The evolution of colour pattern complexity: selection for conspicuousness favours contrasting within-body colour combinations in lizards.

Many animals display complex colour patterns that comprise several adjacent, often contrasting colour patches. Combining patches of complementary colours increases the overall conspicuousness of the complex pattern, enhancing signal detection. Therefore, selection for conspicuousness may act not only on the design of single colour patches, but also on their combination. Contrasting long- and short-wavelength colour patches are located on the ventral and lateral surfaces of many lacertid lizards. As the combination of long- and short-wavelength-based colours generates local chromatic contrast, we hypothesized that selection may favour the co-occurrence of lateral and ventral contrasting patches, resulting in complex colour patterns that maximize the overall conspicuousness of the signal. To test this hypothesis, we performed a comparative phylogenetic study using a categorical colour classification based on spectral data and descriptive information on lacertid coloration collected from the literature. Our results demonstrate that conspicuous ventral (long-wavelength-based) and lateral (short-wavelength-based) colour patches co-occur throughout the lacertid phylogeny more often than expected by chance, especially in the subfamily Lacertini. These results suggest that selection promotes the evolution of the complex pattern rather than the acquisition of a single conspicuous colour patch, possibly due to the increased conspicuousness caused by the combination of colours with contrasting spectral properties.

Using visual modelling to study the evolution of lizard coloration: sexual selection drives the evolution of sexual dichromatism in lacertids.

Sexual selection has been invoked as a major force in the evolution of secondary sexual traits, including sexually dimorphic colourations. For example, previous studies have shown that display complexity and elaborate ornamentation in lizards are associated with variables that reflect the intensity of intrasexual selection. However, these studies have relied on techniques of colour analysis based on human--rather than lizard--visual perception. Here, we use reflectance spectrophotometry and visual modelling to quantify sexual dichromatism considering the overall colour patterns of lacertids, a lizard clade in which visual signalling has traditionally been underrated. These objective methods of colour analysis reveal a large, previously unreported, degree of sexual dichromatism in lacertids. Using a comparative phylogenetic approach, we further demonstrate that sexual dichromatism is positively associated with body size dimorphism (an index of intrasexual selection), suggesting that conspicuous coloration in male lacertids has evolved to improve opponent assessment under conditions of intense male-male competition. Our findings provide the first evidence for the covariation of sexual dichromatism and sexual size dimorphism in lacertids and suggest that the prevalent role of intrasexual selection in the evolution of ornamental coloration is not restricted to the iguanian lineage, but rather may be a general trend common to many diurnal lizards.

Effectiveness of self-esteem and social skills group therapy in adolescent eating disorder patients attending a day hospital treatment programme.

OBJECTIVE: To evaluate self-esteem and social skills in adolescent eating disorder patients before and after specific group therapy as part of a Day Hospital Programme. METHOD: One hundred and sixty adolescent eating disorder patients, classified as anorexia nervosa and related disorders (AN-rd) (N = 116) or bulimia nervosa and related disorders (BN-rd) (N = 44) received structured group therapy for developing self-esteem and social skills. RESULTS: BN-rd patients had poorer perceptions of some self-esteem and social skills variables. After group therapy, both groups presented significant improvements in their perceptions of physical appearance, their self-concept related to weight and shape and to others, happiness and satisfaction, social withdrawal and leadership. BN-rd patients presented more changes on many of the variables. DISCUSSION: Specific self-esteem and social skills group therapy in patients with eating disorders can be useful in improving certain core features.

Putting information back into biological communication.

At the heart of many debates on communication is the concept of information. There is an intuitive sense in which communication implies the transfer of some kind of information, probably the reason why information is an essential ingredient in most definitions of communication. However, information has also been an endless source of misunderstandings, and recent accounts have proposed that information should be dropped from a formal definition of communication. In this article, we re-evaluate the merits and the internal logic of information-based vs. information-free approaches and conclude that information-free approaches are conceptually incomplete and operationally hindered. Instead, we propose a functional notion of information that follows logically from previous adaptationist accounts. The ensuing definition of communication provides a wider, more inclusive theoretical scope that reflects more accurately the evolutionary scenario shaping animal signals. Additionally, it is a definition better equipped to deal with the extraordinary diversity of animal signals, facilitates the distinction of honest and deceptive signals at a proximate level and accommodates a number of conceptual and practical issues (e.g. redundancy, alerting components) that are lost when we fail to acknowledge the informative content of animal signals.

Quantity discrimination in Tenebrio molitor: evidence of numerosity discrimination in an invertebrate?

Numerosity discrimination, the ability to distinguish between sets with more and less items, is recognised as the foundation for higher numerical abilities. Understanding numerosity discrimination from a comparative perspective is hence pivotal in tracing the evolution of numerical representation systems. However, numerosity discrimination has been well studied only in vertebrates, where two innate systems of number representation have been described: an 'analog magnitude system' used to discriminate among numerosities by representing them as cardinal magnitudes and a 'parallel individualisation system' that allows precise discrimination among small arrays of items (< or =4) by representing objects individually. We investigated the existence of quantity discrimination in an insect species (Tenebrio molitor) by using a spontaneous two-choice procedure in which males were exposed to substrates bearing odours from different numbers of females (< or =4) in increasing numerosity ratios (1:4, 1:3 and 1:2). We show that males can discriminate sources of odours reflecting 1 versus 4 and 1 versus 3 females, but not 2 versus 4 or 1 versus 2, indicating that T. molitor males exhibit a marked preference for sources reflecting more female donors only when numerosity ratios are below 1:2. We discuss the functional significance of this finding and whether our pattern of results could be best explained by summation of a non-numerical continuous variable or by the existence of a numerosity discrimination mechanism with an operational signature ratio of 1:2.

Effects of dietary-induced hyperparathyroidism on the parathyroid hormone-receptor-adenylate cyclase system of canine kidney. Evidence for postreceptor mechanism of desensitization.

The present studies were designed to examine the consequences of chronic mild elevations of endogenous parathyroid hormone (PTH) in vivo on the PTH receptor-adenylate cyclase system of canine kidney cortex. Hyperparathyroidism was induced in normal dogs by feeding a diet low in calcium, high in phosphorus to the animals for a period of 6-9 wk. This maneuver resulted in a two to threefold increase in the plasma levels of carboxy-terminal immunoreactive PTH. This degree of hyperparathyroidism is similar to that seen in patients with hyperparathyroidism and normal renal function. After 6-9 wk on the diet the animals were killed and basolateral renal cortical membranes prepared for the study of the PTH receptor-adenylate cyclase system in vitro. The dietary hyperparathyroidism resulted in desensitization of the PTH-responsive adenylate cyclase (Vmax 3,648 +/- 654 pmol cyclic (c)AMP/mg protein per 30 min in hyperparathyroid animals vs. 5,303 +/- 348 in normal controls). The Kact (concentration of PTH required for half-maximal enzyme activation) was unchanged. However, PTH receptor binding (125I-norleucyl8-norleucyl18-tyrosinyl34, 125I[Nle8, Nle18, Tyr34] bPTH (1-34) NH2 as radioligand) was not different in the two groups of animals. Thus, dietary hyperparathyroidism resulted in an uncoupling of the PTH receptor-adenylate cyclase system. This defect was not corrected by guanyl nucleotides in vitro, and the effects of guanyl nucleotides on PTH binding and enzyme activation appeared normal. NaF-stimulated enzyme activity was reduced in the hyperparathyroid animals (8,285 +/- 607 pmol cAMP/mg protein per 30 min vs. 10,851 +/- 247 in controls). These data indicate that desensitization of the PTH-responsive adenylate cyclase system of canine kidney as a result of mild chronic elevations of endogenous PTH is due to a postreceptor defect, demonstrable by NaF activation, not corrected by guanyl nucleotides, leading to abnormal PTH-receptor adenylate cyclase coupling.

Evidence for skeletal resistance to parathyroid hormone in magnesium deficiency. Studies in isolated perfused bone.

Hypocalcemia during magnesium (Mg) depletion has been well described, but the precise mechanism(s) responsible for its occurrence is not yet fully understood. The hypocalcemia has been ascribed to decreased parathyroid hormone (PTH) secretion as well as skeletal resistance to PTH. Whereas the former is well established, controversy exists as to whether or not Mg depletion results in skeletal resistance to PTH. These studies examine the skeletal response to PTH in normal dogs and dogs fed a Mg-free diet for 4-6 mo. Isolated tibia from normal (serum Mg 1.83+/-0.1 mg/100 ml) and experimental dogs (serum Mg 1.34+/-0.15 mg/100 ml) were perfused with Krebs-Henseleit buffer during a constant infusion of 3 ng/ml of synthetic bovine PTH 1-34 (syn b-PTH 1-34). The arteriovenous (A-V) difference for immunoreactive PTH (iPTH) across seven normal bones was 37.5+/-3%. In contrast, the A-V difference for iPTH was markedly depressed to 10.1+/-1% across seven bones from Mg-depleted dogs. These findings correlated well with a biological effect (cyclic AMP [cAMP] production) of syn b-PTH 1-34 on bone. In control bones, cAMP production rose from a basal level of 5.8+/-0.2 to 17.5+/-0.7 pmol/min after syn b-PTH 1-34 infusion. In experimental bones, basal cAMP production was significantly lower than in controls, 4.5+/-0.1 pmol/min, and increased to only 7.1+/-0.4 pmol/min after syn b-PTH 1-34 infusion. Even when PTH concentrations were increased to 20 ng/ml, cAMP production by experimental bones was lower than in control bones perfused with 3 ng/ml. Histological examination of bones from Mg-deficient dogs showed a picture compatible with skeletal inactivity. These studies demonstrate decreased uptake of iPTH and diminished cAMP production by bone, which indicates skeletal resistance to PTH in chronic Mg deficiency.

Chemosensory assessment of sperm competition levels and the evolution of internal spermatophore guarding.

Males of many species adjust their reproductive behaviour according to the perceived risk of sperm competition. Although this phenomenon is widespread in insects and other animals, the mechanisms that allow mates to assess sperm competition levels remain largely unexplored. In this study, we analysed the mating behaviour of pairs of Tenebrio molitor beetles under three odour treatments representing increasing levels of sperm competition risk (SCR) and sperm competition intensity (SCI). Copula duration and male and female post-copulatory behaviour varied significantly with odour treatment. Both copula duration and post-copulatory associations (PCAs) increased significantly in odour treatments reflecting high male density. To our knowledge, this is the first study to report that insects may assess the actual density of potential competitors at the time of mating, a cue to SCR and SCI, on the basis of chemical cues. In T. molitor, males inhibit sperm release from the spermatophore of a rival male when remating takes place at short intervals. We show that, when sperm competition levels are high, PCAs increase female remating interval just above that necessary to prevent spermatophore inhibition by rival males. This finding strongly suggests that strategic male behaviour plays a 'spermatophore guarding' role in this species. Although common in insects with external spermatophore transfer, spermatophore guarding is not expected in species with rapid ejaculate transfer and internal spermatophore delivery. Our results reveal that spermatophore guarding may evolve, even under these circumstances, as an evolutionary response to short-term spermatophore inhibition or displacement mechanisms.

Parathyroid hormone stimulation of renal phosphoinositide metabolism is a cyclic nucleotide-independent effect.

The effects of parathyroid hormone (PTH) and cyclic nucleotides on renal phosphoinositide metabolism were studied using cortical tubules isolated from dog kidneys. PTH stimulated the initial rates of 32Pi incorporation into phosphatidylinositol 4'5'-diphosphate, phosphatidylinositol 4'-monophosphate, phosphatidylinositol and phosphatidic acid. PTH also caused a 45-55% increase in the actual tissue levels of these phospholipids by 5 min of incubation. By 30 min of incubation, the levels of 32Pi incorporated were similar in PTH and control flasks, but the actual levels of the phosphoinositides remained elevated, indicating stimulation of their turnover. Additional evidence of increased turnover of phosphatidylinositol was obtained from tubules pre-incubated with myo-[2-3H]inositol. PTH stimulated a rapid short-lived decrement in [3H]phosphatidylinositol while total phosphatidylinositol levels increased, indicating increased turnover rates of phosphatidylinositol. In tubules pre-incubated with [14C]arachidonic acid, indicating utilization of diacylglycerol produced during turnover for resynthesis of phosphatidic acid and phosphoinositides. Cyclic nucleotides and phosphodiesterase inhibition failed to reproduce the effect of PTH on phosphoinositide metabolism. These studies indicate that PTH stimulates renal phosphoinositide metabolism through a mechanism independent of cAMP which results in a net synthesis of the phosphoinositides.

Massive cerebral calcifications associated with increased renal phosphate reabsorption.

Extensive bilateral cerebral cortical calcifications were demonstrated in a young patient with a history of convulsions since the age of 4 years. Initial metabolic workup showed normal serum calcium levels, hyperphosphatemia, normal renal function, low urinary calcium excretion, and normal serum immunoreactive parathyroid hormone levels. The intravenous infusion of edetate disodium (disodium EDTA) showed a normal phosphaturic and cyclic adenosine monophosphate response, ruling out the diagnosis of pseudohypoparathyroidism. The infusion of acetazolamide produced a blunted phosphaturia with almost no change in the renal phosphorus threshold, suggesting a tubular defect that allows enhanced proximal tubular reabsorption of phosphorus. Although the exact mechanisms responsible for the localized calcifications remain obscure, we suggest that an enhanced proximal tubular reabsorption of phosphorus could be involved in the pathophysiologic basis of this abnormality.

Uncoupling of the parathyroid hormone receptor-adenylate cyclase system of canine kidney during dietary phosphorus deprivation.

The mechanisms involved in the renal resistance to the phosphaturic action of PTH during dietary phosphorus deprivation remain ill defined. Previous studies in dogs from our laboratory demonstrated that baseline excretion of cAMP and the increment after administration of parathyroid extract were markedly reduced during dietary phosphorus deprivation. The present studies examine the initial events in the actions of PTH, namely receptor binding and adenylate cyclase activation, in renal cortical membranes from normal and phosphorus-deprived animals. Mongrel dogs were fed a diet deficient in phosphorus for 4-6 weeks. Plasma phosphorus fell from 4.2 +/- 0.4 to 1.4 +/- 0.3 mg/dl. In renal cortical membranes from these animals, basal adenylate cyclase activity was not different from that in control normal animals. However, PTH-stimulated enzyme activity was markedly reduced (5785 +/- 303 pmol cAMP/mg protein X 30 min in controls vs. 2612 +/- 406 pmol cAMP/mg protein X 30 min; P less than 0.01). Kact (PTH concentration for half-maximal enzyme activation) was unchanged. PTH receptor binding assessed with [Nle8,Nle18,Tyr34]bovine PTH-(1-34) NH2 was not different in the two groups. The decreased PTH-stimulated adenylate cyclase activity was not corrected by GTP. Activation of adenylate cyclase by NaF was reduced in membranes from the phosphorus-deprived animals, whereas enzyme activation by guanylylimidodiphosphate was similar in both groups. Enzyme activity in the presence of Mn++ was not different from the control value. These data indicate that during dietary phosphorus deprivation there is uncoupling of the PTH receptor-adenylate system of canine kidney. This abnormality may play a role in the renal resistance to PTH during dietary phosphorus deprivation.

Effects of aluminum on bovine parathyroid adenylate cyclase.

It is known that the secretion of PTH is often impaired in association with aluminum (Al3+) accumulation in patients with renal failure. The mechanisms involved remain ill defined. Since adenylate cyclase plays a role in the regulation of PTH secretion, these studies examine the effects of Al3+ on parathyroid adenylate cyclase. In membranes from normal bovine parathyroid glands, basal adenylate cyclase activity, in the presence of 0.2 mM ATP and 20 mM Mg2+, increased by 22% as Al3+ was raised from 0-10 microM. Higher Al3+ concentrations caused a progressive decrease in adenylate cyclase activity, reaching 68% inhibition of control activity at 2 mM Al3+. Since adenylate cyclase activation is influenced by the interaction of multiple sites within the adenylate cyclase complex, the nature of the inhibition by Al3+ was explored by examining the interaction of Al3+ with substrate ATP and with Mg2+, an allosteric activating metal ion. In the presence of 20 mM Mg2+, Al3+ concentrations of 1-2 mM resulted in noncompetitive inhibition with respect to ATP [decrease in maximum velocity (Vmax) from 4176 in the absence of Al3+ to 1106 pmol cAMP/mg protein X 15 min; Michaelis Menten constant (Km) for ATP was unchanged]. In contrast, at fixed ATP (0.2 mM), 0.5 mM resulted in competitive inhibition of adenylate cyclase with respect to Mg2+, whereas at higher Al3+ concentrations the inhibition was noncompetitive. When Mg2+ was replaced by Mn2+ (enzyme activity reflects the activity of the catalytic unit), the inhibitory effect of Al3+ on adenylate cyclase activity was abolished. These data suggest that the inhibition of parathyroid adenylate cyclase by Al3+ occurs at the level of the allosteric metal activating site. These data provide a potential mechanism for the inhibition of PTH secretion by Al3+.

Lack of a direct effect of 1,25-dihydroxycholecalciferol on parathyroid hormone secretion by normal bovine parathyroid glands.

Because of differing reports of an effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on parathyroid hormone (PTH) secretion, the present studies were performed in vitro using bovine parathyroid gland slices and isolated parathyroid cells. Both COOH-terminal and NH2-terminal RIAs for PTH were employed. No effect of 1,25(OH)2D3 on PTH secretion was found during a 4-h incubation of parathyroid slices in variable external calcium concentrations. The results from dual RIA measurements also showed no effect of 1,25(OH)2D3 on PTH secretion by isolated parathyroid cells during 90- to 150-min incubations with variable calcium concentrations. In addition, extensive analysis by polyacrylamide gel electrophoresis showed no effect of 1,25(OH)2D3 on cAMP generation. Whereas calcium inhibited and isoproterenol stimulated the production of cAMP, 1,25(OH)2D3 had no effect. We conclude that 1,25(OH)2D3 does not affect parathyroid gland function acutely in vitro.

The arterio-venous difference for immunoreactive parathyroid hormone and the production of adenosine 3,'5'-monophosphate by isolated perfused bone: studies with analogs of parathyroid hormone.

Recent studies suggest that the uptake of immunoreactive parathyroid hormone (iPTH) displays different characteristics in liver, kidney, and bone. Using the isolated perfused canine bone, we have characterized the uptake of two synthetic analogs of PTH, bovine PTH-(3-34) [bPTH-3(3-34)] and [Nle8,Nle18,Tyr34]bPTH-(3-34) amide, which had previously been shown to inhibit PTH-stimulated adenylate cyclase activity in renal membranes. During the infusion of synthetic bPTH-(1-34) (3 ng/ml), extraction of iPTH by isolated perfused bone averaged 37 +/- 1%, and cAMP production rose from 6.2 +/- 2.0 to 21 +/- 3 pmol/min. Extraction of bPTH-(3-34) was similar (35 +/- 2%), but cAMP levels did not increase over baseline with PTH concentrations as high as 100 ng/ml. Simultaneous infusion of bPTH-(1-34) and bPTH-(3-34) at molar ratios of 1:2 led to a 50% inhibition of PTH-stimulated cAMP increases. The extraction by bone of the more potent in vitro inhibitor of renal cortical adenylate cyclase [Nle8,Nle18,Tyr34]bPTH-(3-34) NH2 (3 ng/ml) averaged 39 +/- 2%. In contrast, cAMP production rose from a baseline of 5.6 +/- 0.5 to 12.5 +/- 2.0 pmol/min, demonstrating agonist activity for the analog. These studies show that [Nle3,Nle18,Tyr34]bPTH-(3-34) NH2 has agonist properties in isolated perfused bone, and unsubstituted bPTh-(3-34) inhibits PTH-stimulated cAMP release by perfused bone.

Altered adenylate cyclase kinetics in hyperfunctioning human parathyroid glands.

Current evidence suggests that parathyroid gland adenylate cyclase is involved in the control of parathyroid hormone (PTH) secretion. Thus, the altered control of PTH release in hyperparathyroidism may relate to altered adenylate cyclase activation. Therefore, we examined adenylate cyclase kinetics in membrane preparations from hyperfunctioning human parathyroid glands and normal human and bovine parathyroid tissues. There were no differences in the affinity for ATP between enzymes of normal and pathological tissue. However, the enzyme in 10 hyperfunctioning glands showed increased affinity for Mg++. The activation constant for Mg++ (KaMg) of adenylate cyclase in normal human glands was 10.6 +/- 2 mM, a value not different from that of normal bovine parathyroid tissue (9.5 +/- 1 mM). In contrast, the adenylate cyclase in membrane preparations from three of four hyperplastic and six of seven adenomatous human glands showed a markedly reduced KaMg, ranging from 0.85-1.64 mM and from 1.58-6.46 mM, respectively. In one adenoma and one hyperplastic gland, the Ka of the enzyme for Mg++ was close to normal. The addition of guanylylimidodiphosphate or GTP to the incubation mixture increased, in a dose-dependent manner, the apparent KaMg of the enzyme in the abnormal tissue toward normal, suggesting a defective nucleotide regulatory site in the adenylate cyclase of hyperparathyroid glands. In addition, the hyperparathyroid gland enzyme was less susceptible to inhibition by calcium, requiring 0.7-1 mM Ca++ for 50% inhibition, whereas comparable inhibition of the normal adenylate cyclase was seen at 0.22-0.28 mM Ca++. We conclude that the abnormal control of PTH secretion in hyperparathyroidism may be related, at least in part, to alterations in the characteristics of parathyroid gland adenylate cyclase.

Bone disease in patients with long-term renal transplantation and normal renal function.

Renal osteodystrophy may persist during the early years after renal transplantation. However, information on bone status after a successful long-term renal transplantation is limited. We examined biochemical parameters, bone mineral density (BMD), and bone histomorphometry in 25 asymptomatic men with normal renal function after 7.5 +/- 5.7 years of a renal transplantation. Serum calcium, phosphorus, alkaline phosphatase, and 1,25(OH)(2)D(3) levels and urinary calcium level and cyclic andenosine monophosphate excretion were within normal range in all patients. Serum intact parathyroid hormone (PTH) level was elevated in 11 subjects (133.6 +/- 78 pg/mL) and normal in the other 14 subjects (47.9 +/- 13.6 pg/mL). Mean BMD at the lumbar spine and femoral neck was low in the entire group. However, it progressively increased as time after transplantation increased, approaching normal values after 10 years. Bone histomorphometric analysis showed bone resorption, osteoid volume, and osteoid surface greater than normal range in the majority of patients. Bone formation rate and mineralization surface were low, and mineralization time was delayed in most patients. These lesions were more severe in patients after 3 to 4 years of transplantation but improved with time and approached normal values after a period of 10 years. PTH values did not correlate with bone histological characteristics or BMD. These results show that the bone alterations observed after long-term renal transplantation consist of a mixed bone disease in which features of high bone turnover coexist with altered bone formation and delayed mineralization. These findings may result from the combined effect of preexisting bone disease and immunosuppressive therapy.

Localization of brainstem motoneurons involved in dewlap extension in the lizard, Anolis equestris.

Dewlap extension is a characteristic component of inter- and intraspecific displays of Anolis lizards. Dewlap extension is accomplished by the contraction of ceratohyoid muscles associated with the hyoid apparatus. Retrograde transport of horseradish peroxidase (HRP) was used to investigate the brainstem origins of efferent fibers to the ceratohyoid muscles in Anolis equestris. Following application of HRP to the ceratohyoid muscle or to its nerve supply on one side of the throat, large polygonal motoneurons were found ipsilaterally in the vagal (Amb X) and glossopharyngeal (Amb IX) parts of nucleus ambiguus. Labelled neurons were more abundant and more heavily labelled in Amb X than in Amb IX. In addition, small spindle-shaped cells were labelled ipsilaterally in three parasympathetic nuclei that innervate glandular structures in the pharyngeal floor. HRP injections of the larynx labelled cells in many of the same locations, including Amb X and Amb IX. Thus, the nucleus ambiguus in Anolis contains motoneurons for supply of striated muscles in the hyoid (i.e. ceratohyoid muscles) and the larynx.

Neuron regeneration reverses 3-acetylpyridine-induced cell loss in the cerebral cortex of adult lizards.

Systemic administration of the neurotoxin 3-acetylpyridine to adult lizards results in extensive loss of neurons in the medial cerebral cortex, other brain areas remaining largely unaffected. After the neurotoxic trauma, new cells are produced by mitotic division of cells in the ventricular wall. The new cells migrate along radial glial fibers and replace lost neurons in the medial cortex. Electron microscopic examination of cells labeled with [3H]thymidine confirms that the newly generated cells are neurons. Thus, neuron regeneration can occur in the cerebral cortex of adult lizards.

3-Acetylpyridine-induced degeneration and regeneration in the adult lizard brain: a qualitative and quantitative analysis.

The neurotoxin 3-acetylpyridine (3AP) produces highly selective neuronal damage in specific areas of the lizard brain. Following 3AP intoxication, proliferation and migration of replacement neurons born in the ventricular walls lead to regeneration of the lesioned areas. Earlier studies established the time course of 3AP-induced degeneration and subsequent regeneration in the medial cerebral cortex of adult lizards (Font, E., García-Verdugo, J.M., Alcántara, S. and Lopez-García, C., Neuron regeneration reverses 3-acetylpyridine-induced cell loss in the cerebral cortex of adult lizards, Brain Res., 551 (1991) 230-235 [13]). Complementary to our previous studies, we now provide a qualitative and quantitative account of the extent and distribution of neurotoxic damage in the brain as a whole of lizards treated with 3AP using Nissl and Golgi stains, a degeneration-sensitive reduced-silver method, and electron microscopy. Additionally, [3H]thymidine autoradiography was used to assess changes in the rate of neurogenesis caused by the 3AP treatment. Single doses of 3AP caused degenerative changes in all the cortical areas, anterior dorsal ventricular ridge, deep layers of the lateral cortex, lateral amygdaloid nucleus, and nucleus sphericus, while sparing other brain areas. The most frequent neuropathic change after 3AP treatment was clumping of the nuclear chromatin with formation of pyknotic nuclei. Occasionally, a second type of injury was observed in neurons of the cell layer of the dorsomedial cortex (DMC). 3AP also caused a conspicuous loss of dendritic spines in bipyramidal neurons of the dorsomedial and dorsal cortices possibly representing transneuronal degeneration. Numbers of [3H]thymidine-labeled cells were higher in lizards previously treated with 3AP than in controls. These results demonstrate that the neurotoxic lesion is capable of inducing an increase in the normal rate of adult neurogenesis. Whereas regeneration in the remaining areas was morphologically and histologically complete, in some animals, cell proliferation in the DMC resulted in formation of an abnormal cell plate.

Postnatal neurogenesis in the telencephalon of turtles: evidence for nonradial migration of new neurons from distant proliferative ventricular zones to the olfactory bulbs.

Postnatal neurogenesis in the the turtle telencephalon was investigated by using bromodeoxyuridine immunocytochemistry and [3H]thymidine autoradiography. Red-eared slider turtles Trachemys scripta elegans (Cryptodira, Emydidae) 2-3 months old were injected with the thymidine analogue 5'-bromodeoxyuridine (BrdU) and allowed to survive for 7, 30, 90, and 180 days. Results indicate that cells in the walls of the lateral ventricles continue to proliferate postnatally. Shortly after BrdU treatment (seven days) most labelled cells were found in the walls of the lateral ventricles (ventricular zone: VZ). Labelled cells were particularly abundant in and around the ventricular sulci. The same pattern of labelling was found in the telencephalon of juvenile turtles (> two years old) injected with BrdU and killed seven day later, suggesting that the proliferative activity continues in the telencephalic VZ of turtles during juvenile stages of life and possibly into adulthood. With longer survival periods after BrdU administration (30, 90, and 180 days), the VZ of the telencephalon showed a similar pattern of labelling to that found at seven days. Furthermore, with survival periods of 90 and 180 days labelled cells resembling neurons were found in most telencephalic regions. The largest numbers of these putative neurons were found in the olfactory bulbs. By using [3H]thymidine autoradiography combined with electron microscopy these postnatally generated cells were confirmed as neurons. We conclude that postnatal neurogenesis occurs in the turtle telencephalon. This process is most prominent in the olfactory bulbs. From the pattern of proliferation of neuronal precursors in the VZ we infer that neurons recruited postnatally into the olfactory bulbs come from distant proliferative VZs in the walls of the lateral ventricles.