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Biomedical subjects

G B Azzena

Publications and source records attributed to G B Azzena.

At least 19 recordsLinked to original sources
PubMed1999

Nitric oxide regenerates the normal colonic peristaltic activity in mdx dystrophic mouse.

We demonstrated in vitro that the colonic peristaltic activity is modified in dystrophin-deficient mdx mouse indicating a defect in the enteric nervous system (ENS). Since nitric oxide (NO) has been proposed as a putative inhibitory mediator of ENS, here we have examined the effects of both L-Arginine (L-Arg) and Nomega-nitro-L-arginine methyl ester (L-NAME) on the peristaltic activity of mdx mouse distal colon. The motor pattern of colonic segment showed irregular peristaltic waves. L-Arg (10(-7) - 10(-5) M) induced the peristaltic activity to slow down. At a concentration of 10(-5) M, L-Arg produced hypomotility, characterised by a decrease in amplitude, frequency and ejected fluid volume. Conversely, L-NAME elicited hypermotility, this effect being reversed once again by the subsequent addition of L-Arg. Interestingly the addition of 10(-5) M L-Arg to the organ bath led to the normal progression, in an oral to aboral direction, of 90% of the peristaltic waves. This last result strongly suggests that exogenous application of L-Arg restores the integrative circuits of the ENS responsible for programming and co-ordinating peristaltic activity in the distal colon of mdx mouse.

Animals↗
PubMed1999

Characterization of Ca(2+)-channels responsible for K(+)-evoked [(3)H]noradrenaline release from rat brain cortex synaptosomes and their response to amyotrophic lateral sclerosis IgGs.

The contribution of the different Ca(2+)-channel subtypes to the K(+)-evoked [(3)H]noradrenaline release from rat cerebral cortex synaptosomes has been investigated. In the same experimental model, it was also verified whether the calcium-mediated neurotransmitter release is influenced by IgGs purified from sera of seven patients affected by sporadic amyotrophic lateral sclerosis. Synaptosome treatment with 3.0 microM nifedipine or 2.0 microM calciseptine, which block L-type channels, slightly decreased [(3)H]noradrenaline release, the reduction being 7 and 13% of the control values, respectively. The blockade of N-type Ca(2+)-channels with omega-conotoxin-GVIA (0.001-1.0 microM) induced a concentration-dependent reduction of the neurotransmitter release, with maximum effect of 34%. omega-Agatoxin-IVA failed to significantly affect the studied release, which was instead markedly reduced by omega-conotoxin-MVIIC. After the blockade of N-type channels with maximal concentrations of omega-conotoxin-GVIA, 3.0 microM omega-conotoxin-MVIIC reduced the release by 58%. Synaptosome treatment with amyotrophic lateral sclerosis IgGs enhanced the K(+)-evoked [(3)H]noradrenaline release, which was mostly mediated by P/Q- and N-type Ca(2+)-channels. The increase induced by pathologic IgGs (0.2 mg/ml) ranged from 11 to 62% for the different patients, and it was concentration-dependent. The basal release was instead unaffected by IgG treatment. The results of the present study suggest that the K(+)-evoked [(3)H]noradrenaline release from brain cortex synaptosomes is mainly mediated by activation of P/Q- and N-type Ca(2+)-channels. Autoantibodies present in the sera of patients affected by sporadic amyotrophic lateral sclerosis may interact with these channels by producing an increased calcium influx, with consequent enhancement of the neurotransmitter release. Preliminary results of the present study have been published in abstract form (Martire et al., 1997, Pharmacol. Res. 35:9).

Animals↗
PubMed1999

Auditory steady-state responses to click trains from the rat temporal cortex.

In order to investigate the mechanisms underlying the generation of steady-state responses (SSRs), auditory evoked potentials elicited by click trains presented at several stimulation rates (30, 40, 50, 60 Hz) were recorded in 7 awake rats by means of epidural electrodes placed over the temporal cortex. Mean amplitude-rate function calculated on the recorded responses appeared almost flat and showed the maximum value at 50 Hz, while mean phases showed a linear increase when increasing the stimulation rate. In each rat, predictions of the recorded responses at 30, 40, 50 and 60 Hz were synthesized by superimposing middle-latency auditory evoked potentials (MAEPs) at suitable time intervals at each rate. Mean amplitudes calculated on the predicted curves decreased linearly when increasing the stimulation rate and appeared higher in comparison to those obtained from the recorded SSRs. Predicted phases showed a linear increase when increasing the stimulation rate and were leading with respect to corresponding phase values calculated for recorded SSRs. Our findings indicate that the MAEP superimposition mechanism does not adequately predict the generation of temporal recorded SSRs in rats. This was explained by admitting that phenomena related to the recovery cycle and, to a lesser extent, to rate-dependent facilitating effects come into play.

Acoustic Stimulation↗
PubMed1998

In vitro excitatory actions of corticotropin-releasing factor on rat colonic motility.

Corticotropin-releasing factor (CRF) has been shown to affect gastrointestinal functions, however, a direct effect of CRF on the intestine has not been demonstrated. To determine the direct effect of CRF and its antagonist alpha-helical-CRF9-41 (alpha-h-CRF) on the enteric nervous system, we studied the action of these substances on electrical and mechanical parameters of peristaltic activity on isolated distal colon of the rat. The effects of CRF were evaluated in vitro on rat isolated colonic segments in which intraluminal pressure, longitudinal displacement, ejected fluid volume and extracellular electrical activity were simultaneously recorded during colonic peristaltic reflex. The addition of CRF (10(-10) - 10(-8) M) to the bath fluid provoked a concentration-dependent increase of both mechanical and electrical peristaltic activity. The CRF-receptor antagonist alpha-h-CRF dose-dependently (10(-10) - 10(-7) M) induced a decrease of the colonic mechanical and electrical activity and prevented (10(-8) - 10(-6) M) CRF (10(-8) M) maximal effects. These results indicate: (a) CRF can exert its effects on colon functions by a direct action, (b) a specific CRF-receptor is present in the rat colon. Indeed, CRF effects are antagonized by the specific CRF antagonist alpha-h-CRF, (c) the fact the alpha-h-CRF displays an activity on its own reveals that colonic functions are controlled by an endogenous CRF tonic activity.

Animals↗
PubMed1997

Inhibition of nitric oxide synthase prevents magnesium-free-induced epileptiform activity in guinea-pig piriform cortex neurones in vitro.

The effects of N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, were examined on Mg2+-free-induced epileptiform activity, in guinea-pig piriform cortex slices in vitro. L-NAME (0.1-1 mM) had no effect on neuronal membrane properties or electrically-evoked postsynaptic potentials (PSPs). In contrast, during superfusion of the slices with Mg2+-free solution neurones exhibited spontaneous and stimulus-evoked epileptiform potentials that were suppressed in the presence of L-NAME (100 microM) or the selective NMDA receptor antagonist DL-APV (100 microM). The inhibitory effects induced by L-NAME were reversibly reduced by L-arginine (1 mM), but not D-arginine (1 mM), the latter drug not being a substrate for NO formation. It was concluded that L-NAME can suppress epileptiform activity induced by Mg2+-free exposure primarily through a decrease in presynaptic transmitter release, although additional actions on the NMDA-receptor complex were also considered.

Animals↗
PubMed1996

Sympathetic control of skeletal muscle function: possible co-operation between noradrenaline and neuropeptide Y in rabbit jaw muscles.

Stimulation of the cervical sympathetic nerve at 10/s increases by 12.9 +/- 0.7% peak tension of maximal twitches in the directly stimulated jaw muscles and markedly depresses (41.6 +/- 1.3%) the tonic vibration reflex (TVR) elicited in the same muscles by vibration of the mandible. Both effects are not significantly influenced by administration of beta-adrenoceptor antagonists. When both alpha- and beta-adrenergic receptors are blocked, sympathetic stimulation induces a very small increase in twitch tension (3.8 +/- 0.7%), while no detectable change in the TVR is observed. Close arterial injection of alpha 1-adrenoceptor agonist phenylephrine mimics the effects induced by sympathetic stimulation on twitch tension and TVR, dose-dependently. The noradrenaline co-transmitter neuropeptide Y also produces a long-lasting, dose-dependent increase in the twitch tension which is unaffected by blockade of adrenergic receptors as well as of the neuromuscular junctions. Contribution of neuropeptide Y to the sympathetically-induced reduction of the stretch reflex is not clearly demonstrated. These data suggest that co-operation between noradrenaline and neuropeptide Y may be effective in determining sympathetic modulation of skeletal muscle function.

Animals↗
PubMed1995

Possible modulation of auditory middle latency responses by nitric oxide in the inferior colliculus of anaesthetized rats.

Nitric oxide (NO) is a short-lived radical species endowed with intercellular signalling functions in the mammalian brain. In the present study we have investigated the effects of focal injection into one inferior colliculus of N omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, on the acoustic middle latency responses (MLRs) evoked by click stimuli and recorded from the auditory cortex in anaesthetized rats. Microinfusion of L-NAME (1.0 mM) did not alter the latency of MLRs nor did it affect the evoked brain stem responses (ABRs). By contrast, L-NAME reduced P1a-N1 amplitude of MLRs by 51.7 +/- 6.6% (mean +/- SEM; n = 5) and almost complete recovery to background amplitude was obtained 15-25 min after treatment. The less active isomer, D-NAME (1.0 mM; n = 5), failed to produce consistent effects on the evoked MLRs. A higher concentration of L-NAME (5.0 mM; n = 5) yielded a 69.0 +/- 13.3% inhibition whereas maximum inhibition produced by 0.5 mM (n = 3) L-NAME was approximately equal to 10% of control value. The inhibitory effect typically evoked by 1.0 mM L-NAME was prevented by treating rats with L-arginine (5.0 mM; n = 5), the endogenous precursor of NO synthesis. Reduction of MLR amplitude was also obtained in rats receiving intracollicular injection of dizocilpine (MK801; 1.0 microM) and LY274614 (1.0 mM), two selective N-methyl-D-aspartate (NMDA) receptor antagonists. In conclusion, the present data support a role for intracollicular NO in the processing and transmission of the acoustic input to the auditory cortex in the rat.

Acoustic Stimulation↗
PubMed1995

Analysis of peristaltic reflex in young mdx dystrophic mice.

Experiments have been carried out in isolated distal colon of young normal and mdx dystrophic mice, the animal homologous of Duchenne muscular dystrophy. Intraluminal pressure, longitudinal displacement, ejected fluid volume and changes in morphology during peristaltic events were recorded. In both male and female normal animals, pressure waves were observed to be generally regular in shape, amplitude (14.19 +/- 2.45 (SD) cm H2O), frequency (54.00 +/- 10.78 h-1) and duration (31.12 +/- 3.47 s). The propulsive activity resulted in orthograde transport of intraluminal content. Mdx mice exhibited great changes in relation to sex, since clear and more marked dysfunctions were recorded in female mice. In male mdx animals, an increase of intraluminal pressure (22%) and ejected fluid volume (38%) were recorded. In females, a remarkable significant (P < 0.001) increase (78%) of intraluminal pressure was observed. Simultaneous anterograde and retrograde propulsive activity also occurred. Localized annular constrictions in proximal, central and distal portions of colonic segment were observed. The implications of the results are discussed in terms of injury of myogenic and nervous pathways controlling mdx colonic smooth muscle.

Animals↗
PubMed1995

Generation of human auditory steady-state responses (SSRs). I: Stimulus rate effects.

Auditory evoked responses were recorded in 16 normally hearing subjects in order to investigate the mechanisms underlying the generation of the 40 Hz steady-state response (SSR). In the first part of our study, auditory potentials were evoked by 0.1 ms clicks presented at 105 dB p.e. SPL with repetition rates of 7.9 (to obtain middle latency response, MLR), 20, 30, 40, 50, 60 Hz. In each subject predictions of the responses recorded at stimulus repetition rates of 30, 40, 50, 60 Hz were synthesized by superimposing MLRs at suitable time intervals. The calculated mean amplitude/rate and phase/rate functions behaved similarly for the recorded and predicted curves, showing the highest amplitude at 40 Hz and a linear increase of phase values when increasing the stimulus rate. Nevertheless the synthetic curves closely predicted amplitude and phase values of the recorded responses only at 40 Hz. At frequencies below 40 Hz, the mean amplitude of the predicted curve was lower than that of the recorded one while at frequencies above 40 Hz the mean amplitude was higher. Predicted phase values were found lagging at 30 Hz, and leading at 50 Hz and 60 Hz in comparison to phase values calculated on the recorded responses. Our findings suggest that a model based on the linear addition of transient MLRs is not able to adequately predict steady-state responses at stimulus rates other than at 40 Hz. Other mechanisms related to the recovery cycle of the activated system come into play in the steady-state response generation causing a decrease in amplitude and an increase in phase lag when increasing the stimulus repetition rate.

Acoustic Stimulation↗
PubMed1993

Vestibular projections to hypothalamic supraoptic and paraventricular nuclei.

The effects of electrical stimulation of the eighth nerve and caloric stimulation of the labyrinth were tested on the spontaneous or evoked electrical activity of single neurons located in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei. It was found that these neurons responded to both kinds of stimulation. In particular, the neurons of the SON showed a predominant response pattern characterized by a sequence of excitation-inhibition, whereas the neurons of the PVN showed different patterns of response with various combinations of inhibition and excitation sequences. The latencies of these neuronal responses to the electrically induced eight nerve volleys were compatible only with a polysynaptic connection. The possible pathways involved in this vestibulo-hypothalamic relation as well as their functional role are discussed.

Animals↗
PubMed1991

Penicillin-induced paroxysmal activity in brainstem neurons.

The spontaneous electrical activity of single mesencephalic and bulbar neurons was recorded in hemispherectomized rats, following topical application of the GABA-antagonist penicillin-G on the mesencephalon or on the rhombencephalon, to investigate whether these structures could develop a specific penicillin paroxysmal activity independently of the upper structures. Twenty minutes following penicillin-G, the mesencephalic neurons developed paroxysmal activity characterized by a significant increase in the spontaneous electrical activity, the appearance of multiunit activity and, frequently, phasic activity with rhythmical outbursts. The paroxysmal activity at bulbar level appeared later than that observed in the mesencephalon and was characterized by a significant increase of the spontaneous firing rate of the neurons, single short bursts and sometimes rhythmical outbursts. The bulbar outbursts always discharged at lower frequency than those at the mesencephalic level. Following a midcollicular transection the paroxysmal bulbar activity abruptly disappeared. This phenomenon might be explained by a loss of facilitation from superior structures on the bulbar neurons which in roditors show a poor GABA-receptor distribution. In other words, penicillin alone, due to the scarcity of GABA receptors, might not be sufficient to induce paroxysmal activity in bulbar neurons but the simultaneous presence of both the superior facilitation and the drug might enhance neuronal excitability to a critical level. However, the diffusion of the drug upwards to the mesencephalon, with consequent activation of a system allowing the downward propagation of paroxysmal activity, cannot be excluded. In conclusion, while the mesencephalic neurons demonstrate a proper ability to develop penicillin paroxysmal discharge, the bulbar neurons must be sustained by intact connections with upper structures to be able to do so.

Animals↗
PubMed1989

Volume receptors in guinea pig labyrinth: relevance with respect to ADH and Na control.

We tested the hypothesis that changes in extracellular fluid volume are reflected by pressure changes within structures of the inner ear and that through neural pathways, a control mechanism exerts an influence on antidiuretic hormone (ADH) release and Na excretion. The study was performed on 35 guinea pigs. In protocol 1, 13 animals were studied before and after decompression of the inner ear by bilateral fluid withdrawal in an experimental setting of sustained isotonic expansion that kept the osmoreceptor partially activated and the intrathoracic volume receptors suppressed. A group of six sham-operated animals served as control. In protocol 2, nine animals were studied before and after a unilateral rise in their inner ear pressure during slightly hypertonic low-rate infusions that kept the osmoreceptor and thoracic volume receptors stimulated. A group of seven sham-operated guinea pigs served as controls. Decompression of the inner ear was attended by a rise in plasma ADH from 11.9 +/- 2.4 to 29.1 +/- 6.9 pg/ml, in urine osmolality (Uosmol) from 470 +/- 48 to 712 +/- 46 mosmol/kg (P less than 0.001), and a fall in urine flow rate (V) from 184 +/- 47 to 71 +/- 11 microliters/min (P less than 0.01), whereas plasma Na (PNa) and osmolality (Posmol) did not change. During inner ear hypertension, plasma ADH fell from 25.6 +/- 3.9 to 18.4 +/- 3.1, Uosmol from 829 +/- 58 to 627 +/- 43 (P less than 0.001), and V rose from 51 +/- 11 to 130 +/- 23 (P less than 0.001), whereas glomerular filtration rate, PNa, and Posmol did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Beta-endorphin in experimental canine spinal ischemia.

Plasma and cerebrospinal fluid beta-endorphin concentrations were radioimmunologically assayed in dogs subjected to spinal cord ischemia induced by infrarenal aortic ligature and in control sham-operated dogs. Plasma beta-endorphin levels rose significantly following surgery in control dogs but were unaffected by spinal ischemia. On the other hand, a significant increase in cerebrospinal fluid beta-endorphin concentration occurred after spinal ischemia, while surgical stress had no significant effect. Thus, the origins of plasma and cerebrospinal fluid beta-endorphin may be different, with the former secreted from the hypophysis and the latter from nervous tissue. Observed changes in cerebrospinal fluid beta-endorphin concentration could be related to the ischemic lesion of nervous tissue while the changes in plasma levels may reflect general stressing factors such as the surgery in our experiments.

Animals↗
PubMed1986

The vestibular cortical projection during spinal decompensation.

The removal of spinal afferents in rabbits submitted to unilateral lesion of the labyrinth and fully compensated greatly modified the field potentials as well as the single unit responses recorded from the cortical vestibular area during stimulation of the intact eighth nerve. In particular, an increase of contralateral and a decrease of ipsilateral potentials were observed. These asymmetrical responses indicate that the influence of the spinal cord in compensating the effects of unilateral lesion of the labyrinth is directed to balance not only the electrical activity of the brain-stem structures, but also that of the cerebral cortex. It appears, therefore, that spinal signals intervene not only in the compensation of vestibulospinal and vestibulo-oculomotor functions but also of cortical functions, such as that related to vestibular sensation.

Animals↗
PubMed1983

Omental transposition or transplantation to the brain and superficial temporal artery--middle cerebral artery anastomosis in preventing experimental cerebral ischaemia.

Transposition of lengthened omentum to the brain surface, transplantation of an omental graft, or superficial temporal artery--middle cerebral artery anastomosis were performed in dogs prior to transcranial occlusion of the ipsilateral middle cerebral artery at its origin, including the bifurcation of the internal carotid artery. Both omentum and by-pass were able to reduce the changes in cerebral blood flow, somatosensory evoked responses, cerebral water and electrolyte content, consequent to the ischaemic insult. In the experimental conditions adopted in this study, the effect of omental transposition in maintaining high levels of flow throughout the entire occluded hemisphere was more marked compared to that resulting from the other methods, while the onset of ischaemic cerebral oedema was affected approximately at the same degree by all procedures. The results point to the role of the transposed omentum in providing an effective collateral circulation to the ischaemic brain.

Animals↗
PubMed1981

[The vestibular nuclei as the integration center of central and peripheral afferent projections].

Responses of individual vestibular units were recorded in cat following electrical stimulation of the cerebral cortex and peripheral nerves. Convergence of central and peripheral inputs were recorded from 28 out of 75 cells (37%), localized in the lateral vestibular nucleus. The most important inputs to vestibular neurons come from the areas of sensorimotor cortex and peripheral nerves concerned with the same limb. However, crossed effects were observed in a limited number of vestibular neurons.

Animals↗