum were detected in the following discrete areas, e.g., medial forebrain bundle (MFB), cingulate cortex, septal nucleus, diagonal band of Broca (DBB), lateral preoptic area, bed nucleus of stria terminalis, perifornical area, stria-terminals, raphe nuclei, ventral tegmental area, periaqueductal gray lateral reticular nucleus and nucleus of the solitary tract. The swelling were regarded as the proximal stumps of the chemically injured serotonin fibers. Sprouting serotonin fibers emanating from these swellings were observed 5 days after injection. The swollen thick fibers were seen up to 3 months thereafter throughout the brain, although they gradually decreased in number until 1 month after injection. On the contrary, the sprouting fibers extended their terminal fields throughout the brain. Three types of reorganization pattern of regenerating serotonergic fibers were distinguished: hyperinnervation, normoinnervation (similar to the normal innervation) and hypoinnervation patterns. In the areas with hyperinnervation, the density of the serotonergic fibers gradually increased for 3 months. These hyperinnervation patterns of regenerative serotonergic fibers were observed in the MFB, cingulate cortex, diagonal band of Broca, perifornical area, raphe nuclei, ventral tegmental area, motor trigeminal nucleus, facial nucleus, lateral reticular nucleus, inferior olivary complex and hypoglossal nucleus. On the other hand, the hypoinnervation displayed by a few regenerating serotonergic fibers was observed in the periventricular part of the prosencephalon, the ventromedial part of the hypothalamus, the dorsal hippocampus, the neocortex, the superior and inferior colliculi, the cerebellum, the dorsal tegmental nucleus of Gudden, the vestibular nuclei, the gracile nucleus and the cuneate nucleus. These reorganization patterns were formed 3 months after injection, and continued for a long time (2 years). The mechanisms of serotonergic fiber reorganization are discussed.

5,6-Dihydroxytryptamine↗
PubMed1994

Supersensitization of the oral response to SKF 38393 in neonatal 6-hydroxydopamine-lesioned rats is eliminated by neonatal 5,7-dihydroxytryptamine treatment.

5-Hydroxytryptamine (5-HT) 5-HT2c receptors mediate the enhanced oral activity response to the dopamine (DA) D1 agonist, (+/-)-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393) in neonatal 6-hydroxydopamine (6-OHDA)-lesioned rats. To study the possible involvement of 5-HT fibers on this process, the effect of the 5-HT neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT) was determined. Rats were treated at 3 days after birth with desipramine (20 mg/kg i.p., base) 1 hr before intracerebroventricular vehicle, 6-OHDA (134 micrograms, base) and/or 5,7-DHT (50 micrograms, base). Oral activity was observed at 7 weeks and later. In neonatal 6-OHDA-lesioned rats oral activity dose-effect responses were increased by SKF 38393, 1-(3-chlorophenyl)-piperazine (m-CPP) and pilocarpine-respective DA D1, 5-HT2c and muscarinic receptor agonists. Rats treated neonatally with 5,7-DHT had agonist-induced responses resembling that of the saline control group. However, in rats treated neonatally with both 5,7-DHT and 6-OHDA, oral activity responses were reduced at nearly all doses of SKF 38393 and pilocarpine vs. that of the 6-OHDA group. The response of the 5,7-DHT + 6-OHDA group to m-CPP was reduced at only the 1.0 mg/kg dose. Of a variety of stereotyped behaviors that were observed in separate test sessions, m-CPP-induced grooming activity was less in the 5,7-DHT + 6-OHDA group vs. the 6-OHDA group.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1977

Cytotoxicity of 5,6-dihydroxytryptamine in dimethylhydrazine-induced carcinomas of rat colon.

Male Sprague-Dawley rats were given weekly s.c. injections of 1,2-dimethylhydrazine (21 mg/kg) for 20 weeks. The injections were then discontinued, and, after an interval of 2 to 8 weeks, experimental animals were given i.p. injections of 5,6-dihydroxytryptamine (5,6DHT) at a dose of 40 mg/kg and sacrificed at intervals of 1, 2, 6, 16, and 48 hr later. Specimens of descending colon and carcinomas of the descending or transverse colon from sacrificed animals were examined using light microscopy and transmission electron microscopy. The results show that 5,6DHT at a dose of 40 mg/kg is cytotoxic to malignant colonic epithelial cells but not cytotoxic to adjacent nonmalignant colonic epithelial cells. In malignant colonic epithelial cells, ultrastructural changes in cytoplasmic membranes and mitochondria were evident at 1 hr after 5,6DHT treatment. At 6 hr after 5,6DHT treatment, light microscopy of sections of tumor showed areas of cell necrosis and disrupted tumor morphology. Sections of specimens taken 16 hr after treatment showed widespread destruction of malignant cells.

5,6-Dihydroxytryptamine↗
PubMed1977

Effect of 5,6-dihydroxytryptamine on the structure of nerve fibres in the chronically isolated cat ileum.

The structure of the nerve fibres in the chronically isolated cat ileum was studied by fluorescence and electron microscopy after 5,6-dihydroxytryptamine (5,6-DHT) treatment. Residual fluorescence rapidly disappears after administration of 5,6-DHT. Under the electron miroscope, degeneration of most of the nerve processes containing a special population of 120- to 140-nm diameter granular vesicles could be observed. Also the degeneration of presynaptic terminals in the local ganglia was observed frequently. Some degenerating nerve fibres were found in the inner muscular layer, in the connective tissue surrounding Lieberkühn's glands, and in the storma of the villi. The axons (and/or other nerve processes) undergoing degeneration are assumed to belong to the serotoninergic neurons of the local ganglia. A substantial number of nerve cell processes remaining intact after 5,6-DHT treatment contain different population of vesicles: either 30- to 60-nm agranular and 100- to 120-nm granular vesicles or 30- to 60-nm agranular and 160- to 200-nm diameter neurosecretory type vesicles.

5,6-Dihydroxytryptamine↗
PubMed1996

Plastic responses of neonatal 5-hydroxytryptamine1B receptors to 5,7-dihydroxytryptamine lesions mapped by quantitative autoradiography.

We previously found different effects on behavior, serotonin (5-HT) concentrations, 5-HT uptake sites, and 5-HT1A binding sites of neonatal 5,7-dihydroxytryptamine (5,7-DHT) lesions depending on the route of 5,7-DHT injection. To study the impact of early lesions on 5-HT1B sites as putative 5-HT terminal autoreceptors, we labelled them autoradiographically with [3H]5-HT 4 months after intraperitoneal (i.p.) or intracisternal (i.c.) 5,7-DHT injection during the first postnatal week and quantitated specific binding in 22 brain regions. Changes were confined to the subiculum and substantia nigra, regions with the most 5-HT1B-specific binding and projection areas of structures with high mRNA expression. Both routes of 5,7-DHT injection were associated with increases in specific binding in subiculum (24% for i.p. and 47% for i.c. route). In contrast, there was a 32% increase in specific binding in the substantia nigra in rats with lesions made i.c. but not i.p. No significant differences were found in nucleus accumbens, caudate-putamen or other brain areas. In saturation homogenate binding studies of 5-HT1B sites using [125I]iodocyanopindolol 1 month after i.p. injections, neonatal 5,7-DHT lesions did not significantly alter Bmax or Kd in the neocortex, striatum, diencephalon or brainstem. These data indicate the differential effects of the route of neonatal 5,7-DHT injections on plasticity of 5-HT1B receptor recognition sites and suggest the presence of a subpopulation of post-synaptically located 5-HT1B sites which increases in response to denervation. The data also suggest that sprouting of 5-HT neurons after neonatal 5,7-DHT lesions does not involve 5-HT1B sites.

5,7-Dihydroxytryptamine↗
PubMed1997

Serotonergic function of aging hippocampal CA3 pyramidal neurons: electrophysiological assessment following administration of 5,7-dihydroxytryptamine in the fimbria-fornix and cingulum bundle.

Serotonergic (5-hydroxytryptamine; 5-HT) neurotransmission has been implicated in the regulation of cognitive function and this neurotransmitter system may underlie selective neuronal degeneration found in the aging hippocampus. Age-dependent changes in 5-HT function of hippocampal CA3 subfield pyramidal neurons were evaluated in female Fischer 344 rats (2 and 17 months) following denervation of the serotonergic afferents to the dorsal hippocampus using the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). Vehicle (ascorbic saline) or 5,7-DHT was administered bilaterally in the fimbria-fornix/cingulum bundle and dorsal pyramidal cell responses to microiontophoretic application of 5-HT, the 5-HT1A agonist (+/-)-8-hydroxy-2-(di-N-propylamino) tetralin, the 5-HT1A antagonist WAY 100,135 and N-methyl-D-aspartate were recorded at 3 weeks post-lesion. Independent of changes in sensitivity to the inhibitory effects of 5-HT with aging, the time to recovery of cell firing following application of 5-HT was significantly increased in the 18 months 5,7-DHT group compared to the 18 month Vehicle and 3 month 5,7-DHT groups (3.3- and 2.6-fold, respectively). These results demonstrate that serotonergic neurotransmission is altered with aging following a selective neurotoxic insult to the hippocampus.

5,7-Dihydroxytryptamine↗
PubMed1997

Effects of 5,7-dihydroxytryptamine lesions of the prefrontal cortex on consumption of sucrose-ethanol solutions: relationship to prefrontal monoamines.

Thirty adult male Wistar rats received 8 micrograms bilaterally of 5,7-dihydroxytryptamine into the medial prefrontal cortex (mPFC). Rats were then trained, via a sucrose, fading paradigm, to consume increasing concentrations of alcohol. After death, dopamine (DA), norepinephrine (NE), serotonin (5-HT), and their metabolites were measured in the mPFC, nucleus accumbens (NA), and raphe nucleus. The lesioned group demonstrated a reduction in 5-hydroxyindoleacetic acid (5-HIAA), DA, and NE in the mPFC (p < 0.05), and a trend toward reduction of 5-HT in the NA. In comparison with controls, lesioned animals consumed less of all solutions containing sucrose and alcohol. On regression analyses, monoamines in the mPFC (i.e., 5-HIAA, dihydrophenylacetic acid and NE) predicted consumption of the 5% ethanol solution (p = 0.009), 10% ethanol solution (p = 0.0006), and the 5% sucrose solutions (p = 0.0006), but not the 20% sucrose solutions. In each case, monoamine levels were positively correlated with consumption. No relationships were seen between monoamine levels in the NA and raphe, and in consummatory behavior.

5,7-Dihydroxytryptamine↗
PubMed1998

Alterations in 8-hydroxy-2-(dipropylamino)tetralin-induced neuroendocrine responses after 5,7-dihydroxytryptamine-induced denervation of serotonergic neurons.

In the present study, we examined denervation-induced changes in the sensitivity of hypothalamic postsynaptic serotonin1A (5-HT1A) receptor function with respect to changes in the dose-dependent elevation in plasma hormones [adrenocorticotropic hormone (ACTH), corticosterone, prolactin, oxytocin, prolactin, renin and vasopressin] by the 5-HT1A agonist 8-hydroxy-2-(dipropylamino)tetralin (8-OH-DPAT). Rats received intracerebroventricular (i.c.v.) injections of the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) or vehicle (0.1% ascorbate in saline) 3 weeks before challenge with increasing doses of 8-OH-DPAT (0, 10, 50 or 200 micrograms/kg s.c.). The effectiveness of 5,7-DHT-induced destruction of serotonergic neurons was confirmed by a 93% reduction in [3H]paroxetine-labeled 5-HT uptake sites in the hypothalamus. No changes in basal levels of ACTH, corticosterone, oxytocin, prolactin, renin and vasopressin were observed in rats that received i.c.v. 5,7-DHT injections. The dose-response curves for 8-OH-DPAT-induced elevations of plasma corticosterone and prolactin levels were shifted to the left in rats treated with 5,7-DHT, whereas no significant difference in the ACTH dose-response curve was observed between rats treated with vehicle and rats treated with 5,7-DHT. In contrast, the maximal oxytocin response to 8-OH-DPAT was attenuated in rats treated with 5,7-DHT. A 5,7-DHT-induced decline in the synthesis of oxytocin could explain this phenomenon. Although 8-OH-DPAT did not increase plasma levels of renin or vasopressin in rats treated with vehicle, 8-OH-DPAT produced an elevation (75%) in plasma renin concentration but not in vasopressin levels in rats that received i.c.v. injections of 5,7-DHT. No change was observed in [3H]8-OH-DPAT labeled 5-HT1A receptors in the hypothalamus. In summary, denervation of hypothalamic serotonergic nerve terminals produces supersensitivity of some neuroendocrine responses to 8-OH-DPAT independent of changes in the density of hypothalamic 5-HT1A receptors.

5,7-Dihydroxytryptamine↗
PubMed2001

Compensatory responses in the aging hippocampal serotonergic system following neurodegenerative injury with 5,7-dihydroxytryptamine.

This study utilized a multidisciplinary approach to examine injury-induced compensatory responses in the aging hippocampal serotonin transporter (5-HTT), a membrane protein implicated in a variety of neurodegenerative disorders. Age-dependent cellular, anatomical, and physiological changes of the 5-HTT were evaluated in female Fischer 344 rats (2 and 17 months) following denervation of the serotonergic afferents (fimbria-fornix and cingulum bundle) to the dorsal hippocampus using the neurotoxicant 5,7-dihydroxytryptamine (5,7-DHT). Seven days following 5,7-DHT administration, a uniform loss of the hippocampal 5-HTT immunoreactivity was observed in both age groups. However, at 21 days 5-HTT immunoreactivity in young 5,7-DHT-treated animals was similar to control levels, indicative of recovery, while older animals exposed to 5,7-DHT did not show recovery of hippocampal 5-HTT expression. 5-HTT binding site density, as determined by quantitative autoradiography ([3H]citalopram), supported the immunohistochemical results by demonstrating a recovery of 5-HTT binding sites in young, but not old animals, at 21 days following the lesion (P < 0.001). Furthermore, cellular electrophysiological function of hippocampal CA1 pyramidal neurons in 3- and 18-month-old F344 rats at 21 days following 5,7-DHT or vehicle treatment were assessed using in vivo microiontophoretic application of serotonin (5-HT). Independent of changes in sensitivity to the inhibitory effects of 5-HT application, the time to recovery of cell firing following application of 5-HT was significantly increased in the 18-month 5,7-DHT group compared to the 18-month vehicle and 3-month 5,7-DHT groups (60 and 59% increases, respectively; P < 0.05). Overall, these series of studies comprise a model which can be used to identify cellular events underlying both the formation of injury-induced compensatory processes in younger animals and the lack thereof with advancing age.

Afferent Pathways↗
PubMed1977

Degeneration of possible serotonergic nerves in the myenteric plexus of Mytilus induced by 5,7-dihydroxytryptamine (5,7-DHT).

Initial observations on the effects of 5,7-DHT on the myenteric plexus of Mytilus reveal extensive lesioning of monoamine nerves containing dense-cored vesicles. At least, two types of monoaminergic nerves could be recognized among the degenerating axons. The most affected were profiles with a predominance of large granular vesicles (56-200 nm) which resemble possible indoleamine nerves in the lamprey gut. The other type had small granular vesicles (40-56 nm) resembling catecholamine nerves of vertebrates. These two types of nerves possibly represent serotonergic and dopaminergic nerves, in accordance with pharmacological, biochemical and physiological evidence available in molluscs. There were, however, nerves with a population of medium-sized granular vesicles (56-130 nm) which were also damaged. Two other types of nerve profiles were unaffected by the drug. One conforms to cholinergic nerves while the other resembles "purinergic" nerves in the vertebrate gut. These results confirm previous studies with dihydroxytryptamines on molluscan smooth muscle.

Animals↗
PubMed1976

Activity, avoidance learning and regional 5-hydroxytryptamine following intra-brain stem 5,7-dihydroxytryptamine and electrolytic midbrain raphe lesions in the rat.

Rats underwent one of the following treatments: (1) electrocoagulation of both the dorsal and median midbrain raphe nuclei; (2) 5,7-dihydroxytryptamine creatinine sulfate (5,7-DHT) injection (10 mug, as the salt, in 5 mul vehicle) into the vicinity of each midbrain raphe nucleus; (3) intra-brain stem vehicle (5 mul of 0.2% ascorbic acid in isotonic saline) injections; or, (4) a control operation. Open field activity and one-way avoidance conditioning were examined on postoperative days 16-23. Regional central 5-hydroxytryptamine (5-HT) and catecholamine (CA) concentrations were determined 25-27 days postoperatively. Regional 5-HT levels were greatly reduced following 5,7-DHT administration and electrolytic raphe lesions. The 5,7-DHT rats also showed a reduction in spinal 5-HT content. Central CA concentrations were not affected. Variation in the pattern of regional 5-HT changes after 5,7-DHT treatment was observed but appeared to be related to the adequacy of the dorsal raphe (B7) injection. Only the electrolytic raphe lesion animals, however, showed increased locomotor activity and retarded acquisition and forced-extinction of the one-way avoidance response. In contrast, no significant differences were observed in the open field and avoidance behavior of the 5,7-DHT, vehicle, and control groups. The hyperactivity and impaired one-way avoidance performance observed after electrolytic midbrain raphe lesions are not related simply to reductions in regional forebrain 5-HT and may well be due to damage of non-serotonergic neural systems. Clearly, the behavioral effects of central 5-HT depletion depend on the method employed. The role of 5-HT in regulating activity level and mediating avoidance behavior, furthermore, remains to be determined.

Animals↗