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At least 19 recordsLinked to original sources
PubMed1979

Release of radioactive purines from cat nictitating membrane labeled with 3H-adenine.

Cat nictitating membranes were incubated with 1-2 x 10(-7) M 3H-adenine or 3H-adenosine for 1 h. A tissuebath ratio of about 15 was found for both compounds in intact and denervated membranes. In intact nictitating membranes sympathetic nerve stimulation (4 Hz, 5 min) caused a net release of purines (0.66 +/- 17% of the tissue content), which was reduced by alpha-blockade. Noradrenaline (1-3 microM) or tyramine 60 microM), which produced the same contractile response as did nerve stimulation, increased purine release to the same extent as did nerve stimulation. The effect of either agent was reduced or abolished by phentolamine. Purine release could also be induced by acetylcholine and ATP. This release was not altered after surgical denervation. There was an excellent correlation between the contractile response and the purine release induced by nerve stimulation, noradrenaline, tyramine and acetylcholine. However, ATP caused a larger release of 3H-purines than expected from the contractile responses, possibly indicating displacement. The results indicate that most if not all of the 3H-purines released by nerve stimulation in the cat nictitating membrane are derived from postjunctional elements.

Acetylcholine↗
PubMedDate not supplied

Unconditional-stimulus locus and interstimulus-interval shift in rabbit (Oryctolagus cuniculus) nictitating membrane conditioning.

The nictitating membrane response of rabbits was conditioned at a 200 msec interstimulus interval (ISI) with either circumorbital (C) or paraorbital (P) shock as the unconditional-stimulus locus. After 3 acquisition days half of each group was shifted to a 700 msec interstimuls interval. Results indicated: (1) more rapid acquisition for Group C, (2) postshift response decrements for both groups, (3) more rapid and stable, as well as complete return to preshift performance levels for Group C. Results were discussed in terms of the response-shaping hypothesis and the contiguity-substitution hypothesis in explaining both conditional response emergence and subsequent modifications of CR topography.

Animals↗
PubMed1970

The roles of striated and smooth muscle in the movement of the cat's nictitating membrane.

1. When the movement of the nictitating membrane is recorded in the usual way, pulled out under load in cat, dog, or rabbit, end-plate-depolarizing drugs such as succinylcholine, decamethonium, nicotine, and 2268F, cause a retraction.2. This movement is due to activation of orbital striated muscle, as evidenced by the resistance of the movement to ganglion block or excision of the superior cervical ganglion and to administration of phentolamine or atropine, and by its great sensitivity to dimethyltubocurarine.3. End-plate-depolarizing drugs produce contractions of the superior and inferior oblique and of the recti muscles strong enough to account for the movements of the nictitating membrane, provided the known fascial connexions of the orbit allow transmission of a fraction of the extraocular muscle movement to the membrane.4. In post mortem specimens with the front of the orbit undisturbed, retraction of the central end of any of the ocular muscles produces movement of the nictitating membrane; the movement was greatest with the superior oblique and medial rectus. In vivo, detaching the superior oblique from its insertion into the globe sometimes abolished or reduced the response to end-plate-depolarizing drugs.5. With the membrane unloaded and retracted into the medial canthus, in the lightly anaesthetized or unanaesthetized dog or cat, these drugs cause a protrusion of the membrane, which can be sufficient to cover the cornea. This response also resists ganglion-block and is highly sensitive to dimethyltubocurarine.6. It is suggested that in the normal conscious animal the nictitating membrane is held retracted by a relatively small amount of sympathetic activity, and that its protrusion is an active mechanism under voluntary control mediated by the striated muscles of the orbit.7. The importance of these mechanisms in the interpretation of experiments in which the nictitating membrane is used are discussed.

Animals↗
PubMed1981

Effects of haloperidol and pimozide on classical conditioning of the rabbit nictitating membrane response.

Classical conditioning of the nictitating membrane response of the rabbit was accomplished by presenting tone and light conditioned stimuli for 800 msec before delivery of the unconditioned stimulus, consisting of a 100-msec electric shock to the skin over the paraorbital region of the head. Both haloperidol (250 microgram/kg i.v.) and an equimolar dose of pimozide (308 microgram/kg i.v.) significantly retarded the rate of acquisition of conditioned responses (CRs). Control experiments conducted with separate groups of rabbits indicated that the retardant effect of haloperidol on CR acquisition was not due to an effect on sensitization, pseudoconditioning, base-line responding or the unconditioned nictitating membrane reflex. In previously trained animals, haloperidol produced a significant (12.0 ob) elevation in the intensity threshold of a tone conditioned stimulus for elicitation of CRs. In a separate group of animals, and before any conditioning, haloperidol significantly blocked the amplitude and duration of a tone-induced facilitation of the nictitating membrane reflex. It was concluded that haloperidol blocks both the conditioned and unconditioned excitatory properties of a tone and this accounts for its ability to retard the rate of CR acquisition.

Animals↗
PubMed2006

Repeated acquisitions and extinctions in classical conditioning of the rabbit nictitating membrane response.

The rabbit nictitating membrane (NM) response underwent successive stages of acquisition and extinction training in both delay (Experiment 1) and trace (Experiment 2) classical conditioning. In both cases, successive acquisitions became progressively faster, although the largest, most reliable acceleration occurred between the first and second acquisition. Successive extinctions were similar in rate. The results challenge contextual control theories of extinction but are consistent with attentional and layered-network models. The results are discussed with respect to their implications for the interaction between cerebellar and forebrain pathways for eyeblink conditioning.

Animals↗
PubMed1990

Lesions of the cerebellar interpositus nucleus abolish both nictitating membrane and eyelid EMG conditioned responses.

Both nictitating membrane extension and eyelid EMG activity were measured during classical conditioning of rabbits to tone-airpuff pairings. Both measures were highly correlated. Over trials, learning criterion was met earlier with eyelid EMG activity than with nictitating membrane extension. Within a trial, eyelid EMG preceded and was more robust than nictitating membrane extension. The rabbits were lesioned in the cerebellar interpositus nucleus and then trained for up to 26 days. Detailed analyses of tone alone trials demonstrate that the lesion abolished conditioned responses for both measures. These data confirm that conditioned responses are abolished by lesion of the cerebellar interpositus nucleus.

Animals↗
PubMed1985

Inhibitory effects of alpha, beta-methylene ATP on nerve-mediated contractions of the nictitating membrane in reserpinised cats.

Residual responses of the cat nictitating membrane to nerve stimulation were obtained after reserpine pretreatment (40% of controls), in spite of a pronounced reduction in noradrenaline content. The putative ATP-receptor desensitising agent alpha, beta-methylene ATP (alpha, beta-MATP), administered intraarterially through the lingual artery produced a contraction of the nictitating membrane and subsequently inhibited the residual responses evoked by sympathetic nerve stimulation in reserpinised cats. These doses of alpha, beta-MATP did not modify the contractions evoked by exogenous noradrenaline (i.a.) but antagonized the contractions of the nictitating membrane elicited by beta, gamma-methylene ATP, which is an agonist at P2 receptors. These results are compatible with a co-transmitter role for ATP in the neurally mediated contractile responses of the nictitating membrane following depletion of endogenous noradrenaline stores by pretreatment with reserpine.

Adenosine Triphosphate↗
PubMed1977

The beta-adrenoceptors responsible for a direct relaxation of the uncontracted nictitating membrane of the anaesthetized cat.

Direct relaxation of the nictitating membrane of the anaesthetized cat was produced by close intra-arterial injections of single doses of isoprenaline and other beta-adrenoceptor agonists. This response was relatively resistant to blockade by doses of propranolol that almost abolished the corresponding positive chronotropic and vasodepressor responses. Construction of dose-response curves, however, revealed antagonism of all three parameters by propranolol and different sensitivities of the parameters to isoprenaline. The absence of blockade by practolol, although negative evidence, permitted the nictitating membrane response to be classified as a beta2-adrenoceptor effect, which was supported by the full agonist activity of salbutamol. The blockade of the nictitating membrane response by propranolol was however weaker than of the beta2-adrenoceptor mediated vasodepressor response. Contractile responses were observed with higher doses of isoprenaline and after intravenous injection. These were probably indirect effects induced by local changes in blood pressure at the nictitating membrane due to the concommitant vasodepressor response.

Albuterol↗
PubMed1963

The adrenergic mechanism in the nictitating membrane.

The contractions of the nictitating membrane in response to postganglionic nerve stimulation have been studied in experiments in which cats' heads were perfused. When eserine was added to the perfusion fluid there was a rapid increase in the size of the contractions. In the presence of eserine the contractions produced by injecting acetylcholine into the perfusion fluid were greatly increased. When atropine was injected into the perfusion fluid the contractions caused by postganglionic nerve stimulation returned to the size before eserine was added. In experiments with cats anaesthetized with chloralose, atropine or hyoscine was given first and the effect of eserine on the response to submaximal postganglionic nerve stimulation was determined. Eserine slowly increased the responses to stimulation without increasing the contraction produced by injecting noradrenaline. In other experiments in which maximal stimuli were used, the relation of stimulus frequency to height of contraction was determined. The optimal frequency was low, being 5 to 10 shocks/sec. In the presence of hyoscine, eserine or neostigmine increased the response to stimulation; this increase was greater at lower frequencies, and lessened as the frequency rose to the optimal value.

Acetylcholine↗
PubMed1978

The influence of an extraneuronal compartment on the relaxation of the cat nictitating membrane in vivo.

1 Contractions of the cat nictitating membrane were elicited on stimulation of the internal carotid nerve, and the effects were studied of desipramine and two inhibitors of catechol-O-methyltransferase, U-0521 and pyrogallol, on the subsequent relaxation of the muscle. 2 The relaxation of the nictitating membrane occurred in at least two phases. The late phase of relaxation was prolonged after increase in the period of nerve stimulation and the duration of this phase was further prolonged after treatment with pyrogallol. 3 After inhibition of neuronal uptake of noradrenaline with desipramine both the early and late phases of relaxation were increased in duration, and subsequent administration of pyrogallol or U-0521 caused a further increase in the duration of the late phase of relaxation. 4 The results suggest that the late phase of relaxation of the nictitating membrane is influenced by efflux of noradrenaline from an extraneuronal pool.

Animals↗
PubMed1963

THE RESPONSES TO TYRAMINE OF THE NORMAL AND DENERVATED NICTITATING MEMBRANE OF THE CAT: ANALYSIS OF THE MECHANISMS AND SITES OF ACTION.

The response to tyramine of the denervated nictitating membrane has been analysed by comparing dose/response curves obtained by injections into the femoral vein and into the carotid artery of the spinal cat while recording contractions of innervated and chronically denervated membranes and those of cats treated with reserpine. It is concluded that the effect of tyramine given by these routes is due primarily to catechol amines released from stores within the nictitating membrane itself. Higher doses of tyramine also cause contraction of the membrane by liberating catechol amines into the circulating blood from stores outside the membrane. The response to tyramine of the nictitating membrane after chronic denervation and/or prior treatment with reserpine is partially due to catechol amines released from unidentified stores within the membrane which resist depletion by reserpine and by postganglionic denervation; evidence is presented that adrenaline rather than noradrenaline is concerned. Because of the high sensitivity of the denervated nictitating membrane to adrenaline and to noradrenaline, the response to these amines released from stores outside the membrane by intravenous injections of tyramine becomes greater than that of the normal membrane. Dose/response curves obtained from responses to intravenous sympathomimetic drugs which act away from the membrane are therefore not fully representative of the effect of the drugs on the membrane itself. Tyramine probably has an affinity both for storage sites and for catechol amine receptors in the smooth muscle of the nictitating membrane, the "intrinsic activity," however, being very weak or even absent.

Amines↗
PubMed1977

Influence of apomorphine on sympathetic neural transmission in the nictitating membrane of the cat.

Apomorphine inhibited the nictitating membrane contractions elicited by pre- or postganglionic stimulation of the cervical sympathetic nerve but did not influence even in higher doses the effect of noradrenaline and adrenaline on this organ. The inhibition evoked by apomorphine could be antagonized by haloperidol but was not influenced by phentolamine and propranolol. Dopamine and noradrenaline inhibited the nictitating membrane contractions elicited by nerve stimulation, but clonidine was ineffective in our experiments. Haloperidol antagonized the inhibition evoked by dopamine but did not influence the similar effect of noradrenaline.

Animals↗
PubMed1973

Sensitivity of the nictitating membrane of the cat to succinylcholine after decentralization and denervation.

Seven days after decentralization or denervation, the nictitating membrane of the cat becomes supersensitive to succinylcholine. The supersensitivity to succinylcholine is of a moderate degree (2-3 fold) and there is little difference between the supersensitivity induced by decentralization or denervation. In this respect, it is similar to the decentralization type of supersensitivity observed for other agonists which are not taken up by the adrenergic nerve endings (e.g. acetylcholine and methoxamine). Since succinyloholine causes an apparent contraction of the nictitating membrane through its action on the extraocular muscle and no effect on the nictitating membrane itself, it is concluded that both chronic decentralization and denervation produced a decentralization type supersensitivity in the extraocular muscles. The results suggest that supersensitivity in the extraocular muscles may contribute significantly to the decentralization supersensitivity of the nictitating membrane of the cat, in vivo, especially for those agonists which cause contractions of both the nictitating membrane and the extraocular muscle.

Animals↗
PubMed1984

The role of the accessory abducens nucleus in the rabbit nictitating membrane response.

Electrolytic and knife-cut lesions were employed in the rabbit to examine the role of the VIth cranial nerve, and of the motoneurons in the abducens (ABD) and accessory abducens (ACC) nuclei that supply the VIth nerve, in the reflex extension of the nictitating membrane. The nictitating membrane response (NMR) was elicited by tactual stimulation of the cornea with a puff of air or by electric shock delivered to the skin over the paraorbital region of the head. Total destruction of the VIth nerve or interruption of all ACC inputs to the VIth nerve (while leaving ABD inputs intact) produced a large and comparable reduction in the magnitude of the NMR elicited by air puff, although a small residual NMR of less than 1 mm could still be detected. In contrast, the magnitude of the NMR elicited by shock was not affected by ACC isolation and only reduced by 50% after VIth nerve lesions. Total isolation of ABD inputs to the VIth nerve (while leaving ACC inputs intact) had no effect on NMR magnitude elicited by either air puff or shock. The small residual NMRs to air puff and the larger NMRs to shock remaining after total destruction of the VIth nerve were not eliminated by the removal of all extraocular muscles (while leaving the retractor bulbi muscle intact). However, knife cut lesions that interrupted all ACC inputs to the VIth nerve and transected the VIIth (facial) nerve completely eliminated NMRs elicited by both air puff and shock. The results of this study indicate that NMRs elicited by tactual stimulation of the cornea are primarily mediated by retractor bulbi motoneurons in the ACC nucleus via the VIth nerve. In contrast, NMRs elicited by electric shock delivered to the skin over the paraorbital region of the head are produced by contraction of the retractor bulbi muscle via the VIth nerve and by contraction of the orbicularis oculi muscle via the VIIth nerve which then squeezes the nictitating membrane over the cornea.

Abducens Nerve↗
PubMed1975

The effects of morphine on the release of noradrenaline from the cat isolated nictitating membrane and the guinea-pig ileum myenteric plexus-longitudinal muscle preparation.

1. Electrical field stimulation of either the cat isolated nictitating membrane or the guinea-pig ileum myenteric plexus-longitudinal muscle preparation caused the release of noradrenaline into the bathing medium. 2. In the cat nictitating membrane, the output per pulse of noradrenaline was constant at frequencies of stimulation from 0.5 to 15 Hz. In the guinea-pig myenteric plexus preparation the output per pulse of noradrenaline increased as the frequency of stimulation was increased from 2 to 16 Hz. 3. Phenoxybenzamine (29.3 muM) caused a marked increase in the noradrenaline output from both the cat nictitating membrane and guinea-pig myenteric plexus preparations. 4. Morphine (0.13-8 muM) inhibited the contractions of the cat nictitating membrane caused by electrical stimulation. This effect was greater at low (1Hz) than at high (15Hz) frequencies of stimulat The site of action is at the nerve-smooth muscle junction. 5. The action of narcotic analgesic drugs on the cat nictitating membrane showed stereospecificity. Naloxone (0.1 muM) reversed the inhibition caused by normorphine (3.2 muM). 6. Morphine (3 muM) reduced the noradrenaline output from the cat nictitating membrane stimulated at 1 Hz but not at 15 Hz. At 1 Hz, the inhibition of noradrenaline output by normorphine (muM) was reversed by naloxone (0.25 muM). 7. Morphine (1.5 muM) did not alter the noradrenaline output from the guinea-pig myenteric plexus preparation stimulated at 2 or 16 Hz.

Animals↗
PubMed1983

Effects of scopolamine and methylscopolamine on classical conditioning of the rabbit nictitating membrane response.

Classical conditioning of the rabbit nictitating membrane response was accomplished by presenting tone- and light-conditioned stimuli for 800 msec before delivery of a 100-msec shock as the unconditioned stimulus. Scopolamine significantly retarded the rate of acquisition and final asymptotic performance of conditioned responses to the tone- and light-conditioned stimuli. Methylscopolamine was approximately 20 times less potent than scopolamine in retarding the rate of acquisition, and had no effect on the final asymptotic performance of conditioned responses. The retardation in acquisition of conditioned responses produced by scopolamine could still be detected 5 days after cessation of drug injections, indicating that the effects of scopolamine were on acquisition and not performance. In contrast, scopolamine and methylscopolamine had no affect on the development of long-term habituation produced by the unpaired presentations of tone, light and shock stimuli. Control experiments indicated that the acquisition of conditioned responses by animals injected with saline, scopolamine or methylscopolamine was not contaminated by the presence of changes in base-line responding, sensitization or pseudoconditioning. In addition, scopolamine and methylscopolamine did not affect the unconditioned nictitating membrane reflex. In previously trained animals, scopolamine produced a significant, approximately 25-db elevation in the intensity threshold of a tone-conditioned stimulus for elicitation of conditioned responses. It was concluded that scopolamine blocks the excitatory properties of tone stimuli and this accounts for its ability to retard the rate of acquisition of conditioned responses.

Acoustic Stimulation↗
PubMed1986

Effects of morphine, ethylketocyclazocine, and N-allylnormetazocine on classical conditioning of the rabbit nictitating membrane response.

The rabbit's nictitating membrane response was classically conditioned to tone and light conditioned stimuli presented for 800 ms before delivery of a 100-ms unconditioned shock stimulus. Both the mu receptor agonist morphine (5 mg/kg) and the kappa receptor agonist ethylketocyclazocine (1 mg/kg) significantly retarded the acquisition of conditioned responses (CRs). The retardant effects of both morphine and ethylketocyclazocine on CR acquisition could still be detected when the rabbits were tested 5 days after cessation of drug injections. At the dose employed in this study (5 mg/kg), the sigma receptor agonist N-allylnormetazocine had no effect on acquisition. The retardant effects of morphine and ethylketocyclazocine on acquisition were significantly antagonized by both naloxone (1 mg/kg) and N-allylnormetazocine (5 mg/kg). It was suggested that mu and possibly kappa receptors are involved in the retardant effects of opiates on the acquisition of classically conditioned responses.

Animals↗
PubMed1990

Characterization of adrenergic receptors of the cat iris and nictitating membrane.

Graded pupillary dilations and nictitating membrane (NM) contractions were elicited in anesthetized cats by electrical stimulation of the preganglionic sympathetic nerve or by i.a. administration of norepinephrine (NE) or phenylephrine into the carotid artery. Pupil and NM responses were measured simultaneously from the same side. Alpha-adrenoceptor antagonists were administered intravenously. All of the alpha 1-adrenoceptor blockers tested produced a dose-related reduction of NM responses to both neural and agonist activation; the potency rank order was prazosin greater than WB-4101 greater than phentolamine greater than phenoxybenzamine (PBZ). In contrast, responses of the iris dilator were antagonized only by WB-4101 and PBZ. The iris was almost totally refractory to doses of prazosin and phentolamine that blocked NM responses by more than 75% of control. Neither alpha 2- nor beta-adrenoceptor antagonism produced significant inhibition of neural or agonist activation of either organ (with the exception of high doses of yohimbine on the NM). These results suggest that the postjunctional adrenoceptors of the NM are exclusively of the alpha 1-adrenoceptor subtype. In contrast, those of the iris dilator muscle cannot be easily classified pharmacologically as either alpha 1 or alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗