Publications by authors named "Gaffori O"

Oxytocin (OXT) reduced locomotion, rearing, grooming and bolus production in a circular open field at 15 min, but not at 60 min, after a subcutaneous (s.c.) injection.

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The potency of various C-terminal fragments of the neurohypophyseal hormone [Arg8]vasopressin [AVP-(1-9)] was determined using different avoidance behavioral test procedures in rats. Passive avoidance behavior was facilitated by these peptides. The fragments [Cyt6]AVP-(5-8) and [Cyt6]AVP-(5-9) were the most potent peptides tested after postlearning injection (consolidation) and preretention treatment (retrieval), respectively, after s.

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The present study was designed to investigate critical time periods for the memory modulating effect of vasopressin and several analogues in rats using a passive avoidance test as the behavioral paradigm. AVP, AVP-(4-8) and AVP-(5-8) were more effective when given immediately after the learning trial (consolidation), while AVP-(1-8) (DGAVP) and AVP-(5-9) were more active when administered one hour prior to the retention test (retrieval). DDAVP and AVP-(4-9) were highly active both when given immediately after the learning trial or 1 hour before the retention test.

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The behavioral changes induced by low doses of melatonin bilaterally injected into the nucleus accumbens of rats (decrease of locomotor activity and rearing and increase of grooming and sniffing behavior) were not affected by local pretreatment with beta-endorphin, but could be completely antagonized by alpha-type and gamma-type endorphins. Structure activity relationship studies revealed that the peptide beta-endorphin-(10-16) contains the essential information in this respect. The lowest effective dose of this peptide was 10 pg.

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N alpha-acetyl-gamma-endorphin (Ac gamma E) was identified in the rat neurointermediate pituitary, based on its immunological properties, comigration with synthetic Ac gamma E on HPLC and resistance to aminopeptidase-M degradation. The peptide appeared to be the main form of gamma-endorphin (gamma E) in this tissue and in brain areas remote from the hypothalamus (hippocampus, septum, amygdala). The anterior pituitary, the hypothalamus and the thalamus contained almost exclusively the non-acetylated form of gamma E.

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Small doses of melatonin (0.1-100 ng), injected into the nucleus accumbens of rats, decreased locomotor activity and rearing, and increased grooming and sniffing behaviour when the animals were tested in small test-cages. Larger doses of melatonin appeared to be less effective.

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The influence of AVP on open field behavior was studied at 15 and 60 min after s.c. injection.

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The aim of the present study was to differentiate between the postulated central behavioral effects of vasopressin and its pressor response, which is mainly mediated by peripheral vascular receptors. Thus, the interaction between the vasopressor antagonists dPTyr(Me)AVP (AAVPa) and d(CH2)5Tyr(Me)AVP (AAVPb) with the effects of [Arg8]vasopressin (AVP-(1-9)) and [pGlu4,Cyt6]AVP-(4-8) (referred to as AVP-(4-8)) was examined using passive avoidance behavior and the pressor response as parameters. AVP-(4-8) was approximately 4 and 200 times more potent than AVP-(1-9) in facilitating passive avoidance behavior after subcutaneous (SC) or intracerebroventricular (ICV) administration respectively.

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The concentration of immunoreactive arginine-vasopressin (IR-AVP) was measured in the cerebrospinal fluid (CSF) during acquisition and retention of passive avoidance behavior. IR-AVP level in CSF of male Wistar rats immediately after the learning trial was increased; the rate of which was related to the intensity of the electric footshock during the learning trial and the avoidance latency as measured 1 day after the learning trial. Immediately after the 24 h retention test IR-AVP levels were significantly increased in rats subjected to the low (0.

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Low doses (10 ng) of the dopamine agonist apomorphine induced hypolocomotion when injected into the nucleus accumbens of rats. This behavioral response was antagonized by local treatment with either the opioid peptide gamma-endorphin (gamma E) or the non-opioid peptide N alpha-acetyl-gamma-endorphin (Ac gamma E) in a dose of 100 pg. High doses of apomorphine (10 micrograms) r amphetamine (2 micrograms) injected into the nucleus accumbens resulted in hyperlocomotion.

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The neurohypophysial hormone vasopressin exerts antidiuretic, vasopressor and behavioural effects (for example, facilitation of memory processes). Vasopressin may alter animal behaviour via direct effect on brain processes. Recently, however, it has been suggested that vasopressin acts mainly at peripheral receptor systems and influences behavioural mechanisms by altering visceral afferent signals.

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N-terminal and C-terminal fragments of substance P (SP) have been shown to exert opposite effects on antinociception, grooming and fighting in mice. The present experiments explored whether these findings could be generalized to passive avoidance behavior. Substance P (SP-(1-11] and the C-terminal fragment pyroglutamyl-SP-(7-11) attenuated passive avoidance behavior when picogram amounts were injected into the nucleus accumbens.

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Arginine-vasopressin (AVP) is involved in memory processes. The memory effects of AVP are mediated by neuronal mechanisms taking place in limbic-midbrain structures. Therefore, immunoreactive AVP (IR-AVP) was measured in hippocampus and amygdala of male Wistar rats during acquisition and retention of passive avoidance behavior.

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The action of some CCK-8 related peptides, desulphated CCK-8 (CCK-DS), the sulphated form of CCK-8 (CCK-8-S) and ceruletide was explored in a number of test procedures with rats, in which antipsychotic agents are active. Following injection into the nucleus accumbens, all three peptides antagonized the hypolocomotion induced by low doses of apomorphine (10 ng). Ceruletide appeared to be the most potent in this respect (ED50: approximately 5 pg).

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The effect of subcutaneously injected DT gamma E (beta-endorphin, (beta E)2-17) on the pineal melatonin level was compared with that of closely related peptides and the neuroleptic drug haloperidol. As found previously, DT gamma E (3 ng/rat and 300 ng/rat) increased the melatonin levels. Similar doses of DT alpha E (beta E 2-16), DT beta E (beta E 2-31), gamma E (beta E 1-17), alpha E (beta E 1-16) and beta E failed to significantly change the melatonin levels in both the dark and the light phase.

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Immunoreactive arginine-vasopressin (IR-AVP) was measured in various hypothalamic and extrahypothalamic nuclei of male Wistar rats immediately after the 24 h retention test of a passive avoidance response. IR-AVP concentrations in paraventricular, suprachiasmatic and lateral septal nuclei were significantly decreased in comparison with the non-shocked rats, while IR-AVP was increased in the central amygdala nucleus, subfornical organ and locus coeruleus. No significant differences in IR-AVP levels were found in the habenular and periventricular hypothalamic nucleus, organum vasculosum of lamina terminalis and medial and dorsal raphe nucleus.

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Bilateral injection of gamma-endorphin into the nucleus accumbens of rats antagonizes the hyperlocomotion elicited by local treatment with relatively high doses of apomorphine. beta-Endorphin, alpha-endorphin, [Met]enkephalin, [Leu]enkephalin and des-Tyr1-gamma-endorphin do not mimic this effect of gamma-endorphin. Previous studies have shown that this antagonism by gamma-endorphin is mediated by a naloxone sensitive receptor system.

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The potency of two beta-endorphin fragments, des-Tyr1-gamma-endorphin (DT gamma E, beta E-(2-17) and des-enkephalin-gamma-endorphin (DE gamma E-(6-17) was compared on extinction of pole-jumping avoidance behavior and on retention of a one-trial step-through passive avoidance procedure. Both peptides facilitated the extinction of pole-jumping avoidance behavior and attenuated passive avoidance behavior. The gamma-type endorphin exhibited an inverted U-shaped dose-response curve on passive avoidance behavior but not on extinction of pole-jumping avoidance behavior.

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In this experiment we investigated in rats the effects of chronic injections (13 X 1.0 microgram and 13 X 2 micrograms i.m.

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Systemic injection or arginine vasopressin (AVP) (1 micrograms/rat) significantly prolonged extinction of a pole-jump, active avoidance response in rats; lateral ventricular injection of 1000-fold less AVP (1 ng/rat) produced similar results. A new AVP analogue, [1-deaminopenicillamine-2-(O-methyl)tyrosine]arginine vasopressin (dPTyr-(Me)AVP), is known to antagonize behavioral and vascular effects of exogenous AVP at molar ratios of 5 : 1. At a dose of 100 micrograms/rat (subcutaneously) dPTyr-(Me)AVP produces, by itself, a behavioral effect opposite to that of exogenous AVP, namely a facilitation of extinction.

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The lesion of the ventral mesencephalic tegmentum (VMT) and especially of the dopaminergic (DA) A10 neurons induced disturbances of spontaneous activity in the rat. Measured in different situations (circular corridor, open field, hole box), locomotor activity was dramatically and permanently increased (5 days of recording) without modifications of the circadian rhythm, although exploratory patterns of behavior were reduced. In contrast, the administration of a low dose of D-amphetamine (1 and 2 mg/kg i.

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The effects of ventral mesencephalic tegmentum (VMT) radio-frequency lessions on spontaneous and complex behaviors, such as food hoarding and alimentary patterns, were investigated. Activity measures indicated that VMT lesions increased horizontal activity in a circular corridor as well as in an open field whereas vertical activity (rearing) was decreased. After 12 hr of food deprivation, food hoarding and alimentary patterns were evaluated in a square open field to which rats had free access from their home cage.

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