the role of inhibitory gabaergic and glycinergic nervous systems in neural regulation of escaping...

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The Role of Inhibitory Gabaergic and GlycinergicNervous Systems in Neural Regulation of EscapingMovements and Rapid Feather Shedding in JapaneseQuail (Coturnix Coturnix Japonica)Alina Šveistytė a & Daina Malickienė aa Institute of Ecology of Vilnius University , Akademijos 2, 2600 , Vilnius , LithuaniaPublished online: 23 Jul 2012.

To cite this article: Alina Šveistytė & Daina Malickienė (2003) The Role of Inhibitory Gabaergic and Glycinergic NervousSystems in Neural Regulation of Escaping Movements and Rapid Feather Shedding in Japanese Quail (Coturnix CoturnixJaponica), Acta Zoologica Lituanica, 13:3, 330-341, DOI: 10.1080/13921657.2003.10512690

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330 Acta Zoologica Lituanica, 2003, Volumen 13, Numerus 3

ISSN 1648-6919

THE ROLE OF INHIBITORY GABAERGIC AND GLYCINERGICNERVOUS SYSTEMS IN NEURAL REGULATION OF ESCAPINGMOVEMENTS AND RAPID FEATHER SHEDDING IN JAPANESE QUAIL(COTURNIX COTURNIX JAPONICA)

Alina ÐVEISTYTË, Daina MALICKIENË

Institute of Ecology of Vilnius University, Akademijos 2, 2600 Vilnius, Lithuania. E-mail: [email protected]

Abstract. The escaping reactions under treatment with GABA-receptor agonist diazepam, GABAantagonist picrotoxin and glycinergic agonist glycine, antagonist strychnine and NMDA receptorantagonist MgSO4 were investigated in Japanese Quail (Coturnix coturnix japonica). Escaping move-ments but not feather shedding were sensitive to agonists and antagonists of these systems. The influ-ence of neuroactine agents on feather shedding and on escaping movements was revealed by activationof dopamine receptors with apomorphine which induced rapid feather shedding and alteration in es-caping movements. The effect of glycinergic and GABAergic agents on apomorphine-induced featherrelease and on apomorphine reaction suppression by noradrenergic system activated by yohimbine wasdifferent. Attenuation of apomorphine reaction by cholinergic agonists was abolished by diazepam andglycine. Diazepam and glycine influence on escaping movements were prevailed over the influence ofapomorphine or physostigmine. Distress calls induced by yohimbine + apomorphine were enhanced byglycine and diminished by diazepam. Results have revealed the participation and the differences ofinhibitory neurotransmissions in regulation processes of feather release and escaping movements in quails.Key words: quail, autotomy, feather shedding, escaping movements, neuroactive agents

INTRODUCTION

Our previous study (Ðveistytë 2000a) has revealed thatfluttering of wings and an extreme escaping reaction �feather shedding (bird autotomy) � induced underexperimental conditions in Japanese Quails (Coturnixcoturnix japonica) can be evoked by the activation ofpostsynaptic dopamine D1 and D2, or by suppressionof cholinergic muscarinic receptors. Moreover, this in-vestigation also has shown that feather shedding in quailinduced by dopamine receptor agonist apomorphine canbe attenuated by activation of noradrenergic or cholin-ergic neurotransmissions. There is some evidence thatgamma-aminobutyric acid (GABA) and glycinergic sys-tems participate in the autotomy of rats. Injections ofGABA A receptors agonist muscimol into the substan-tia nigra of rat brain produces numerous stereotyped acts,antinociception and self-injurious behaviour (autotomy;Baumeister & Frye 1986; Baumeister et al. 1987). Au-totomy in rats also can be augmented by blocking theglycinergic inhibition (Seltzer et al. 1991) as well.GABA and glycine are major inhibitory neurotrans-mitters in the nervous system. Autoradiographic bind-ing studies have shown that GABA, glycine and their

antagonists are bound to many neurones, but not toglial cells of the central nervous system of cultured ratCNS (Hosli & Hosli 1983). The synaptoneurosomesfrom different parts of the rat brain respond to bothglycine and GABA with chloride fluxus in a picro-toxin (GABA antagonist) sensitive manner. However,GABA has no effect on the response to glycine andvice versa (Engblom et al. 1996). The spinal interneu-rons release both glycine and GABA (Jonas et al.1998). GABA is an inhibitory transmitter in spinalinterneurons that function both pre- and post-synaptically; glycine is an inhibitory transmitter thatfunctions post-synaptically (Shapiro 1997).GABAergic and glycinergic inhibitory pathways in thespinal cord play an important role in establishing thepattern of motor discharge (Ho 1998). Glycine is notonly a major inhibitory neurotransmitter in the spinalcord and brain stem of vertebrates (Zafra et al. 1997),but it may also play a functional role in the control ofexcitatory activity in the amygdala, particularly dur-ing the periods of decreased GABAergic influences(Danober & Pape 1998). The inhibitory action of gly-cine is mediated by strychnine-sensitive glycinereceptors; strychnine is a competitive antagonist of

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331The role of inhibitory neurotransmitters in autotomy of quails

glycine-gated Cl- channels; strychnine effect is shownin rat hippocampal neurons (Matsubayashi et al. 1998)and in rat caudate putamen (Darstein et al. 1997). Inaddition, glycine can participate in excitatoryneurotransmissions by modulating the activity of theN-methyl-D-aspartate (NMDA) subtype of glutamatereceptors (Zafra et al. 1997). It has been found thatglycine has biphasic modulatory effects on the gluta-mate-mediated excitatory post-synaptic potential in thechick brain stem (nucleus tractus solitarius; Sato etal. 1996).Taking into account the abundant influences ofGABAergic and glycinergic systems on neuralstructures, it can be suspected that these bothneurotransmissions are able to participate in regulationof behavioural escaping reactions. Their role in birdautotomy has not been investigated yet. Therefore, thefollowing study was conducted to evaluate the roleplayed by glycinergic and GABAergic neurotrans-mission in mediating effects of dopaminergic,noradrenergic and cholinergic systems on feathershedding and escaping movements in quails.

MATERIAL AND METHODS

Subjects. Adult male Japanese Quails, weighing from120 to 170 g served as subjects. The quails were hatchedfrom eggs obtained from one commercial supplier. Thebirds were housed in groups, 5�7 per cage (0.62 × 0.54× 0.66 m), and they had free access to food and water.Compounds. Apomorphine hydrochloride (0.65�0.75mg/kg), diazepam (Seduxen, Gedeon Richter, 6.7�8.0mg/kg), glycine (glicine, Roanal, Hungary, 300.0�900.0 mg/kg), MgSO

4 (200.0�800.0 mg/kg), neostig-

mine methylsulphate (0.07 mg/kg), physostigminesalycilate (0.1 mg/kg), picrotoxin (Serva, 0.7�0.8 mg/kg),strychnini nitras (0.3�2.7 mg/kg), yohimbine, HCl(Serva, 4.0�5.0 mg/kg), physiological saline.For the investigation of single drugs and theircombinations, apomorphine was administered 7�18,diazepam 10�40, glycine 20�82, MgSO

4 60�80,

neostigmine 15�32, physostigmine 5�30, picrotoxin15�36, strychnine 5�45, yohimbine 18�81 andphysiological saline 5�30 min before behaviouraltesting. More details about the dose of drugs and thelength of time between pre-treatment of separate drugsare presented in the Results. All drugs were adminis-tered intraperitoneally.Behavioural testing. All behavioural testing wascarried out between 10:00 a.m. and 2:00 p.m.Birds tried to break out from human hands in whichthey were held, and that consequently evoked escaping

movements in quails. The bird movements wereunrestricted. At that time, there was registered theoccurrence of wings and body fluttering, pushing upwith legs, no movements and a distress call. Quail inan observer�s hand was held for 1 min, although themajority of quails were trying to escape from the humanhand immediately or a few seconds after they had beencaught. At the same time, the test of feather sheddingwas performed. The ability to shed feathers was testedby running the observer�s hand gently over the quail�splumage. Feathers (of various sizes) shed by singlequails were counted.The individual behaviour of quails was observed in theirhome cage and in the strange cage. The behaviouraltest was made by two observers. One of them was wellaware about pre-treatment of animal. Some tests wererepeated with the same animals two months later. Thebirds have contacts with humans every day duringnormal housing.The results were analysed by the Mann-Whitney U-test. Value of P < 0.05 was considered to indicatestatistically significant differences.

RESULTS

In the present study, feather shedding, escapingmovements and distress calls in quails under thetreatment with glycinergic, GABAergic, dopaminergic,cholinergic and noradrenergic neuroactive agents wereinvestigated. Drugs were administered separately andin two- or three-drug combinations.

The effect of glycinergic agents alone and in com-bination with dopamine D1/D2 receptor agonistapomorphine on feather shedding and escapingmovements.The influence of neurotransmitter glycine of glycinergicsystem, and strychnine, the antagonist of this system,on the feather release and escaping movements wasinvestigated. Strychnine influences glycine receptorswhich are sensitive to strychnine. In addition, glycineaction by means of glutamate NMDA receptors wasinvestigated. The activity of these receptors wasblocked by MgSO

4. Mg2+ has an inhibitory effect on

NMDA receptors; NMDA receptors are highly sensi-tive to extracellular magnesium (Escames et al. 1998).The Mg2+ ions block NMDA channels by entering thepore from either extracellular, or the cytoplasmic sideof the membrane in a voltage dependent manner(Kupper et al. 1996).The effect on feather shedding. The shedding of featherin quails under glycine or strychnine treatment was small

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332Ðveistytë A., Malickienë D.

and did not differ from the control (saline) group (Tab-le 1). However, both glycine and its antagonist strychninesignificantly diminished the effect of apomorphine onfeather shedding. Among the birds treated with strychninein combination with apomorphine, there were more birdswith weak feather relaxation in comparison to the quailsof the glycine + apomorphine group. Moreover, apomor-phine effect was diminished under the combined treatmentwith strychnine, glycine and apomorphine. These results

show that the glycine effect on apomorphine feather shed-ding is not mediated by strychnine receptors.MgSO

4 (200.0�800.0 mg/kg) did not change the apo-

morphine (at dose of 0.6 mg/kg, N = 12) effect on thisreaction. But at a high apomorphine dose (0.7 mg/kg)which induced abundant feather shedding (51.3 ± 5.7,range 17�74, N = 14), MgSO

4 significantly diminished

apomorphine effect (27.4 ± 4.8, range 6�62, N = 14).The percentage of birds with small feather shedding was

Table 1. The influence of glycinergic agents alone and in combination with apomorphine on feather shedding in quails.

Drugs Dose, Min after N Mean ±SE Range % of quails shedding the following number of feathers

mg/kg treatment 0 1�5 6�15 16�30 31�50 >51

Saline 0 10�25 31 1.2 ± 0.6 0�18 64.6 29.0 3.2 3.2

Glycine 667.0�900.0 20�35 13 0.69 ± 0.4 0�4 61.5 38.5

Apomorphine 0.65 8�18 11 37.6 ± 7.0a 8�76 18.2 18.2 36.4 27.3

Glycine + 700.0 38�50 19 15.0 ± 3.4a, b 0�54 5.2 26.3 31.6 26.3 5.2 5.2apomorphine 0.65 8�20

Strychnine 0.3�0.9 5�15 11 4.4 ± 2.3 0�22 63.6 9.1 18.2 9.1

Strychnine + 0.7 18�25 12 11.3 ± 4.1b 0�36 25.0 25.0 25.0 8.3 16.7apomorphine 0.65 8�15

Strychnine + 2.7 30�45 7 9.7 ± 4.7 0�24 14.5 28.5 28.5 28.5glycine + 300.0 28�35apomorphine 0.65 8�15

Mann-Whitney U-test, two-tailed: a � with respect to saline; b � with respect to apomorphine p < 0.05

Table 2. Escaping movements in quails induced by glycinergic agents alone and in combination with apomorphine.

% of quails showing escaping movementsDistress

Drugs Dose, Min after N No Fluttering of Pushing up callsmg/kg treatment

movements wings body with legs %

Saline 0 10�25 25 24.0 28.0 32.0 8.0 20.0

Glycine 667.0�900.0 20�35 13 15.5 15.5 69.2 7.1 15.5

Apomorphine 0.65 8�18 11 27.3 54.5 18.2 9.2

Glycine + 700.0 38�50 19 36.8 31.6 31.6 10.5apomorphine 0.65 8�20

Strychnine 0.3�0.9 5�15 11 100.0 9.1

Strychnine + 0.7 18�25 12 8.3 58.3 50.0 25.0apomorphine 0.65 8�15

Strychnine + 2.7 30�45 6 83.3 33.3glycine + 300.0 28�35apomorphine 0.65 8�15

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significantly augmented. Thus, it appears that the apo-morphine effect on feather shedding could be augmentedbut not suppressed under activation of NMDA receptors.Therefore, it seems that NMDA receptors do not takepart in the glycine suppression of apomorphine, whichevoked feather release.The effect on escaping movements. Under glycinetreatment markedly more quails were showing body flut-tering in comparison to the quails of the control or apo-morphine groups (Table 2). Only some birds were show-ing wings fluttering, and that was a contrast to the quailsin the apomorphine group.Most of the birds were showing wings fluttering whiletreated with strychnine (Table 2). It indicated that wingsfluttering suppression evoked by glycine was mediatedby strychnine-sensitive glycine receptors.Escaping movements in the apomorphine group underglycine treatment resembled those recorded in thecontrol group: the difference in number between birdsshowing wings fluttering and body fluttering wasabolished. Under strychnine + apomorphine treatment,apomorphine as well as strychnine effects on escapingmovements had changed: almost no one case of wingsfluttering was observed in the group.Under the treatment with MgSO

4 (200.0�800.0 mg/kg),

about a half of the birds manifested no movements. Bodyfluttering was observed in 38.5% of birds. About a half(53.5%) of the birds also manifested no movements whenthey were treated by MgSO

4 + apomorphine (0.6 mg/kg,

N = 12). The percentage of birds showing wings flutter-ing also decreased in comparison to that of the apomor-phine group. In the latter group, 75% of birds showedwings fluttering, whereas in the MgSO

4 + apomorphine

group, there were only 38.5% of such birds. Neverthe-less, this escaping behaviour prevailed among other pat-

terns of active behaviour. Thus, the results of this studyshow that under suppression of glutamate NMDAreceptors the activity of birds and the frequency of theirwings fluttering diminished. Therefore, it appears that thedecrease in occurrence of wings fluttering under the gly-cine treatment was not mediated by glycine activation ofNMDA receptors.Thus, the findings of this study show that the glycinergicsystem is able to change by its separate action a profileof escaping movements (body fluttering was augmented),but it failed to evoke feather shedding. However, theshedding of feathers and an increase in wings flutteringinduced by apomorphine were diminished by the acti-vation as well as by suppression of glycinergicneurotransmission. It seems that attenuation of wingsfluttering activity by glycine was mediated by strych-nine-sensitive but not by NMDA receptors.

The effect of the neuroactive agents of GABAergicsystem alone and in combination with apomorphineon feather shedding and escaping movements ofquails.The influence of GABA-benzodiazepine receptor ago-nist diazepam and GABA antagonist picrotoxin on thefeather release and escaping movements was investi-gated. Picrotoxin blocks the channels of chlorine.The effect on feather shedding. Diazepam alone didnot augment the shedding of feathers in quails in com-parison to the quails of the control group (Table 3). Butunder the treatment with picrotoxin, no feathers wereshed. Diazepam did not change the intensity of apomor-phine-induced feather release as well (Table 3). Butunder the treatment with picrotoxin + apomorphine, theeffect was significantly lower. There were no birds withabundant feather shedding. Therefore, the latter data may

Table 3. The influence of GABAergic agents alone and in combination with apomorphine on feather shedding in quails.


mg/kg treatment 0 1�5 6�15 16�30 31�50 >51

Saline 0 13 2.1 ± 1.4 0�18 61.5 30.8 7.7

Apomorphine 0.65�0.75 8�16 21 36.8 ± 8.0a 1�160 19.0 14.3 23.8 9.5 33.3

Diazepam 6.7�8.0 10�30 12 1.3 ± 0.7 0�8 66.7 25.0 8.3

Picrotoxine 0.7�0.8 15�18 13 0 0 100.0

Diazepam + 6.7�8.0 20�30 16 36.3 ± 5.9a 2�73 6.2 12.5 25.0 25.0 31.2apomorphine 0.65�0.75 8�16

Picrotoxine + 0.7�0.8 26�36 13 15.8 ± 3.6b 0�42 7.7 15.4 38.5 23.1 15.4apomorphine 0.65 8�16

Mann-Whitney U-test, two tailed: a � with respect to saline, one tailed: b � with respect to apomorphine, p < 0.05

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support the opinion that the GABAergic system takespart in quail feather release.The effect on escaping movements. Wings flutteringwas the most frequently displayed escaping movementamong the other escaping patterns in quails kept in hu-man hands under the treatment with diazepam (Table 4),although in the home cage all quails fell asleep afterdiazepam injections. But under the treatment with di-azepam combined with the same dose of apomorphine,all quails remained asleep when they were kept in ob-servers� hands too. No escaping movements occurred.Some alteration in the apomorphine effect on the behav-ioural movements was evoked by picrotoxin. The numberof birds showing wings fluttering decreased and the numberof birds showing body fluttering increased (Table 4).The findings of the study indicated that GABA-benzodiazepine receptors regulate wings fluttering, al-though this GABA influence was not revealed by thesimultaneous treatment with the activated dopaminergicsystem. Contrarily, diazepam induced sleeping was in-tensified by apomorphine. However, results obtainedunder picrotoxin treatment indicated that GABA couldtake part in increase of wings fluttering and feather re-lease induced by apomorphine, although this effect, itseems, was not mediated by benzodiazepine receptors.

Diazepam and glycine influence on the apomor-phine effect on feather shedding and escapingmovements under the activated cholinergic system.Activation of the cholinergic system was induced byphysostigmine and neostigmine, cholinergic agonists.As it was shown in our previous study (Ðveistytë2000a), apomorphine-induced feather shedding wasdiminished and most of the birds showed no movementsunder the treatment with cholinergic agents andapomorphine in combination.

The effect on feather shedding. Apomorphine-inducedfeather shedding decreased under the physostigmine andneostigmine treatment as well (Table 5). However, phys-ostigmine or neostigmine induced attenuation of apomor-phine feather release was not revealed under the diazepamtreatment (Table 5). Under the treatment of quails withdiazepam and physostigmine in combination, but with-out apomorphine, no feather release was evoked.Physostigmine-elicited attenuation of apomorphine-in-duced feather release was not revealed under glycine aswell as under the diazepam treatment (Table 5). Moreo-ver, the number of birds showing abundant feather shed-ding was augmented in comparison to that of the apo-morphine group (Table 3). It seems that under the con-dition induced by the interaction between glycinergic,cholinergic and dopaminergic neurotransmissions, theglycine attenuating effect on apomorphine-inducedfeather release was abolished as well.Glycine and diazepam in combination did not induceany feather shedding (1.0 ± 0.1, range 0�2, N = 6).The effect on escaping movements. Physostigmine andneostigmine changed the apomorphine-induced behav-ioural profile: about a half of the birds did not manifestany movements, and wings fluttering did not prevail overbody fluttering (Table 6). Under the simultaneous treat-ment with diazepam and physostigmine, only diazepambut not physostigmine effects were observed (Tables 4and 6). But under the diazepam, physostigmine (or ne-ostigmine) and apomorphine combined treatment, wingsfluttering was not evoked and percentage of birds withno movements was higher. Which of these neurotrans-missions predominated in this behavioural profile, israther difficult to consider, since in contrast to the ef-fect of diazepam + physostigmine, both diazepam +apomorphine and cholinergic agonist + apomorphinestimulated neither movements, nor wings fluttering.

Table 4. Escaping movements in quails induced by GABAergic agents alone and in combination with apomorphine.




Saline 0 13 38.5 30.8 23.1 15.4

Apomorphine 0.65 8�16 11 36.4 36.4 9.1 18.2 20.3

Diazepam 6.7�8.0 10�30 20 15.0 75.0 20.0

Diazepam + 6.7�8.0 20�30 16 100.0 sleeping sleepingapomorphine 0.65�0.75 8�16

Picrotoxine + 0.7�0.8 26�36 13 38.5 30.7 46.1 7.7apomorphine 0.65 8�16

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Table 5. The influence of diazepam and glycine on cholinergic agonists physostigmine or neostigmine induced suppressionof apomorphine feather shedding.


mg/kg treatment 0 1�5 6�15 16�30 31�50 >51

Physostigmine + 0.1 15�25 11 8.6 ± 3.2 0�29 36.4 18.2 18.2 27.3apomorphine 0.65 7�15

Neostigmine + 0.07 15�25 11 6.4 ± 2.5 0�24 18.2 54.5 9.1 18.2apomorphine 0.6 7�20

Diazepam + 8.0 25�30 6 2.7 ± 1.6 0�8 50.0 33.3 16.7physostigmine 0.1 5�10

Diazepam + 8.0 20�38 6 38.8 ± 8.3b 6�60 16.7 66.7 16.7physostigmine + 0.1 20�28apomorphine 0.65 8�16

Diazepam + 6.7 36�46 14 34.7 ± 4.9c 2�68 7.1 7.1 21.4 50.0 14.2neostigmine + 0.075 22�32apomorphine 0.7 6�16

Glycine + 700.0 85�92 13 50.8 ± 6.4a 15�82 7.7 15.4 30.8 46.1physostigmine + 0.1 23�30apomorphine 0.65 7�14

Mann-Whitney U-test, two tailed: a � with respect to physostigmine + apomorphine, p < 0.05; b � with respect to di-azepam + physostigmine, p < 0.05; c � with respect to neostigmine + apomorphine, p < 0.05

Table 6. The effect of diazepam and glycine on escaping movements induced by physostigmine or neostigmine withapomorphine in combination.




Physostigmine + 0.1 15�25 11 54.5 9.1 36.4 9.1apomorphine 0.65 7�15

Neostigmine + 0.07 15�25 11 54.5 18.2 18.2 27.3apomorphine 0.6 7�20

Diazepam + 8.0 25�30 6 16.7 66.7 16.7physostigmine 0.1 5�10

Diazepam + 8.0 20�38 6 50.0 50.0physostigmine + 0.1 20�28apomorphine 0.65 8�16

Diazepam + 6.7 36�46 14 92.8 7.1neostigmine + 0.075 22�32apomorphine 0.7 6�16

Glycine + 700.0 85�92 13 23.1 61.5 7.7 23.1physostigmine + 0.1 23�30apomorphine 0.65 7�14

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Therefore, there is not enough evidence to judge aboutthe abolition of cholinergic influence by diazepam asit was seen in feather shedding reaction.Under the combined glycine, physostigmine andapomorphine treatment, neither apomorphine, norphysostigmine + apomorphine effect was revealed(Table 6). Evoked behavioural profile seems to beglycine alone effect alike.Thus, the results showed that cholinergic suppressionof apomorphine feather release was not revealed underactivated GABAergic or glycinergic systems. Glycineinfluence on behavioural movements predominated theinfluence of physostigmine and apomorphine under thetreatment with glycine in combination with thesecompounds.

Diazepam and glycine influence on the apomor-phine induced effects on feather shedding andescaping movements under activation of noradre-nergic system.The noradrenergic system was activated by yohimbine,a presynaptic alpha-2-adrenoreceptor antagonist.According to the results of our previous investigation(Ðveistytë 2000a), yohimbine failed to evoke feathershedding in quails, but it suppressed apomorphine-induced feather release. Moreover, distress calls wereaugmented in a group of quails by yohimbine andparticularly by yohimbine + apomorphine.The effect on feather shedding. Diazepam failed tochange yohimbine evoked attenuation of apomorphine-induced feather release, whereas glycine enhanced thisyohimbine effect: about a half of birds did not shed theirfeathers at all (Table 7). However, by an injection ofyohimbine before glycine, only the influence of glycine

on apomorphine-induced feather shedding was observed.It can be supposed that these different effects of glycineand yohimbine could depend on some peculiarities ofglycine and yohimbine interaction or on the length ofthe period between the administration of drugs andfeather shedding examination.The effect on escaping movements. Diazepam andglycine failed to change yohimbine + apomorphineinduced alteration in escaping movements by anexception of the distress call (Table 8). The percentageof birds making distress calls, which were evoked underyohimbine + apomorpine treatment, was augmented byglycine and diminished by diazepam. Distress callswere also not observed under diazepam alone anddiazepam with apomorphine, diazepam with physostig-mine, diazepam with cholinergic agonists andapomorphine treatment in combination (Tables 4 and6). Diazepam induced a sleeping state which wasintensified by apomorphine, but was not observed underthe yohimbine treatment.Thus, the findings indicate that glycine (not diazepam)enhances noradrenergic inhibition of the apomorphinefeather shedding. Glycine augments the percentage ofbirds making distress calls evoked under the yohimbine+ apomorphine treatment. Diazepam, in contrast toglycine, diminishes the distress call alone and in com-bination with other neuroactive agents.

DISCUSSION

In this and in our previous study (Ðveistytë 2000a;2000b), the mechanism of sensory inputs that inspirefeather shedding and escaping movements reactions was

Table 7. The influence of diazepam and glycine on yohimbine induced suppression of apomorphine feather shedding.


mg/kg treatment 0 1�5 6�15 16�30 31�50 >51

Yohimbine + 4.0�5.0 44�50 13 6.5 ± 1.7 0�24 7.7 46.1 38.5 7.7apomorphine 0.6 7�13

Diazepam + 6.7 30�44 18 7.7 ± 2.8 0�51 5.5 50.0 38.9 5.5yohimbine + 4.0 18�32apomorphine 0.75 7�21

Glycine + 450�900 80�95 16 2.5 ± 1.1 0�16 56.2 31.2 6.2 6.2yohimbine + 4.0 55�65apomorphine 0.65 8�15

Yohimbine + 4.0 75�81 11 21.9 ± 6.1 0�52 18.2 9.1 18.2 27.3 9.1glycine + 600�900 35�41apomorphine 0.65 9�15

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not investigated. Our investigation deals with monoam-inergic, cholinergic and inhibitory neurotransmissionsthat can be involved in realisation of these reactions.The results of the present investigation show that bothinhibitory GABAergic and glycinergic systems partici-pate in the process of regulation of feather shedding andescaping movements. Although GABAergic and glyci-nergic agonists and antagonists by their separate actionand by action of diazepam plus glycine did not inducethe shedding of feathers, all these neuroactive agentswere able to influence dopamine agonist apomorphine-induced feather release. However, there was some dif-ference between the effects of GABAergic andglycinergic agents on the apomorphine-induced feathershedding. Apomorphine feather shedding was decreasedby glycine, whereas diazepam did not affect this apo-morphine reaction. However, both GABA antagonistpicrotoxin and glycine antagonist strychnine diminishedapomorphine feather shedding intensity implying thatsome level of activity of these neurotransmission facili-tates apomorphine feather shedding reaction. Both gly-cine and diazepam abolished a decrease in apomorphinefeather shedding induced by cholinergic agonists. Buttheir effects on suppression of apomorphine- featherrelease, which was evoked by activated noradrenergicsystem with yohimbine, were different: glycine activatednoradrenegic inhibition, whereas diazepam had no ef-fect on it at all.Although the results of this study showed that diazepamfailed to activate apomorphine-induced feather shedding,

in our previous investigation (Ðveistytë 2000a), di-azepam, under a small dose of nitrate treatment, aug-mented significantly apomorphine effect on feather shed-ding. There is convincing evidence that benzodiazepinereduces the frequency of Ca2+ oscillation in smoothmuscle cells of airway along with the inducement of itsrelaxation (Savineau & Marthan 2000). Therefore, somerole of diazepam on the relaxation of feather myocytesshould not be rejected. In addition, our present resultsshow that activation of the apomorphine reaction byGABA-benzodiazepine receptors agonist diazepamcould be realised by the abolition of cholinergic influ-ence on apomorphine feather shedding reaction. Thereis some evidence showing that activated GABAergictransmission by benzodiazepine receptors agonist de-creases activated cortical acetylcholine efflux (Sarter& Bruno 1994). This study also revealed that GABAantagonist picrotoxin diminished the apomorphine ef-fect. Therefore, it seems that GABAergic transmissionfacilitates post-synaptic dopamine receptors agonist apo-morphine effect on feather release. It appears that GABAeffects are mediated not only by benzodiazepinereceptors but also by other receptors of GABA. Sinceall neuroactive agents were administered systemically,it was not possible to conclude which neuroanatomicalsites mediated the observed effects.Our results revealed that glycinergic influence on apo-morphine-induced feather shedding is more complicatedwhen compared to that of GABAergic. A decrease inapomorphine reaction induced by glycine is not medi-

Table 8. The effect of yohimbine and apomorphine in combination on escaping movements in quails under diazepam orglycine treatment.




Yohimbine + 4.0�5.0 44�50 13 7.7 30.8 46.1 15.4 53.8apomorphine 0.6 7�13

Diazepam + 6.7 30�44 18 23.1 61.5 7.7 23.1yohimbine + 4.0 18�30apomorphine 0.75 7�21

Glycine + 450�900 80�95 16 12.5 25.0 50.0 18.7 75.0yohimbine + 4.0 55�65apomorphine 0.65 8�15

Yohimbine + 4.0 75�81 11 27.3 27.3 45.4 63.6glycine + 600�900 35�41apomorphine 0.65 9�15

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ated by strychnine-sensitive glycine receptors, because,under the treatment with strychnine, apomorphine reac-tion diminishes as well. According to our results, thisglycine effect was not mediated by activation of NMDAreceptors by glycine as well. Therefore, it could be sug-gested that the other systems, which inhibit apomorphinereaction, were activated by glycine. Our findings indi-cate that glycine (unlike diazepam) enhances noradrener-gic suppression of apomorphine feather release. Thereis convincing evidence that glycine enhances noradrena-line release in the brain structures. An increase in no-radrenaline release from slices of rat hippocampus byactivating receptors of the strychnine-sensitive subtypewas found (Raiteri et al. 1990; Schmidt & Taylor 1990).In addition, there is evidence that glycine induces no-radrenaline release in the striatal and hippocampalsynaptosomes by strychnine � insensitive glycine recep-tors (Raiteri et al. 1992). Some investigators have dem-onstrated that acetylcholine release is activated by gly-cine. Glycine, activating by strychnine-sensitive recep-tors in nucleus tractus solitarius, induces acetylcholinerelease, which depends upon interaction betweenglycinergic and cholinergic neuronal elements, as it hasbeen shown, and in slices of hippocampus and striatum(Talman et al. 1994). It has been shown that increase inacetylcholine release from the slices of rat brain couldbe expressed under the treatment with strychnine-sensi-tive glycine and under the NMDA receptors activation(Nishimura & Boegman 1990). Glycine receptors in sym-pathetic neurons of cultured chickens are excitatory, andthey trigger acetylcholine and noradrenaline release(Boehm et al. 1997). However, strychnine-sensitive gly-cine evokes acetylcholinesterase release from the slicesand synaptosomes of the spinal horn (Rodriguez-Ithurralde et al. 1996). Moreover, glycine also stimulatesstriatal dopamine release in conscious rats. Strychninemarkedly attenuated these responses (Yadid et al. 1993).However, strychnine-insensitive glycine receptors(NMDA) also induced dopamine release in the striataland hippocampal synaptosomes (Raiteri et al. 1992).Taking into consideration these different effects ofglycinergic systems, it is rather difficult to explain theability of glycine to abolish a decrease in apomorphinefeather shedding reaction induced by the cholinergicsystem. According to our results, not only cholinergicinhibition was abolished but also a decrease inapomorphine effect induced by glycine was notrevealed. Thus, it appears that glycine is capable totake part in apomorphine feather shedding reaction onlyafter the cholinergic system has been activated. Takingall these aspects together, it is possible to hypothesizethat with the enhancement of the cholinergic systemactivity the activity of some other processes interfering

with glycine in this reaction is reduced. As aconsequence, the glycine efficacy to suppresscholinergic activity could be elevated. It should benoted that although GABAergic, glycinergic andcholinergic transmissions are able to take part in feathershedding reaction, activation of the dopaminergicsystem is most important in this reaction. Diazepamplus glycine or diazepam plus physostigmine incombination did not evoke feather shedding.In contrast to feather shedding, escaping movementswere influenced by glycine, strychnine, diazepam andpicrotoxin when they were applied separately. How-ever, some differences between the effects induced byGABAergic and glycinergic agents on the escapingmovements were observed. Diazepam evoked wingsbut not body fluttering, whereas glycine had the oppo-site effect. Therefore, it could be suggested that in regu-lation of escaping from predators by flying, theGABAergic system could take part, whereas by slip-ping out � the glycinergic system could participate. Itseems that glycine effect on body movements wasmediated by the strychnine-sensitive glycine receptorsbut not by the NMDA receptors.The effect of glycine on escaping movementspredominated over the effect of apomorphine or theeffect of cholinergic agonist + apomorphine under thetreatment with glycine combined with these com-pounds. However, by suppression of the glycinergicactivity by the strychnine + apomorphine, the effect onthe escaping movements was also changed. Therefore,it appears that a certain level of the glycinergic systemactivity is necessary for the apomorphine effect on therealisation of escaping movements as it was seen infeather shedding reaction.Diazepam effect on the escaping movements prevailedover the effects of apomorphine or cholinergic agonistsas well. Under the treatment with diazepam with thoseneuroactive agents, two different but characteristicfeatures of the diazepam effect were observed: wingsfluttering with physostigmine and sleeping state withapomorphine. Apomorphine effect on feather sheddingwas not hampered by the sleep of quails. Sleeping andfeather release, induced at the same time by theactivation of GABAergic and dopaminergic receptorssimultaneously, can be considered as one of thedeceptive behavioural reactions in birds. In spite of theeffect induced by the GABA-benzodiazepine receptoragonist diazepam with apomorphine in combination,GABA antagonist picrotoxin diminishes apomorphine-induced feather release and the activation of wingsfluttering. Therefore, it could be suggested that theGABAergic system facilitates apomorphine inducedfeather release and wings fluttering reaction.

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GABAergic and glycinergic systems had differenteffects on the distress calls evoked by yohimbine plusapomorphine in combination: glycine augmented thepercentage of quails making a distress call, whereasdiazepam decreased it. If a distress call indicates anxietyor fear of birds, glycine is able to enhance this stateand diazepam � to diminish it. However, under the fearor anxiety situation induced by the simultaneous actionof yohimbine and apomorphine, feather release was notevoked.According to our observations, feather sheddingreaction without any drugs occurs in some quails whenthey try to escape from human hands by flying. Butunder our experimental conditions, when featherrelease was induced by drugs, feather shedding couldoccur not only with wings fluttering, but also with bodyfluttering and during the sleep. Thus, in order to obtainbetter knowledge of the feather shedding in quails undernatural conditions, other studies and observationsshould be conducted.

CONCLUSIONS

The findings of this study show that GABAergic andglycinergic neurotransmissions take part in theregulatory processes of rapid feather shedding andescaping movements in quails. The influence inducedby these two systems was different. The rapid feathershedding reaction evoked by dopamine agonistapomorphine could be enhanced or not affected byGABA, but it was never diminished by it. It seems thatdifferent receptors of GABA play a different role inthis apomorphine reaction. GABA-benzodiazepinereceptors agonist diazepam did not activate apomor-phine reaction, but diazepam abolished its cholinergicsuppression. Moreover, GABA antagonist picrotoxindiminished apomorphine-induced feather release.Therefore, it could be suggested that GABAergictransmission participates in feather shedding reactionevoked by dopaminergic agonist apomorphine. Glycinediminished apomorphine-induced feather shedding.However, a certain level of glycinergic activity seemsto be necessary for the apomorphine feather release.Glycine, the same as diazepam, abolished cholinergicsuppression of this apomorphine reaction, but glycineenhanced noradrenergic inhibition of apomorphinefeather release which was not observed under thetreatment with diazepam.The influence of GABAergic and glycinergic systemson the escaping movements differed as well. Wingsfluttering was activated by diazepam and bodyfluttering by glycine. Under the simultaneous action

of these inhibitory systems with apomorphine orcholinergic agonists, the influence of GABAergic orglycinergic transmissions on the behavioural profilewas prevailed over the dopaminergic or cholinergiceffects. Although diazepam induced wings flutteringpredominated behavioural effect evoked by cholinergicagonist, no wings fluttering was displayed under thesimultaneous action of diazepam with apomorphine;the other property of diazepam � to induce sleeping inquail was intensified by apomorphine. However, underthe inhibition of GABA activity with the picrotoxin,the apomorphine effect on wings fluttering, as well ason feather shedding, was diminished.Both inhibitory systems did not change the behaviouralprofile induced by yohimbine and apomorphine incombination, with the exception of the distress call:glycine enhanced it, whereas diazepam � diminished.Therefore, it can be suggested that fear reaction inducedby activation of the monoaminergic system could bediminished by diazepam and enhanced by glycine.Thus, the study at the behavioural level revealed thatGABAergic and glycinergic systems played a role indopaminergic, cholinergic and noradrenergic regulationof extreme escaping reaction � feather shedding andescaping movements induced under experimentalcondition. Moreover, the difference between theinfluences induced by these two inhibitory neurotrans-missions was elucidated.

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SLOPINANÈIOSIOS GASRERGINËS IR

GLYCINERGINËS NERVØ SISTEMOS VAIDMUO PUTPELIØ

(COTURNIX COTURNIX JAPONICA) IÐVENGIMO JUDESIØ

IR GREITO PLUNKSNØ IÐMETIMO NERVINËJE

REGULIACIJOJE

A. Ðveistytë, D. Malickienë

SANTRAUKA

Buvo tirta GASR-benzodiazepinø receptoriø agonistodiazepamo, GASR antagonisto pikrotoksino, gliciner-ginio agonisto glicino ir antagonisto strichnino beiNMDA receptoriø antagonisto magnio sulfato átakaapsauginëms reakcijoms. Iðvengimo judesiø, bet neplunksnø iðmetimo reakcija buvo jautri ðiø nerviniøsistemø agonistams ir antagonistams. Neuroaktyviømedþiagø átaka plunksnø iðmetimui ir iðvengimojudesiams iðryðkëjo aktyvinant dopamino receptoriusapomorfinu, kuris sukëlë greità plunksnø iðmetimà irkai kuriuos iðvengimo judesiø pokyèius. Glycinerginësir GASRerginës neuroaktyvios medþiagos skirtingaipaveikë apomorfinu sukeltà plunksnø atpalaidavimà irðios reakcijos slopinimà, kurá sukëlë yohimbinu

suaktyvinta noradrenerginë sistema. Glicinas didinoyohimbino poveiká, diazepamas neturëjo jam átakos.Taèiau apomorfino plunksnø iðmetimo reakcijosslopinimas, kurá sukelia cholinerginiai agonistaifizostigminas ir neostigminas, nepasireiðkë, kaipaukðèiai buvo paveikti glicinu ar diazepamu. Iðvengimojudesiø reakcijai glicino ar diazepamo átaka buvovyraujanti, kai ðios medþiagos veikë kartu suapomorfinu, fizostigminu ar fizostigminu + apomorfinu.Taèiau, slopinant GASR pikrotoksinu, apomorfinopoveikis iðvengimo judesiams, kaip kad ir plunksnøiðmetimui, maþëjo. Glicinas ir diazepamas nepaveikëyohimbino + apomorfino sàlygoto iðvengimo judesiøcharakterio, iðskyrus nelaimës ðûksnius, kuriesuaktyvëjo veikiant yohimbinui + apomorfinui: glicinasjuos skatino, diazepamas maþino. Rezultatai parodë,kad GASRerginë ir glicinerginë neurotransmisijosdalyvauja dopaminerginëje, cholinerginëje ir noradre-nerginëje greito plunksnø atpalaidavimo ir iðvengimojudesiø reguliacijoje. Tyrimai iðryðkino ðiø slopinan-èiøjø nerviniø sistemø reguliacijos skirtumus.

Received: 3 March 2003Accepted: 25 September 2003

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the role of inhibitory gabaergic and glycinergic nervous systems in neural regulation of escaping...

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