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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↗
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↗
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↗
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↗
PubMed1979

Effects of baroreceptor activation on spontaneous activity in the sweat glands and nictitating membrane of the cat.

(1) In chloralose-anesthetized cats, elevation of carotid sinus pressure caused blood pressure, sweat gland potentials and nictitating membrane tension to decrease. (2) The onset and recovery of the sweat gland and nictitating membrane responses usually preceded the respective phases of the blood pressure (depressor) response; the latencies of the sweat gland and nictitating membrane responses agreed with the latencies predicted for neural reflex pathways. (3) The sweat gland and nictitating membrane responses were evoked less consistently than the depressor response. (4) In experiments where only the sweat gland potentials and blood pressure were studied: (a) the sinus pressure threshold for inhibition of sweat gland activity was similar to the threshold for the depressor response; (b) cutting the sinus nerves, or blocking the efferent neural activity to the sweat glands, eliminated the effects of sinus pressure elevation on the sweat gland potentials; (c) with carotid sinus pressure held constant, decreases in blood pressure, produced by stimulating the peripheral end of the vagus nerve, did not affect the sweat gland potentials. (5) These results indicate that baroreceptors can reflexly modulate activity in sympathetic neurons whose target organs are not fundamentally involved in blood pressure regulation.

Adrenergic Fibers↗
PubMed1976

Possible involvement of a transmitter different from norepinephrine in the residual responses to nerve stimulation of the cat nictitating membrane after pretreatment with reserpine.

Pretreatment with reserpine (0.3 or 3 mg/kg, 24 hours before the experiment) reduced the norepinephrine (NE) levels in the medial muscle of the cat nictitating membrane to approximately 2% of the control values. Under these experimental conditions, the responses to postganglionic nerve stimulation were not abolished, reaching up to 50% of the maximum development of tension to exogenous sympathomimetic amines both in vivo and in vitro. In contrast to the responses to nerve stimulation obtained in normal nictitating membranes, the residual responses to nerve stimulation obtained after pretreatment with reserpine were not blocked by phentolamine (3.1 and 31 muM) or by 0.29 muM phenoxybenzamine. The effectiveness of phentolamine and phenoxybenzamine in blocking responses to exogenous NE was the same when the normal nictitating membrane was compared to the smooth muscle obtained from cats pretreated with reserpine. The residual responses to nerve stimulation were reduced when the calcium concentration in the medium was decreased to 0.65 mM. These residual responses were abolished in the presence of tetrodotoxin. Scopolamine, 0.078 muM, did not reduce the residual responses to nerve stimulation while it antagonized the responses to exogenous acetylcholine, indicating that a cholinergic mechanism is not involved in this phenomenon. Adenosine triphosphate (ATP) and adenosine diphosphosphate (ADP) behaved as agonists on the smooth muscle of the normal and of the reserpine-pretreated nictitating membrane and the responses to ATP were not blocked by phentolamine. It is concluded that the residual responses to nerve stimulation obtained after pretreatment with reserpine could be due to the release of a transmitter different from NE. The possibility that ATP or ADP might be involved in these residual responses to nerve stimulation is discussed.

Adenosine Triphosphate↗
PubMed1979

Effects of LSD on learning as measured by classical conditioning of the rabbit nictitating membrane response.

Acquisition of the classically conditioned, nictitating membrane response was used to assess effects of LSD on learning. Tone and light conditioned stimuli (CS) were presented 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. Extension of the membrane to the CSs in the 800 msec prior to shock onset was recorded as a conditioned response (CR), while extension to shock onset was recorded as an unconditioned response (UCR). LSD (1, 10, 30, 100 or 300 nmol/kg) was injected i.v., 30 min before each daily conditioning session. Dosages of 1 to 100 nmol/kg of LSD produced a dose-dependent enhancement of CR acquisition. Acquisition to a criterion of 10 successive CRs required 184 trials at 30 nmol/kg of LSD as compared to 293 trials with controls. Separate groups of rabbits received explicity unpaired presentations of stimuli (tone alone, light alone and shock alone). The frequency of responding within 800 msec of CS onset or in the 800 msec before shock onset was low (2-3%) and was not affected by any dosage of LSD, indicating that the effects of LSD on acquisition were not due to sensitization, pseudoconditioning or changes in baseline responding. LSD also had no effect on UCR amplitude. Hence, the systematic effects of LSD on acquisition of CRs reflects the action of the drug on learning.

Acoustic Stimulation↗
PubMed1976

Characteristics of the sympathetic innervation of the nictitating membrane and of the vasculature of the nose and tongue of the cat.

Vasomotor responses from the nasal mucosa and tongue, and contractions of the nictitating membrane, were recorded on stimulation of the cervical sympathetic or internal carotid nerves. Preganglionic sympathetic nerve fibres which elicited a membrane response possessed a lower threshold than those which evoked nasal vasoconstriction, while the latter displayed a lower threshold than fibres which evoked tongue vasoconstriction. The sympathetic vasodilator fibres to the tongue whose activity was revealed after alpha-receptor blockade, had a similar threshold to the vasoconstrictor fibres. Membrane contraction, nasal vasoconstriction and occasionally tongue vasoconstriction could be evoked by stimulating the internal carotid nerve. The postganglionic fibres innervating the nasal mucosa had a similar threshold to those of the nictitating membrane, which may indicate that there are small myelinated fibres innervating the mucosa. The preganglionic compound nerve action potential had four major components, S1-S4. S1, S2 and usually S3 fibres were associated with membrane contraction; S2, S3 and sometimes S1 fibres were associated with nasal vasoconstriction; and S3, usually S2 and occasionally S1 fibres were associated with vasoconstriction in the tongue. It is concluded that each of these three groups of nerve fibres, but not S4 fibres, may include fibres associated functionally with the three effectors. There was a considerable difference between the relative amplitude of the responses of the three effectors elicited by stimulation of the cervical sympathetic nerve at frequencies between 0.2 and 2 Hz. Vasoconstrictor responses were relatively larger than membrane contractions suggesting differences in the mechanisms of neurotransmission at the neuroeffector junctions.

Animals↗
PubMed1977

Properties of the peripheral opiate receptors in the cat nictitating membrane.

The noradrenaline overflow and the contractile response elicited by nerve stimulation of the muscle were inhibited by 1 micron morphine in the cat nictitating membrane. This concentration of morphine did not modify the response of the muscle to exogenous noradrenaline. The inhibitory effect of morphine was increased by low Na+ (50 mM), whereas the capacity of naloxone as antagonist to morphine was higher with 150 mM than with 50 mM Na+. These results suggest that the peripheral opiate receptors which interact with noradrenergic neurotransmission could show a sodium allosteric transformation similar to that described for the brain opiate receptor. The effect of morphine was enhanced by manganese ion in the presence of normal Na+. The responses of the cat nictitating membrane to nerve stimulation were not altered in the presence of the protein modifying reagent DTNB [5,5'-dithiobis-(2-nitrobenzoic acid)] but the effect of morphine on the adrenergic neurotransmission was diminished by DTNB with 150 mM Na+. It is postulated that the affinity of the ligands for presynaptic receptors which regulate adrenergic neurotransmission might be modified during the physiological changes in ion concentration which accompany nerve depolarization.

Animals↗
PubMed1977

The influence of the nictitating membrane on steroid inhibition of limbal wound healing.

In a study involving 34 rabbits, it was found that local corticosteroids inhibit limbal wound healing in normal rabbit eyes, and do not inhibit similar wounds if the nictitating membrane has been removed. It was further found that the contact time of fluorescein labelled corticosteroids is almost 3 times longer in rabbit eyes with nictitating membranes than those in which the membranes have been removed.

Administration, Topical↗
PubMed1978

Differences between presynaptic and postsynaptic alpha-adrenoceptors in the isolated nictitating membrane of the cat: effects of metanephrine and tolazoline.

The alpha-adrenoceptor blocking agent, tolazoline, and the O-methylated metabolite of adrenaline, metanephrine, produced a concentration-dependent increase of tension in the smooth muscle of the cat isolated nictitating membrane. These effects were considered to be due to the activation of postsynaptic alpha-adrenoceptors. 2 The responses to nerve stimulation of this muscle were neither potentiated nor blocked by tolazoline (0.1 to 10 micrometer) or metanephrine (1 to 10 micrometer). 3 3H-transmitter overflow evoked by electrical stimulation was not modified by tolazoline or metanephrine in concentrations in which these drugs stimulated the postsynaptic alpha-adrenoceptors. 4 Since tolazoline and metanephrine failed to activate the presynaptic alpha-adrenoceptors of the cat nictitating membrane under experimental conditions in which they stimulated the postsynaptic alpha-adrenoceptors, these results further support the view that the presynaptic (alpha2) adrenoceptors differ from the postsynaptic (alpha1) adrenoceptors.

Animals↗
PubMed1979

Contraction of cat nictitating membrane by tetramisole.

Tetramisole produced a dose-dependent persistent contraction of cat nictitating membrane. This was not significantly altered by prior adrenalectomy or reserpinisation and tyraminisation, but was abolished by prior alpha blockade.

Adrenalectomy↗
PubMed1979

Stimulation of abducens nucleus supports classical conditioning of the nictitating membrane response.

The acquisition and terminal performance of a classical conditioning group compared with a control group indicated that extension of the nictitating membrane elicited by direct electrical stimulation of the abducens nucleus was successfully conditioned to a previously neutral stimulus. The conditioning so obtained was associative and not due to such nonassociative factors as sensitization, pseudo-conditioning, or alteration in base-rate responding.

Abducens Nerve↗
PubMed1979

Neuronal unit activity in the abducens nucleus during classical conditioning of the nictitating membrane response in the rabbit (Oryctolagus cuniculus).

Neuronal unit activity was recorded from the abducens (6th nerve) nucleus, the "final common path," during classical conditioning of the nictitating membrane (NM) response in the rabbit, with the use of a tone conditioned stimulus, an air puff unconditioned stimulus (UCS), 250-msec interstimulus interval, and 60-sec intertrial interval. Animals were given 2 days of conditioning training (104 trials in eight blocks per day) and 1 day of extinction. Control animals were given comparable periods of stimulus presentations, explicitly unpaired. Activity of small clusters of units--"multiple unit" recording--was compared with the amplitude-time course of the NM response. Between-blocks comparisons of neural and behavioral responses indicated an essentially perfect correlation during acquisition of the conditioned response (Day 1, r = .99; Day 2, r = .98) and a slightly lower correlation during extinction (r = .93) for the conditioning animals. Within-blocks comparisons indicated a close correspondence between the histograms of unit activity and the amplitude-time course of the NM response for the conditioning animals in all phase of training and for the control animals in the UCS trial blocks.

Abducens Nerve↗
PubMed1977

Classical nictitating membrane conditioning in the awake, normal, restrained cat.

Present knowledge of its central nervous system makes the cat a desirable subject for studies of brain-behavior relationships. Response frequencies and latency characteristics in conditioning and control groups indicate that the response of the nictitating membrane can be classically conditioned in a new restraint system in which detailed brain and behavior measures can be easily obtained.

Animals↗
PubMed1978

Neuronal plasticity in the limbic system during classical conditioning of the rabbit nictitating membrane response. I. The hippocampus.

Hippocampal unit responses were recorded throughout classical conditioning of the rabbit nictitating membrane response to a tone conditioned stimulus (CS) using a corneal air-puff unconditioned stimulus (UCS). Multiple unit analysis revealed that a rapidly developing increase in cell discharges (relative to spontaneous activity) occurs within the first block of paired trials and continues to increment with subsequent training, initially in the UCS period and then in the CS period. The pattern of hippocampal activity within paired trials closely parallels the amplitude-time course of the behavioral response and precedes it temporally. Identical recordsings from animals given unpaired CS-alone and UCS-alone presentations showed no such changes. These control results and additional lines of evidence point to the critical necessity of the learning paradigm for the development of the hippocampal response seen in conditioning animals. A single unit analysis indicates that not all hippocampal neurons exhibit the described conditioned discharge pattern. Hippocampal long-term potentiation is considered as a possible mechanism for mediating this early and rapid neuronal plasticity dependent on specific 'contingent' patterns of stimulation.

Acoustic Stimulation↗