Biomedical subjects

J H Pazo

Publications and source records attributed to J H Pazo.

At least 37 records · Page 2Linked to original sources

PubMed1990

Responses elicited by species-specific models in the cichlid Crenicichla lepidota (Heckel).

Species recognition by the cichlid fish C. lepidota was studied by measuring species-specific aggressive behavior toward either live conspecifics (control) or toward different two-dimensional models. A plain fish-shaped model elicited aggressive behavior, but the responses were mostly absent when the model was a rectangle. Adding heavy stripes to the fish-shaped form increased the responses, which were further enhanced by adding a spot. Comparable aggressive responses were also induced by adding spots and eye to dummies with thin stripes. We conclude that in our experimental conditions, fish-like shape and contrast seem to be of great significance for recognition of conspecifics in the cichlid C. lepidota (Heckel).

Aggression↗

PubMed1989

Automatic temperature controller for maintaining body temperature in experimental animals.

A system for autoregulation of body temperature of large and small animals is described. The device uses the IC AD590 as a temperature transducer. It operates on the basis of continuous regulation of the heating current, and does not emit transients which interfere with electrical recordings. A panel meter shows either the rectal temperature of the animal or the current flow to the blanket.

Body Temperature Regulation↗

PubMed1989

Changes in pancreatic exocrine secretion after repeated haloperidol administration.

The effect of repeated administration of haloperidol on the pancreatic secretion was studied in urethane-anesthetized Swiss mice. Haloperidol (2 mg/kg) injected daily i.p. for 7 days, increase the volume and protein content of the basal pancreatic juice significantly. This secretory activity was partially blocked by i.p. injection of atropine (5 mg/kg), both in control and treated animals. The volume of the secretory response to bethanechol, a cholinergic agonist, was decreased by haloperidol without any change in amylase release. From these findings it is concluded that repeated haloperidol treatment produces an increase of basal pancreatic secretion, which is probably the result of changes in the sensitivity of dopamine receptors of the gland.

Adrenergic Fibers↗

PubMed1989

Increase of muscarinic cholinergic receptors in the rat submandibular glands after parasympathectomy and repeated administration of haloperidol.

1. The mechanisms of the supersensitivity to cholinergic drugs after chronic haloperidol was studied in normal and parasympathectomized submandibular glands of the rats. 2. Both parasympathectomy and haloperidol treatment for 7 days (2 mg/kg/day, i.p.) increased the sialogogue response of the glands to methacholine, a cholinomimetic drug. 3. Both denervation and haloperidol administration induce up-regulation of the muscarinic receptors as expressed per gram of the tissue. 4. Haloperidol causes no further increase in sensitivity than denervation alone. 5. These data demonstrate that secretory supersensitivity to cholinergic drugs in the rat submandibular glands, after chronic haloperidol and parasympathectomy is related to an increase in muscarinic cholinergic receptors.

Animals↗

PubMed1989

Central and peripheral modulation of spontaneous neuronal activity in the caudate nucleus.

The modulatory action of the caudate on the neural activity of the contralateral nucleus was studied in locally anesthetized, paralysed and artificially ventilated cats. This type of preparation was necessary because of a complete suppression of spontaneous spike activity after subanesthetic doses of general anesthesia. Two types of caudate action potential were characterized according to their waveform: biphasic and triphasic spikes, with a predominance of the former. These waveforms appeared to be independent of recording distance; however, their responses were similar to both central and peripheral stimuli. Caudate stimulation modified the spontaneous activity of the majority of the single units recorded within the opposite nucleus. This effect was mainly inhibitory and keeps up certain somatotopic distribution in the rostrocaudal extent of the nucleus. Kainic lesion of the site of stimulation suppressed the responses in the contralateral caudate nucleus, whereas the responses to substantia nigra and precruciate cortex remained unaltered. On the other hand, stimulation of the precruciate cortex opposite to the recording sites always excited the caudate neurons. The responses evoked by stimulation of ipsilateral substantia nigra and of contralateral sciatic nerve followed a similar pattern to those elicited by caudate stimuli. These results suggest a mostly inhibitory effect of the caudate on neuronal activity within the opposite nucleus, which is reinforced by the action of central and peripheral somatosensory inputs.

Action Potentials↗

PubMed1987

Selective increase of alpha 1-adrenoceptors and muscarinic cholinergic receptors in rat cerebral cortex after chronic haloperidol.

The effect of chronic administration of haloperidol on alpha 1-, alpha 2-, and beta-adrenoceptors, cholinergic muscarinic, GABAA and benzodiazepine receptors in the cerebral cortex of the rat was investigated. Doses of 0.3 and 2 mg/kg of haloperidol during 7 days increased markedly the density of alpha 1-adrenoceptors without changes in affinity. The alpha 2- and beta-adrenoceptors were not modified after neuroleptic administration. The number of muscarinic receptors were also increased after haloperidol treatment (2 mg/kg/day). However, the GABAA and benzodiazepine binding sites remained unchanged. In the brainstem an increment in the alpha 1-, but not the beta-adrenoceptors was observed. The well known increase in the dopamine receptors in the striatum was confirmed. These observations demonstrate a multireceptor effect of haloperidol in the cerebral cortex.

Animals↗

PubMed1987

Effect of chronic administration of haloperidol on secretory response mediated by cholinergic receptors in rat submandibular glands.

Administration of haloperidol influences peripheral non-dopaminergic receptors. The sialagogue response of the submandibular glands of the rats to methacholine was enhanced by chronic administration of haloperidol. The binding of [3H]QNB to muscarinic receptors in the submandibular glands was not changed by chronic haloperidol. The supersensitivity of postsynaptic cholinergic receptors to drugs in haloperidol treated rats is not related to changes in the number or affinity of such receptors. This paper confirmed the sialagogue supersensitivity to adrenergic drugs related to an increase in alpha 1-adrenoceptors in the submandibular glands of haloperidol injected rats.

Animals↗

PubMed1987

Spinal cord substrate of the turning behavior induced by unilateral lesion of the entopeduncular nucleus.

The neural pathways in the spinal cord mediating circling behavior in animals with unilateral kainic acid lesion of the entopeduncular nucleus were studied in rats. The circling activity toward the lesioned side was indiced by i.p. administration of apomorphine (3 mg/kg). Section of the lateral funiculus ipsilateral to the lesioned entopeduncular nucleus, reduced significantly the rate of drug induced rotations. The above was a common lesion of ventrolateral and dorsolateral transections of the cervical spinal cord. However, the latter transection was more effective than the former to block the circling. On the other hand, lesion of the contralateral spinal cord fails to modify turning behavior. These findings suggest that crossed fibers descending in the dorsolateral quadrant directly from the basal ganglia or mediating synaptic relay in the lower brainstem may be the anatomical substrate of the circling produced by striatal stimulation.

Animals↗

PubMed1986

The sialagogue response of striatal dopamine receptors to L-dopa is not influenced by castration or chronic estrogen treatment.

The secretory response of salivary glands to L-dopa, elicited by stimulation of dopamine receptors in the striatum and the circling behavior induced by apomorphine in animals bearing a unilateral kainic lesion of the entopeduncular nucleus, was studied in intact and ovariectomized female rats. Castration did not modify the sialagogue response to L-dopa, while the turning behavior was significantly increased. Daily administration of 17-beta-estradiol benzoate during 7 days to ovariectomized rats decreased the circling activity to the level of intact female rats, while the salivary secretion to L-dopa was unaffected. The above findings suggest that the sialagogue response induced by L-dopa may be due to the interaction of this agonist with D1 striatal receptors, whose activity is not influenced by estrogens. However, we cannot rule out any possible alteration in the metabolism and/or presynaptic conversion of L-dopa to dopamine by estrogen treatment. The changes in turning behavior may be attributed to an antidopaminergic effect of estrogens and/or, like L-dopa, to modifications in the metabolism of apomorphine induced by the hormone.

Animals↗

PubMed1985

Chronic haloperidol causes increase in salivary response and alpha 1-adrenoceptors in submandibular gland of the rat.

The effect of chronic haloperidol on the receptor-secretion coupling of the submandibular glands of the rat was studied. After injection of 2 mg/kg haloperidol daily for 7 days, the dose-response curve to L-noradrenaline was displaced to the left, with lowering of the threshold and enhancement of the maximal response. This was accompanied by a 73% increase in alpha 1-adrenoceptors in the glands. The effect was selective, since no changes were observed in alpha 2- and beta-adrenoceptors.

Animals↗

PubMed1984

Salivary secretion induced by L-DOPA in haloperidol-treated rats.

The effect of chronic haloperidol treatment on salivary secretion induced by L-dopa, was studied in male Sprague-Dawley rats. Dose-response relationships for L-dopa, obtained 24 h after haloperidol treatment, showed that salivary secretion was greater in rats that had been injected with haloperidol (2 mg/kg/day, i.p.) for 7 days than in controls. The threshold doses requirements were significantly reduced in that group. Pretreatment with carbidopa suppressed the salivary secretion produced by L-dopa in haloperidol-treated and control rats whose glands had been denervated. The secretory response in innervated glands was higher in haloperidol-treated animals than in controls. Haloperidol treatment also increased salivation induced by L-noradrenaline as determined by dose-response relationships. This was associated with a decrease in the threshold doses requirement. In controls and in rats chronically treated with haloperidol, the salivary responses to L-noradrenaline were temporarily depressed by 80-90% by a prior acute injection of haloperidol (2 mg/kg, i.v.) presumably acting as an alpha blocker. A similar reduction was observed after acute treatment with phentolamine (3 mg/kg, i.v.). The data obtained in this study, i.e. that chronic administration of haloperidol increases the salivary response to L-dopa and L-noradrenaline, suggests that such an affect could be due to the development of supersensitivity of striatal dopamine receptors as well as of peripheral alpha-adrenergic receptors.

Animals↗

PubMed1983

Cholinergic mechanisms within the caudate nucleus mediate changes in blood pressure.

Microinjections of 10 micrograms of carbachol into the caudate nucleus induced changes in the blood pressure of cats anesthetized locally, paralyzed and artificially respired. These responses were dependent on the site of injection. Carbachol, microinjected at rostral levels of the caudate nucleus, elicited pressor responses while a decrease in blood pressure was observed following injections at caudal levels. Both of these effects were blocked by prior microinjection of atropine. Microinjections of carbachol outside the caudate did not affect the resting blood pressure. However, injections of carbachol into the lateral ventricle always produced pressor responses independent of the site of injection along the antero-posterior extension of the ventricle. On the other hand, microinjections of dopamine (20 micrograms) into the caudate nucleus failed to modify blood pressure. From this study, it is concluded that within the caudate nucleus there are two different muscarinic mechanisms, which when activated, mediate changes in blood pressure, possibly through the sympathetic nervous system.

Acetylcholine↗

PubMed1982

Changes in multiunit activity of nigral neurons induced by cholinergic and dopaminergic stimulation of the caudate nucleus.

The effects of stimulation of the caudate cholinergic and dopaminergic receptors on multiunit activity in the ipsilateral substantia nigra were studied in cats locally anesthetized, paralyzed and artificially respired. Cholinergic stimulation by intracaudate microinjections of 10 micrograms of carbachol diminished multiunit activity by 36% in the ventral substantia nigra (SN) and increased activity by 48% in the dorsal SN. This effect was abolished after electrolytic lesion of the ipsilateral striatonigral pathway. Opposite responses were observed following intracaudate administration of 20 micrograms of dopamine or 20 micrograms of D-amphetamine. Multiunit activity in the ventral SN increased by 36% and 34%, respectively, while the activity in the dorsal SN was reduced by 56% and 53%, respectively. Similar results were obtained in response to systemic administration of D-amphetamine. Extracaudate microinjections of carbachol and dopamine left multiunit activity in the SN unaffected. In conclusion, our results indicate an opposite action of caudate cholinergic and dopaminergic receptors on multiunit activity in the SN of the cat.

Animals↗

PubMed1982

Study of the neural basis of circling behavior induced by L-dopa in lesioned entopeduncular cats.

Experiments were carried out in cats bearing unilateral electrolytic lesion of the entopeduncular nucleus. The animals were tested for circling 1-2 weeks after surgery. Postoperatively the cats displayed transient spontaneous ipsiversive turning. The administration i.p. of L-DOPA (80 mg/kg) plus CarbiDOPA (30 mg/kg), suspended in 10% Tween 80, induced rotational behavior toward the lesioned side. This effect began about 26 min after drug administration and reached its maximum 40-110 min after the injection. Electrolytic lesions placed in the superior colliculus, strionigral pathway or pedunculopontine nucleus, contralateral to the lesioned entopeduncular nucleus did not modify the circling behavior induced by L-DOPA. Similar results were observed following unilateral lesion of the sensorimotor cortex or the VL thalamic nucleus. These results suggest that the circus movements induced by L-DOPA, in animals with unilateral lesion of the entopeduncular nucleus, is not mediated by the classic outflow of the striopallidal system.

Animals↗

PubMed1982

The role of the caudate-putamen nucleus in salivary secretion induced by L-DOPA.

Experiments were performed in rats of the Wistar strain anesthetized with alpha-chloralose (100 mg/kg). Electrolytic lesion of either components of the striopallidal complex (corpus striatum, globus pallidus or entopeduncular nucleus) reduced the sensory response to L-DOPA in the contralateral submaxillary glands. Damage to other neural structures, directly or indirectly related to the striopallidal system, left the salivary response unaffected. These structures were: substantia nigra, cerebral cortex, ventromedial and center median-parafascicular thalamic nuclei, nucleus accumbens and posterior hypothalamic areas, including the medial forebrain bundle and lateral habenular nucleus. However, lesions placed in H1-H2 fields of Forel and reticular formation, lateral to the periaqueductal gray, reduced the salivary response in the contralateral glands. This effect was similar to that observed in animals with lesions of the striopallidal complex. From this study, it is concluded that the striatum is the target area for the central effect of L-DOPA on salivary secretion, by activation of pathways descending through the fields of Forel and mesencephalic reticular formation to the contralateral lower brain stem.

Animals↗

PubMed1982

Somatotopic organization of caudate-caudate relationships in the cat.

Experiments were carried out on cats locally anesthetized and paralyzed with Flaxedil. Stimulation of the caudate nucleus and the sciatic nerve evoked biphasic positive-negative field potentials in the contralateral nucleus with mean latencies of 16.1 +/- 1.8 msec and 18.1 +/- 1.6 msec, and peak to peak amplitudes of 185.5 +/- 19.8 microV and 236.9 +/- 11.5 microV, respectively. A mediolateral distribution was observed in the caudate connections. The medial and lateral halves of one nucleus project to medial and lateral halves of the contralateral caudate, respectively. However, maximum amplitude responses were grouped in the middle-external two-thirds of the caudate. No responses could be evoked in the caudate tail by stimulation of any part of the opposite nucleus. On the other hand, the somatic afferents are distributed to all levels of the caudate nucleus. Although the largest responses were recorded in the same areas where the highest potentials were evoked by contralateral caudate stimulation. It is concluded that, in the cat, a topographic organization of the caudate-caudate relations exist in the mediolateral axis of the nucleus, and that its middle regions could be the primary receptive fields for caudate and somatic afferents.

Afferent Pathways↗

PubMed1981

Studies on the mechanisms of L-dopa-induced salivary secretion.

Systemic administration of L-dopa and dopamine elicited a marked and sustained secretory response in the rat's submaxillary glands. These effects were blocked by pretreatment with phentolamine plus propranolol. Acute unilateral sympathectomy (decentralization or denervation) reduced the response to L-dopa by about 41-48%. But it left unchanged the secretory response to dopamine. Chemical sympathectomy by hexamethonium caused a similar reduction (45%) in the secretory response to L-dopa while parasympathectomy was unable to modify the salivary secretion caused by L-dopa or dopamine. Pretreatment with haloperidol reduced the salivary secretion to L-dopa in normal animals (unoperated glands), while the response to dopamine was unaffected. On the other hand, haloperidol did not alter the salivary response to L-dopa in animals with surgical sympathectomy (denervation) as compared to the same animals treated with L-dopa alone. From this study we conclude that the salivary secretion induced by L-dopa is mediated by both central and peripheral mechanisms. Dopaminergic receptors may be involved in the central effect and alpha- and beta-receptors in the peripheral response.

Animals↗

PubMed1981

Electrophysiological study of evoked electrical activity in the pineal gland.

Experiments were carried out in rats, unanesthetized, paralyzed and artificially respirated. The electrical activity from the pineal gland was recorded with bipolar electrodes. Field potentials were evoked in the pineal after peripheral (photic and sciatic nerve) and central (septal area, habenular complex and optic tract) stimulations. In general these potentials were biphasic with the exception of that evoked by the sciatic nerve and optic tract, which exhibited a complex response and a triphasic field potential, respectively. Bilateral sympathectomy did not modify the pineal evoked responses, but when the pineal stalk was sectioned all the responses were immediately suppressed after the lesion. On the basis of the above experimental data one could conclude that the bulk of the inputs to the pineal gland come through its stalk. At the present, the physiological significance of these findings is not clear.

Animals↗