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Evidence in the human of a hypotensive and a bradycardic effect after mouth opening maintained for 10 min
No full textPURPOSE:
We have recently shown that in humans submaximal mouth opening associated with partial masticatory movements for 10 min is followed by a small but significant and prolonged reduction of blood pressure and heart rate. We here report the effects of a fixed mouth opener.
METHODS:
In 22 seated normotensive volunteers the effect on blood pressure and heart rate was studied in randomized order after fixed mandibular extension and after a control procedure consisting in keeping a stick between the incisor teeth (both for 10 min). Automated recordings every 10 min were done for 40 min before and 120 min following the procedure.
RESULTS:
Two-way ANOVA for repeated measures on absolute values (actual recordings) and on changes from baseline revealed that, compared to controls, systolic, diastolic and mean blood pressure and heart rate were significantly lower after mandibular extension. Compared to controls, mandibular extension induced an average blood pressure drop of 2.88 mmHg (systolic), 2.55 mmHg (diastolic) and 2.42 mmHg (mean) over the entire observation period. The average decline over the central part of the observation period (30th to 80th min) was, respectively, of 3.62, 3.70 and 3.61 mmHg. The decrements of heart rate were of 2.11 and 2.66 beats per min. All these differences were statistically significant. The hypotensive and bradycardic responses persisted for 70-120 min.
CONCLUSIONS:
This study shows that, in normotensives, a single fixed submaximal mouth opening for 10 min is followed by prolonged albeit small reductions of blood pressure and heart rate
Acetyl-L-Carnitine affects the electrical activity of mechanosensory neurons in Hirudo medicinalis ganglia
Full text linkWas previously discovered that in the leech Hirudo medicinalis, acetyl-l-carnitine (ALC) affects forms of non-associative learning, such as sensitization and dishabituation, due to nociceptive stimulation of the dorsal skin in the swim induction behavioural paradigm, likely through modulating the activity of the mechanosensory tactile (T) neurons, which initiate swimming. Since was found that ALC impaired sensitization and dishabituation, both of which are mediated by the neurotransmitter serotonin, the present study analyzed how ALC may interfere with the sensitizing response. Was already found that ALC reduced the activity of nociceptive (N) neurons, which modulate T cell activity through serotonergic mediation
Transcription and protein synthesis inhibitors influence long-term effects of acetyl-l-carnitine on non-associative learning in the leech
No full textAcetyl-l-carnitine (ALC) is the principal acetyl ester of L-carnitine and it plays an essential role in intermediary metabolism. ALC affects several targets in the nervous system. Along this line of investigation, we analyzed the long-term effects of ALC on elementary nonassociative learning in the swimming induction model of the leech Hirudo medicinalis, in which nociceptive stimulation of the dorsal skin produces a more rapid swim response to a test stimulus (sensitization). In this simplified model a single ALC administration blocked the sensitizing effects of nociceptive stimulation in swim induction showing increasingly long lasting effects. Herein, we have analyzed the long-term effects of ALC on sensitization and dishabituation. Leeches were treated with inhibitors of either transcription or protein synthesis 30 min after the administration of ALC and, subsequently, subjected to noxious stimuli: the animals exhibited a sensitized swimming response 6 days after ALC treatment but not after 2 hours indicating that the long-term suppressive effects of ALC on sensitization/dishabituation needed mRNA and protein synthesis
Cyclic AMP mediates the inhibition of the Na+/K+ electrogenic pump by serotonin in t sensory neurones of the leech
No full textActivity-dependent increase of the AHP amplitude in T sensory neurons of the leech
No full textWe identified a new form of activity-dependent
modulation of the afterhyperpolarization (AHP) in tactile (T)
sensory neurons of the leech Hirudo medicinalis. Repetitive intracellular
stimulation with 30 trains of depolarizing impulses at 15-s
inter-stimulus interval (ISI) led to an increase of the AHP amplitude
(60% of the control). The enhancement of AHP lasted for 15 min.
The AHP increase was also elicited when a T neuron was activated by
repetitive stimulation of its receptive field. The ISI was a critical
parameter for the induction and maintenance of AHP enhancement.
ISI duration had to fit within a time window with the upper limit of
20 s to make the training effective to induce an enhancement of the
AHP amplitude. After recovery from potentiation, AHP amplitude
could be enhanced once again by delivering another training session.
The increase of AHP amplitude persisted in high Mg2 saline, suggesting
an intrinsic cellular mechanism for its induction. Previous
investigations reported that AHP of leech T neurons was mainly due
to the activity of the Na/K ATPase and to a Ca2-dependent K
current (IK/Ca). In addition, it has been demonstrated that serotonin
(5HT) reduces AHP amplitude through the inhibition of the Na/K
ATPase. By blocking the IK/Ca with pharmacological agents, such as
cadmium and apamin, we still observed an increase of the AHP
amplitude after repetitive stimulation, whereas 5HT application completely
inhibited the AHP increment. These data indicate that the
Na/K ATPase is involved in the induction and maintenance of the
AHP increase after repetitive stimulation. Moreover, the AHP increase
was affected by the level of serotonin in the CNS. Finally, the
increase of the AHP amplitude produced a lasting depression of the
synaptic connection between two T neurons, suggesting that this
activity-dependent phenomenon might be involved in short-term plasticity
associated with learning processes
Octopamine and Leydig cell stimulation depress the after-hyperpolarization in T sensory neurons of the leech
No full textIn touch sensory neurons of the leech, a train of spikes evoked by intracellular electrical stimulation leads to an afterhyperpolarization, mainly due to the activation of the Na+/K+ electrogenic pump and partly to a Ca’+ -activated K+ conductance. It has been found that serotonin is able to reduce
the afterhyperpolarization through the inhibition of the Na+/K+ electrogenic pump. We have investigated the possible modulation of the afterhyperpolarization by other endogenous neurotransmitters and we have found that octopamine is also able to reduce its amplitude. The electrical stimulation of the octopaminergic Leydig neurons mimics this effect. We have compared the actions of the two amines and found that
the effect of serotonin is blocked by methysergide but not by high [Mg2+] or by phentolamine, and it is still present in touch cells isolated in culture. On the contrary, the octopamine modulation of the afterhyperpolarization does not occur in single touch cells in culture and it is blocked by all these treatments.
These data suggest that while serotonin should act monosynaptically, octopamine should act through
a serotonergic pathway
Role for Calcium Signaling and Arachidonic Acid metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T sensory neurons
No full textPrevious studies have revealed a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) neurons of the leech Hirudo medicinalis. The firing of T cells is characterized by an AHP, which is mainly due to the activity of the Na+/K+ ATPase.
Low-frequency repetitive stimulation of T neurons leads to a robust increment of the AHP amplitude, which is correlated with a synaptic
depression between T neuron and follower cells. In the present study, we explored the molecular cascades underlying the AHP increase. We tested the hypothesis that this activity-dependent phenomenon was triggered by calcium influx during neural activity by applying blockers of voltage-dependent Ca2+ channels. We report that AHP increase requires calcium influx that, in turn, induces release of calcium from intracellular stores so sustaining the enhancement of AHP. An elevation of the intracellular calcium can activate the cytosolic isoforms of the phosholipase A2 (PLA2). Therefore we analyzed the role of PLA2 in the increase of the AHP, and we provide evidence that not only PLA2 but also the recruitment of arachidonic acid metabolites generated by the 5-lipoxygenase pathway are necessary for the induction of AHP increase. These data indicate that a sophisticated cascade of intracellular signals links the repetitive discharge of T neurons to the activation of molecular pathways, which finally may alter the activity
of critical enzymes such as the Na+/K+ ATPase, that sustains the generation of the AHP and its increase during repetitive stimulation.
These results also suggest the potential importance of the poorly studied 5-lipoxygenase pathway in forms of neuronal plasticity
DIFFERENTIAL EFFECTS OF PACAP-38 ON SYNAPTIC RESPONSES IN RAT HIPPOCAMPAL CA1 REGION
No full textPituitary adenylate cyclase-activating polypeptide (PACAP-38) is a member of the vasointestinal polypeptide (VIP)/secretin/glucagon family of neuropeptides for which neuroregulatory functions have been postulated.
PACAP-38 receptors are expressed in different brain regions, including hippocampus. In this study, we examined the dose-dependent effects of PACAP-38 on the excitatory postsynaptic field potential (fEPSP)evoked at the Schaffer collateral-CA1 synapse in rat hippocampal slices. Bath application of low dose (0.05 nM)of PACAP-38 induced long-lasting facilitation of the fEPSP. This enhancement was blocked by the
cholinergic receptor antagonist atropine and partially by the NMDA receptor antagonist 2-amino-5-phosphonovalerate (APV) and therefore, shares a common mechanism with LTP. In contrast, a high dose (1 μM)of PACAP-38 induced a persistent depression of the fEPSP that was not blocked by antagonists of
cholinergic receptors (i.e., atropine and mecamylamine), adenosine receptors (i.e., DCPCX), or glutamatergic NMDA receptors (APV). Intermediate doses (0.1–0.5 μM) of PACAP-38 produced an initial decrease of the fEPSP followed by an enhancement. This decrease was not blocked by atropine whereas the facilitation was.
These results show that PACAP-38 modulates CA1 synaptic transmission in a dose-dependent manner and that the peptide interacts with cholinergic and glutamatergic systems
Inhibition of Na+/K+ ATPase potentiates synaptic transmission in tactile sensory neurons of the leech
No full textIncreasing evidence indicates that modulation of Na+⁄K+ ATPase activity is involved in forms of neuronal and synaptic plasticity. In
tactile (T) neurons of the leech Hirudo medicinalis, Na+⁄K+ ATPase is the main determinant of the afterhyperpolarization (AHP),
which characterizes the firing of these mechanosensory neurons. Previously, it has been reported that cAMP (3',5'-cyclic adenosine
monophosphate), which mediates the effects of serotonin (5HT) in some forms of learning in the leech, negatively modulates Na+⁄K+ ATPase activity, thereby reducing the AHP amplitude in T neurons. Here, we show that a transient inhibition of Na+⁄K+ ATPase can affect the synaptic connection between two ipsilateral T neurons. Bath application of 10 nm dihydroouabain (DHO), an ouabain analogue, causes an increase in the amplitude of the synaptic potential (SP) recorded in the postsynaptic element when a test stimulus is applied in the presynaptic neuron. Iontophoretic injection of cAMP into the presynaptic T neuron also produces an increase of SP. Simulations carried out by using a computational model of the T neuron suggest that a reduction of the pump rate and a consequent depression of the AHP might facilitate the conduction of action potentials to the synaptic terminals. Moreover, nearly
intact leeches injected with 10 nm DHO respond with a swimming episode more quickly to an electrical stimulation, which selectively activates T neurons exhibiting sensitization of swimming induction. Collectively, our results show that inhibition of Na+⁄K+ ATPase is critical for short-term plasticity
Acetyl-L-carnitine prevents serotonin-induced behavioural sensitization and dishabituation in Hirudo medicinalis
No full textSeveral studies suggest that acetyl-L-carnitine (ALC) might influence learning processes. Along this line of investigation, we have previously shown that ALC impaired sensitization and dishabituation induced by nociceptive stimulation of the dorsal skin of the leech Hirudo medicinalis, in the behavioral paradigm of the swim induction (SI). In previous works we showed that 5HT was involved in both sensitization and dishabituation of SI acting through the second messenger cAMP.
In this work, we have reported that for given doses and temporal ranges ALC was able to block sensitization and to impair dishabituation mimicked by the injection of 5-HT or 8Br-cAMP, a
membrane permeable analogue of cAMP. Our results show that a single treatment with 2 mM ALC was the most effective concentration to block the onset of sensitization induced by 5-HT injection and its major effects occurred 11 days after ALC treatment. 2 mM ALC also blocked sensitization induced by 8Br-cAMP injection, whereas, ALC did not completely abolish dishabituation induced by 5-HT or 8Br-cAMP injection at the tested concentrations and at every time point
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