English Journal

Alpha-adrenoceptive dual modulation of inhibitory GABAergic inputs to Purkinje cells in the mouse cerebellum.

Hirono M, Obata K.Author information Neuronal Circuit Mechanisms Research Group, Brain Science Institute, RIKEN, Wako, Saitama 351-0198, Japan. hironom@brain.riken.jpAbstractNoradrenaline (NA) modulates synaptic transmission in various sites of the CNS. In the cerebellar cortex, several studies have revealed that NA enhances inhibitory synaptic transmission by beta-adrenoceptor-and cyclic AMP-dependent pathways. However, the effects of alpha-adrenoceptor activation on cerebellar inhibitory neurotransmission have not yet been fully elucidated. Therefore we investigated the effects of the alpha1- or alpha2-adrenoceptor agonist on inhibitory postsynaptic currents (IPSCs) recorded from mouse Purkinje cells (PCs). We found that the nonselective alpha-adrenoceptor agonist 6-fluoro-norepinephrine increased both the frequency and amplitude of spontaneous IPSCs (sIPSCs). This enhancement was mostly mimicked by the selective alpha1-adrenoceptor agonist phenylephrine (PE). PE also enhanced the amplitude of evoked IPSCs (eIPSCs) and increased the frequency but not the amplitude of miniature IPSCs (mIPSCs). Moreover, PE decreased the paired-pulse ratio of eIPSCs and did not change gamma-aminobutyric acid (GABA) receptor sensitivity in PCs. Conversely, the selective alpha2-adrenoceptor agonist clonidine significantly reduced both the frequency and the amplitude of sIPSCs. Neither eIPSCs nor mIPSCs were affected by clonidine. Furthermore, presynaptic cell-attached recordings showed that spontaneous activity of GABAergic interneurons was enhanced by PE but reduced by clonidine. These results suggest that NA enhances inhibitory neurotransmitter release by alpha1-adrenoceptors, which are expressed in presynaptic terminals and somatodendritic domains, whereas NA suppresses the excitability of interneurons by alpha2-adrenoceptors, which are expressed in presynaptic somatodendritic domains. Thus cerebellar alpha-adrenoceptors play roles in a presynaptic dual modulation of GABAergic inputs from interneurons to PCs, thereby providing a likely mechanism for the fine-tuning of information flow in the cerebellar cortex.
Journal of neurophysiology.J Neurophysiol.2006 Feb;95(2):700-8. Epub 2005 Oct 26.
Noradrenaline (NA) modulates synaptic transmission in various sites of the CNS. In the cerebellar cortex, several studies have revealed that NA enhances inhibitory synaptic transmission by beta-adrenoceptor-and cyclic AMP-dependent pathways. However, the effects of alpha-adrenoceptor activation on c
PMID 16251261

Adrenergic involvement in the locus ceruleus and adjoining regions in the facilitation of predatory attack behavior as induced by hypothalamic stimulation in cats.

Saha SN, Bhatia SC, Nayar U.Author information Department of Physiology, All India Institute of Medical Sciences, New Delhi--110 029.AbstractThe present study was carried out in five cats which did not attack the rats spontaneously. Predatory attack on an anaesthetized rat was elicited by electrical stimulation of extreme lateral regions of hypothalamus. These sites were stimulated at a current strength from 300-700 microa to evoke a predatory attack on an anaesthetized rat. The attack was accompanied by minimal affective display such as alertness, pupillary dilatation, and culminated in beck biting at higher current strength. A scoring system allowed the construction of stimulus response curves, which remained fairly constant when repeated over a period of 3-4 weeks. Microinfusions of norepineprine and clonidine in 4.0 and 5.0 microg dose respectively in locus ceruleus and adjoining tegmental fields facilitated the predatory attack and there was a significant reduction in the threshold current strength for the elicitation of affective and somatomotor components. Microinfusions of yohimbine, an alpha-2 blocker, in 5 microg dose completely blocked the predatory attach response as indicated by an increase in the threshold current strength for the affective components. The somatomotor components were completely inhibited and could not be elicited even when the current strength was increased to 1000 microA. The predatory attack behavior remained completely inhibited for almost two hours following microinfusion of yohimbine. During this period, the animal was extremely drowsy and reacted very slowly even to a painful stimulus such as pinching of tail. Microinfusions of propranalol (beta-blocker), practalol (beta-1 blocker), prazosin (alpha-1 antagonist), propylene glycol as well as saline in similar volumes (0.5 microl) as control failed to produce any blocking effect, thus indicating the involvement of alpha-2 adrenoceptive mechanisms in the modulation of predatory attack in this region of midbrain. The facilitatory effects of norepinephrine and clonidine were significant at P<0.01 and P<0.05 respectively with Wilcoxon's signed rank test. The inhibitory effects of yohimbine were significant at P<0.05. The present study indicates the involvement of alpha-2 adrenoceptive mechanisms in the facilitation of hypothalamically elicited predatory attack.
Indian journal of physiology and pharmacology.Indian J Physiol Pharmacol.2004 Jan;48(1):51-8.
The present study was carried out in five cats which did not attack the rats spontaneously. Predatory attack on an anaesthetized rat was elicited by electrical stimulation of extreme lateral regions of hypothalamus. These sites were stimulated at a current strength from 300-700 microa to evoke a pre
PMID 15270369

[Neosynephrine mydriasis combined with general anesthesia with halothane in ocular surgery].

Giuri S.AbstractOphthalmologic surgical interventions are performed in numerous cases under general anaesthesia with halothane, many of which requiring a preoperatory mydriasis. Neosinerfin is alpha-adrenoceptive sympathomimetic. Local use, in a 10% concentration produces a strong mydriasis, resistant to the opening of the aqueous chamber during the intervention. Its systemic effects are remarkable: it induces a peripheral blood vessel constriction which can unleash a reflex bradycardia followed by a shortcoming of the cardiac flow. The halothane has various effects upon the heart: reduces the cardiac frequency, reduces the conduction speed of the cardiac impulse stimulating rhythm disorders, sensitizes the myocardium to the action of adrenaline, diminishes the heart's contraction force and the cardiac flow. The cumulative effects of seosinefrin and halothane cause major cardio-vascular changes: sinus bradycardia, ventricular arrhythmia, arterial hypotension. These are reasons for which the pre- and intraoperatory use of neosinefrin is unadvisable. Under this circumstances the collaboration between the ophthalmologist and anesthesiologist is very important, each of them having specific tasks. The ophthalmologist: preoperatory, the optimal pupillary dilatation may be obtained with tropicamide and diclofenac 0.1%, preoperatory, if the general anesthesia must be combined with local anesthesia, anesthetics in association with adrenalin should not be used; immediately postoperatory local use of atropine should be applied with cautiousness. The anesthesiologist: preoperatory he will not interrupt anti-hypertensive, anti-arrhythmia, anti-angina medication, with the mention that adrenoceptive alpha blockers (Prazosin) are indicated in comparison to adrenoceptive beta blockers because they diminish the risk of rhythm disorders; the use of clonidine and avoiding of phenobarbital in the premedication of the patient. As far as it is possible, it is recommended that halothane is replaced with izofluran or enfluran or enfluran which have a great tolerance to exogenous adrenoceptives.
Oftalmologia (Bucharest, Romania : 1990).Oftalmologia.2002;52(1):97-100.
Ophthalmologic surgical interventions are performed in numerous cases under general anaesthesia with halothane, many of which requiring a preoperatory mydriasis. Neosinerfin is alpha-adrenoceptive sympathomimetic. Local use, in a 10% concentration produces a strong mydriasis, resistant to the openin
PMID 12677810