REFERATe GENERALe / GENERAL STUDIES

Relaia dintre neurotransmitori, comportament i abuz: O

privire retrospectiv/ O analiz
Relationship between neurotransmitters, behavior,
and maltreatment: A review
Adrian V. Rus 1, Sheri R. Parris2
Rezumat

Aceast retrospectiv examineaz urmtorii opt Neurotransmitori: dopamina, norepinefrina, epinefrina, serotonina, histamina, feniletilamina (FEA),
glutamatul i acidul gama aminobutiric (GABA). Mai precis, lucrarea examineaz relaia dintre aceti neurotransmitori i comportamente psihopatologice care indic problemele psihologice latente sau antecedente de abuz. Cunoaterea acestor legturi poate oferi o nelegere profund a acestor comportamente i i poate ajuta pe specialiti n luarea unor decizii de tratament bine documentate.
Cuvinte cheie : neurotransmitori, comportamente, abuz

ABSTRACT

This review paper examined the following eight neurotransmitters: dopamine, norepinephrine, epinephrine, serotonin, histamine, phenylethylamine (PEA),
glutamate, and gamma-aminobutyric acid (GABA). Specifically, we examined the relationship between these neurotransmitters and psychopathological
behaviors that indicate underlying psychological problems or histories of maltreatment. Awareness of these links can provide a deeper understanding of
these behaviors as well as assist practitioners in making more informed treatment decisions.
Keywords : neurotransmitters, behavior, maltreatment

Introducere
Aceast lucrare retrospectiv examineaz urmtorii opt neurotransmitori: dopamina, norepinefrina,
epinefrina, serotonina, histamina, feniletilamina (FEA),
glutamatul i acidul gama-aminobutiric (GABA). n
continuare se va discuta relaia dintre comportament
1 Universitatea Cretin Sudvest, Statul Texas, SUA
2 Universitatea Cretin Texas, Statul Texas, SUA

E-mail: aadrianrus@gmail.com | adrian.rus@swcu.edu

i aceti neurotransmitori. Unii dintre compuii

neuro chimici enumerai mai sus nu sunt definii n
mod consecvent ca neurotransmitori n literatura
de specialitate datorit ambiguitii modului n care
acioneaz, dac afecteaz sistemul nervos central sau
pe cel periferic. Dar, pentru a uura lectura i vom
considera pe toi neurotransmitori.
1 Southwestern Christian University, TX, USA
2 Texas Christian University, TX, USA

E-mail: aadrianrus@gmail.com | adrian.rus@swcu.edu

Revista de Neurologie i Psihiatrie a Copilului i Adolescentului din Romnia Iunie 2013 vol. 16 nr. 2

Adrian V. Rus Relaia dintre neurotransmitori, comportament i abuz: O privire retrospectiv/ O analiz

Neurotransmitorii, definii drept mesageri chimici ai sistemului nervos, susin transmiterea semnalelor de la un neuron la altul i n cele din urm
permit ca semnalul s fie purtat prin toate organele
din corp. Neurotransmitorii sunt prezeni n toate
fluidele corpului, cum ar fi limfa, lichidul cefalorahidian (LCR), saliva i urina (Ailts, Ailts, & Bull, 2007).
Dei sunt prezeni n tot corpul, Neurotransmitorii
sunt n primul rnd sintetizai, depozitai i secretai
de ctre sistemul nervos central (SNC). Cei mai
muli dintre Neurotransmitori sunt sintetizai din
aminoacizii obinui din hran i de aceea precursorii neurotransmitorilor pot trece de bariera snge
creier (Ailts, Ailts, & Bull, 2007).
Neurotransmitorii catecolaminergici - dopamina, epinefrina i
norepinefrina
Principalele catecolamine din sistemul nervos sunt
amine biogene i includ dopamina, norepinefrina i
epinefrina (Smeets & Gonzlez, 2000). Catecolaminele sunt prezente n mai multe comportamente care
includ, reglarea proceselor afective, comportamentul
de cutare de compensaii i modularea funciei cardiovasculare, precum i comportamentele de auto-reglare, funciile cognitive i consolidarea memoriei. n
continuare vom discuta despre aceste catecolamine i
relaia lor cu comportamentele normale i psihopatologice.
Dopamina
Dopamina, care are att efecte excitatorii ct i
inhibitorii (Carlson, 2007), este implicat n reglarea
proceselor afective, i joac un rol central n comportamentul cutrii de compensaii cum ar fi abordarea,
consumul i dependena; activarea comportamental;
i comportamentul orientat spre scop (Baar & Gntekin, 2008; Pessiglione et al., 2006; Wise, 2004). n
special, transmisia dopaminei din substantia nigra i
tegmental ventral ctre structurile cortexului frontal
cum sunt nucleus accumbens i neostriatum joac un rol
important n medierea valorii de recompens a hranei, buturii, sexului, recunoaterii sociale, abuzului de
droguri i stimulrii creierului (Berridge & Robinson,
1998). Mai mult, n poziia de catecolamin principal din creierul mamiferelor, dopamina contribuie,
de asemenea, la modularea funciei cardiovasculare, la
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REFERATe GENERALe

secreia catecolaminelor i hormonilor, la tonusul vascular, la funcia renal i la motilitatea gastrointestinal (Missale, Nash, Robinson, Jaber, & Caron, 1998).
Dopamina are un rol i n funciile cognitive, n
memoria de lucru (memoria de scurt durat) i n
procesele intenionale i atenionale (Herschkowitz,
2000). Tulburri n dezvoltarea sistemului dopaminergic pot duce la numeroase dereglri i anomalii
cum ar fi diskinezia, distonia, ticurile, tulburri obsesiv-compulsive i micri anormale ale ochilor (Herlenius & Lagererantz, 2001). mpreun cu serotonina,
GABA, glutamatul, opioidele i oxitocina, dopamina
a fost de asemenea legat de autism (Penn, 2006).
Beard i Conner (2003) sugereaz c deficitul de fier
timpuriu n cursul vieii are ca rezultat modificri n
metabolismul dopaminei, fapt care poate cauza probleme de percepie i motivaie; i de aceea probleme
cu dezvoltarea cognitiv i comportamental. Georgieff (2007) a notat c deficitul de fier n perioada fetal i neonatal poate duce la niveluri sczute ale dopaminei. Aceste niveluri sczute ale dopaminei au fost
corelate cu probleme de atenie i ADHD (Volkow et
al., 2009; Konrad, Gauggel, & Scurek, 2003). Nivelurile ridicate au fost corelate cu probleme cognitive, de
atenie(Herschkowitz, 2000), i cu simptomele tulburrii stresului posttraumatic la femeile adulte (Glover
et al., 2003).
Mai mult, De Bellis et al. (1999a) au descoperit niveluri ridicate ale dopaminei n urin la copiii abuzai
aflai n perioada de prepubertate cu tulburri de stres
posttraumatic (TSPT). n mod specific, acest studiu a
comparat 18 copii maltratai, suferind de TSPT cu 24
de copii neabuzai ntr-un grup de control. n grupul
TSPT au fost descoperite niveluri semnificativ mai
mari de catecolamide (inclusiv dopamina) dect n
grupul de control al copiilor neabuzai. n plus, nivelul catecolaminelor din urin i cel al cortisolului
s-au corelat pozitiv cu gndurile suprtoare, evitarea
i hiperexcitabilitatea. ntr-un alt studiu, De Bellis et
al. (1999b) a descoperit c 44 de copii i adolesceni
abuzai cu TSPT, care au fost evaluai prin scanarea
creierului prin rezonan magnetic aveau un volum
intracranian i cerebral cu 7% i 8% mai mic dect cei
din grupul de control (61 de copii care se potriveau n
ceea ce privete vrsta, sexul, ndemnarea, poziia pe
scala Tanner, rasa, nlimea i greutatea). n plus, copiii abuzai din grupul TSPT, prezentau n proporii
crescute tulburri de internalizare i externalizare n
concordan cu rezultatele descoperite n alte studii

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REFERATe GENERALe 

Adrian V. Rus Relaia dintre neurotransmitori, comportament i abuz: O privire retrospectiv/ O analiz

asupra copiilor abuzai. n general, aceste rezultate

pot fi explicate, conform autorilor acelui studiu, ca
un efect al abuzului cronic asupra copiilor cu TSPT,
care le-a alterat sistemele majore ale stresului biologic
(inclusiv neurotransmitorii catecolaminergici dopamina, epinefrina i norepinefrina) i a avut efecte
adverse asupra dezvoltrii creierului.
Mai mult, Yehuda, Southwick, Giller, Ma, i Mason (1992) au descoperit de asemenea niveluri nalte ale dopaminei la veteranii rzboiului din Vietnam
cu tulburri de stres posttraumatic (TSPT) . n acest
studiu, autorii au explicat nivelurile mari ale dopaminei ca fiind rezultatul activitii crescute a sistemului
nervos simpatic la persoanele cu TSPT, legnd severitatea grupurilor de simptome ale TSPT de nivelul
excitaiei sistemului nervos simpatic.
Norepinefrina
Norepinefrina are att efecte excitatorii ct i inhibitorii, totui efectele comportamentale ale norepinefrinei sunt excitatorii (Carlson, 2007). Sistemul
norepinefrinei este destinat funciilor autoregulatorii
cum ar fi medierea rspunsului de orientare, atenia
selectiv i posibil a vigilenei (Solanto, 1998). Norepinefrina (noradrenalina) este implicat de asemenea
n somn, visare i nvare; deoarece este eliberat n
vasele sanguine, ea cauzeaz contracia vaselor sanguine i astfel ritmul btilor inimii crete. (Baar
& Gntekin, 2008). Beane and Marrocco (2004) au
sugerat ideea c o eliberare insuficient de norepinefrin poate explica problemele care afecteaz atenia
reflex i pe cea voluntar. Viggiano (2008) nota c o
descretere n sinteza norepinefrinei are, de obicei, ca
rezultat, un comportament hipoactiv. Cu toate acestea, i o cretere cronic poate avea ca rezultat hipoactivitatea. Norepinefrina este asociat, de asemenea,
cu tulburri afective cum ar fi depresia maniacal,
cunoscut i sub numele de tulburare bipolar (Baar & Gntekin, 2008); modularea strii de excitare
(arousal); i cu manifestarea unei sensibiliti a organismului fa de factorii de mediu, care poate avea ca
rezultat reacii negative la stimuli noi sau ostili din
mediul nconjurtor (Berman & Coccaro, 1998). Rogeness (1991) a descoperit c acei copii care aveau un
precedent de neglijare prezentau niveluri sczute de
norepinefrin n urin.
Mai mult, Yehuda, Southwick, Giller, Ma, i Mason (1992) au artat faptul c veterani ai rzboiului

din Vietnam cu TSPT aveau niveluri de norepinefrin

mai ridicate dect pacienii externi i dect membrii
normali ai grupului de control. Ca i n cazul nivelurilor de dopamin semnificativ mai ridicate, nivelurile
ridicate de norepinefrin erau corelate cu o activare
mrit a sistemului nervos simpatic la persoanele cu
TSPT.
Modelele animale arat c stresul traumatic activeaz locus coeruleus (acel nucleu din creier care conine
catecolamine n special norepinefrina) precum i
faptul c sistemul nervos simpatic conduce spre un
rspuns de tip lupt sau fugi. n consecin, acest
mecanism influeneaz creterea cantitii de catecolamine din creier, din sistemul nervos simpatic i
din miezul glandei suprarenale fapt care influeneaz
creterea btilor inimii, a tensiunii arteriale, a strii
de alert i a circulaiei epinefrinei, norepinefrinei i
dopaminei. Totui, n timpul stresului sever, locus coeruleus stimuleaz axa hipotalamo-hipofizo-corticosuprarenal (HPA) i se elimin hormonul de eliberare
a corticotropinei (CHR) stimulnd secreia hormonului adrenocorticotrop (ACTH) i a cortisolului.
Aceast cascad de modificri chimice stimuleaz activarea biologic i stimularea intens fapt care se exprim n anxietate i hipervigilen (De Bellis, 2002).
Echilibrul norepinefrinei este afectat nu doar de
stresul traumatic ci i i de niveluri nalte ale stresului
fiziologic cronic aa cum au artat Babisch, Fromme, Beyer, i Ising (2001) n cercetrile efectuate pe
subieci expui la zgomot. Mai precis, ei au aflat c
volumul traficului, ca indicator al expunerii la zgomot,
era asociat cu o concentraie mai mare a noradrenalinei n urin.
Epinefrina
Epinefrina (adrenalina) este un neurotransmitor
cu aciune excitatorie (Feldman, Meyer, & Quenzer,
1997) i se consider c are un efect n consolidarea
memoriei umane (Cahill, Gorski, & Le, 2003) i n
stres (Charmandari, Kino, Souvatzoglou, & Chrousos, 2003). Delahanty, Nugent, Christopher, i Walsh
(2005) au raportat c niveluri ridicate ale epinefrinei
n urin se corelau n mod pozitiv cu nivelurile tulburrilor de stres posttraumatic la copii de ase sptmni, care suferiser un eveniment traumatic. Krantz,
Forsman, i Lundberg (2004) au gsit de asemenea
c stresul crete nivelurile de epinefrin. Ei au legat
epinefrina de activitatea cardiovascular i de tensi-

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Adrian V. Rus Relaia dintre neurotransmitori, comportament i abuz: O privire retrospectiv/ O analiz

unea muscular. Garde, Hansen, Persson, Ohlsson,

i rbk (2003) au descoperit c stimularea (arousal) att cea pozitiv ct i cea negativ, se asociaz
cu concentraii crescute de adrenalin n urin; astfel,
att emoiile pozitive ct i cele negative se asociaz cu concentraii mrite ale epinefrinei. Epinefrina,
ca i dopamina i norepinefrina a fost corelat i cu
ADHD (Konrad, Gauggel, & Schurek, 2003). Mai
mult, Yehuda, Southwick, Giller, Ma, i Mason (1992)
au demonstrat niveluri mai crescute ale epinefrinei
la veteranii rzboiului din Vietnam care sufereau de
TSPT dect la pacienii externi i la persoanele din
grupul de control.
Catecolamine Concluzii
Niveluri ridicate ale epinefrinei, norepinefrinei i
cortisolului n urin pot indica prezena unei stri de
stres acut i cronic (Babisch, Fromme, Beyer, & Ising,
2001). n plus, studii asupra animalelor au artat norepinefrin i efedrin alterate n plasm ca rezultat
al unui stresor intermitent cronic (Marby, Gold, &
McCarty, 1994).
Eliberarea de norepinefrin i dopamin n cortexul prefrontal se coreleaz cu o stare de stimulare (arousal) (Arnsten & Pliszka, 2011). n condiii de stres,
nivelurile mari de catecolamine (dopamina i norepinefrina) sunt eliberate n cortex-ul prefrontal (Finlay,
Zigmond, & Abercrombie, 1995). n plus, niveluri
sczute ale stimulrii (arousal) se coreleaz cu niveluri sczute ale norepinefrinei (Foote, Aston-Jones, &
Bloom, 1980). Efectele norepinefrinei i dopaminei
asupra strii emoionale, stimulrii, i comportamentului sunt mediate prin receptori localizai n cortexul prefrontal care este sensibil la mediul neurochimic
(Arnsten & Pliszka, 2011). n consecin, eliberarea
de catecolamine, care este fie insuficient, fie n exces, va conduce la deteriorarea funciei cortexului prefrontal. Mai precis, att norepinefrina ct i dopamina
sunt prezente n cantiti sczute n timpul oboselii
i plictiselii i n cantiti moderate cnd o stare de
alert este provocat de stimuli relevani sau n timpul
mersului fr stres. Niveluri insuficiente de dopamin
sunt corelate cu atenia/reacia nedirijat, cu confuzia
i un control slab al impulsurilor (ADHD netratat).
Niveluri moderate de norepinefrin sunt corelate cu
atenie i reacie dirijate i cu comportamente flexibile, organizate i canalizate (ADHD tratat n mod optim). Norepinefrina n cantiti mari este corelat cu
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atenia sau reacia direcionate greit, cu inflexibilitate

mental, doze excesive de stimulente i deteriorarea
funcionrii cortexului prefrontal (Arnsten & Pliszka,
2011). n timp ce cauza specific a ADHD nu a fost
identificat, exist dovezi c aceast tulburare implic
modularea disfuncional a circuitului cortico-limbicstriat de ctre catecolamine (n special dopamina i
noradrenalina) precum i de serotonin (Dalley, Mar,
Economidou, & Robbins, 2008).
Serotonina
Serotonin (5-hidroxitriptamina 5-HT), are att
efecte excitatorii ct i inhibitorii (Carlson, 2007)
i poate fi implicat ntr-o serie larg de comportamente cum sunt pofta de mncare, emoiile, funciile
cognitive i motorii, modularea funciei neuroendocrine, i ritmul circadian (Hensler, 2006). Anomalii
serotoninergice au fost depistate att n autism ct i
n epilepsie(Chugani, 2004); n depresie i tulburri
de anxietate(Ressler & Nemeroff, 2000) i n ADHD
(Hawi et al., 2002). Ali cercettori au corelat activitatea redus a serotoninei cu comportamentul agresiv
fa de ali oameni, fa de proprietile altor oameni
i fa de propria persoan (Meyer et al., 2008; Berman & Coccaro, 1998; Meyer et al., 2008; Mitsis et
al., 2000; Oades et al., 2008; Tuinier, Verhoeven, &
Van Praag, 1996). Niveluri sub valorile optime indic
posibilitatea depresiei (Booij, Van der Does, & Riedel,
2003) i o slab reglare a impulsurilor (Kent et al.,
2002). Kaufman et al. (1998) a descoperit c abuzul la
copil poate duce la un sistem al serotoninei care opereaz ineficient provocnd probleme la nivel cognitiv
i comportamental. O cauz a acestei situaii se poate datora monoaminoxidazei A (MAO-A), o enzim
care catalizeaz degradarea dopaminei, serotoninei i
norepinefrinei. Studiile au artat c expresia MAO-A
este influenat de factorii de mediu, cum ar fi abuzul n copilrie (Caspi et al., 2002; Foley et al., 2004;
Nilsson, 2006; Nilsson, Sjoberg, Wargelius, & Leppert, 2006). Cnd activitatea MAO-A este declanat
de abuz, nivelurile de dopamin, serotonin i norepinefrin sunt i ele afectate (Oreland, Nilsson, Damberg, & Hallman 2007; Shih & Thompson, 1999).
Histamina
Histamina are att efecte excitatorii ct i inhibitorii (Feldman, Meyer, & Quenzer, 1997) i este im-

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Adrian V. Rus Relaia dintre neurotransmitori, comportament i abuz: O privire retrospectiv/ O analiz

plicat n diferite funcii ale sistemului nervos central

cum ar fi stimularea (arousal), anxietatea, activarea
sistemului nervos simpatic, reglarea ciclului somnveghe, retenia de ap, i suprimarea alimentaiei
(Brown et al., 2001). Unii cercettori consider c
histamina joac un rol important n reglarea energiei
i a homeostazei endocrine precum i n plasticitatea
sinaptic i n nvare (Haas & Panula, 2003). Histamina a fost descris, de asemenea, ca avnd un rol
modulator n rspunsul imun (Hough & Leurs, 2006;
Tanaka & Ichikawa, 2006).
O concentraie mare a histaminei se gsete n
multe alimente, n special n produsele obinute prin
fermentaie microbiologic cum ar fi brnza maturat,
varza acr, vinul, carnea prelucrat i alimentele citrice
(Bodmer, Imark & Kneubhl, 1999; Mainz & Novak,
2007; Ruiz-Capillas, & Jimnez-Colmenero, 2004).
Cantitatea de histamine gsit n anumite alimente
poate fi un factor care contribuie la nivelurile nalte
ale histaminelor la copii. Legislaia european permite niveluri ale histaminelor de dou ori mai mari dect
cele permise de ctre Food and Drug Administration
n Statele Unite ale Americii. Unii cercettori atrag
atenia fa de toxicitatea histaminelor din alimente
i buturi; astfel, este necesar ca autoritile sanitare
s stabileasc limite legale de siguran asupra aminelor biogene aa cum este histamina (Ruiz-Capillas &
Jimnez-Colmenero, 2004).
Alergiile, mastocitoza, bacteriile sau hemoragiile gastrointestinale pot de asemenea s produc un
exces de histamine(Mainz & Novak, 2007). Mainz
i Novak (2007) au raportat c histaminele produc
contracia celulelor musculare netede, vasodilatare,
permeabilitate vascular crescut, secreia de mucus,
tahicardie, modificri ale tensiunii arteriale i aritmii.
Sistemul histaminic, propus ca un sistem de rspuns la pericole, elibereaz mai mult histamin n
condiii extreme ca deshidratare, hipoglicemie sau
stres (Brown, Stevens, & Haas, 2001). n studiile
pe animale, histamina a fost corelat cu provocarea
anxietii experimentale, ceea ce sugereaz faptul c
histamina poate juca un rol important n reglarea
anxietii (Ikarashi & Yuzurihara, 2002).
Histamina a fost legat, de asemenea, de boala Alzheimer i de schizofrenie (Fernndez-Novoa
& Cacabelos, 2001) precum i de sindromul Down
i de boala Parkinson (Haas & Panula, 2003). Conform unor cercettori, histamina are i un efect asupra
proceselor memoriei (Blandina, Efoudebe, Cenni,

Manaioni, & Passani, 2004; Philippu & Prast, 2001).

Histamina a mai fost asociat cu anxietata i cu
problemele de somn (Brown et al., 2001; Hough &
Leurs, 2006; Tanaka & Ichikawa, 2006). Stimulri
psihologice adverse, cum ar fi stresul imobilizrii sau
izolarea social au ca rezultat eliberarea substanei
P n creier (Ebner, Rupniak, Saria, & Singewald,
2004). Substana P, o neuropeptid, provoac eliberarea de histamin ceea ce duce la inflamri i la stri
emoionale negative, team i anxietate (Rosenkranz,
2007).
HCL
Beta-feniletilamina
(HCL)
este
un
neurotransmitor excitator care funcioneaz ca o
amfetamin (Kahane, 2009). Niveluri sczute ale
HCL au fost asociate cu depresia (Nakagawara,
1992;) i cu ADHD (Kusaga et al., 2002). Niveluri
crescute au fost observate la indivizi cu anxietate i
schizofrenie (vezi Burchett & Hicks, 2006). Exist o asociere foarte puternic ntre monoamioxidaza
B (MAO-B), o enzim care catalizeaz degradarea
HCL, i mediile psiho-sociale adverse (de exemplu,
abuzul) i comportamentul criminal (Oreland, 2007).
n plus, MAO-B este asociat cu susceptibilitatea fa
de multe tulburri psihiatrice (pentru o trecere n revist, vezi Volavka, 1999), i joac un rol n reglarea
strilor afective (Bortolato, Godar, Davarian, Chen,
& Shih, 2009); a reaciilor emoionale, inclusiv activitatea exploratorie, stimularea (arousal), i ntrirea
comportamentului (Sabelli & Javaid, 1995); criminalitate violent (Asberg, 1997; Belfrage, Lindberg,
& Oreland, 1992; Longato-Stadler, af Klinteberg,
Garpenstrand, Oreland, & Hallman, 2002); i suicid
(Verkes et al., 1998). n concluzie, studiile au artat
c mediul psiho-social al unui individ influeneaz
att activitatea MAO (care are un efect direct asupra
nivelurilor HCL) ct i expresia comportamental a
individului respectiv.
Glutamatul
Glutamatul este un neurotransmitor excitator (Carlson, 2007) i este considerat principalul
mediator al informaiei senzoriale, coordonrii
motorii, emoiilor i cunoaterii, inclusiv formarea memoriei i regsire a informaiilor memo-

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Adrian V. Rus Relaia dintre neurotransmitori, comportament i abuz: O privire retrospectiv/ O analiz

rate (Hassel & Dingledine, 2006). Glutamatul

joac de asemenea un rol n alinarea efectelor
neuronale ale stresului, anxietii i moduleaz
activitatea neuronal de-a lungul sistemului nervos central ( Johnson et al., 2005; Niswender, Jones, & Conn, 2005). El a fost implicat n iniierea
i propagarea atacurilor (Holmes, 1995) precum
i n patofiziologia tulburrilor afective (Sanacora, Zarate, Krystal, & Manji, 2008). Glutamatul
a fost implicat i n tulburarea de depersonalizare, care a fost asociat cu abuzul emoional i
trauma n copilrie (Simeon, 2004). Mai mult,
un exces de glutamat a fost asociat cu tulburarea
obsesiv complusiv (Carlsson, 2000), n timp
ce un deficit a fost asociat cu ADHD (Moore et
al., 2006) i cu simptomele depresive (Tordera
et al., 2011). Disfuncia glutamatului a fost asociat cu autismul (Page et al., 2006; Shinohe et
al., 2006) i schizofrenia (Coyle, 2006). Stresul
acut modific eliberarea de glutamat n creier
(Musazzi et al., 2010), iar mediile n care copiii
sunt crescui i care sunt marcate de neglijen i
izolare sunt asociate cu o expresie redus a glutamatului n creier, fapt care duce la deficit cognitiv i tulburri psihiatrice. Se suspecteaz c
disfuncia glutamatului produs de stres ar juca
un rol n schizofrenie i dependen (Melendez,
Gregory, Bardo, & Kalivas, 2004). Niveluri ale
glutamatului exterm de ridicate, care conduc
spre degradarea celulelor/moarte au fost descoperite la copii cu leziuni traumatice ale creierului care au fost de asemenea victime ale abuzului
(Ruppel, 2001).
GABA
Acidul gama-amino-butiric (GABA), neurotransmitorul inhibitor cel mai important al
Sistemului Nervos Central (SNC), joac un rol
trofic n timpul dezvoltrii timpurii a creierului,
incluznd ramificaiile neuronale, plasticitatea
reelei neuronale i organizarea neuronal (Herlenius & Lagercrantz, 2001). Sinteza GABA
atinge o activitate de vrf n al doilea an de via;
astfel, la vrsta de doi ani, copiii ar trebui s
prezinte mbuntiri n integrarea informaiei
(Herschkowitz, 2000). Olsen i Betz (2006) au
12

REFERATe GENERALe

raportat o legtur ntre funcia GABA-ergic

defectuoas i tulburrile neurologice i psihiatrice, legate n primul rnd de hiperexcitabilitate,
inclusiv deficiene n dezvoltare; retard mintal i
epilepsie, tulburri de somn; dependen de droguri, procesare senzori-motorie, i coordonare
motorie. Brambila, Perez, Barale, Schettini, i
Soares (2003) au raportat niveluri sczute att
la pacieni deprimai ct i la pacieni maniacali.
Johnston i Singer (2001) au raportat niveluri
sczute ale GABA n lichidul cerbero-spinal la
indivizii cu convulsii. Mai mult, au fost gsite
niveluri ridicate de GABA n plasm la tineri cu
tulburri autiste i unii cercettori consider c
GABA este un marker biochimic al autismului
(Dhossche et al., 2002) precum i al ADHD cu
tulburri de conduit (Prosser et al., 1997).
Concluzii
n concluzie, abuzul poate afecta nivelurile neurotransmitorilor prezentai mai sus.
Specialitii care lucreaz n domeniul sntii
i ocrotirii copilului ar trebui s fie contieni c
acei copii cu un istoric de traume, neglijare i
alte forme de abuz, prezint adesea un comportament care este determinat de niveluri neregulate ale neurotransmitorilor care sunt generate
de abuz (Purvis, McKenzie, Cross, Kellermann,
& Huisman, 2011). Probe de urin pentru msurarea nivelurilor specifice corespunztoare fiecrui neurotransmitor cu scopul de a determina dac el se gsete n parametri optimi, pot
fi utile n planificarea terapiilor i interveniilor
adecvate (de exemplu, intervenii psihologice
i comportamentale, suplimente, sau medicaii)
dar i n evaluarea eficienei interveniilor.
ntr-un studiu recent, s-a observat o reducere
substanial a comportamentului inadaptabil la
copiii cu risc atunci cnd nivelurile de serotonin i de GABA au fost mrite cu ajutorul suplimentelor naturale (Cross, Kellermann, McKenzie, Purvis, Hill, & Huisman, 2011). Mai mult,
s-a utilizat screening-ul translucenei nucale
pentru a detecta abuzul asupra copiilor. ntr-un
studiu de caz, o mam urmrea s restabileasc
custodia total asupra copilului ei care se afla n

Revista de Neurologie i Psihiatrie a Copilului i Adolescentului din Romnia Iunie 2013 vol. 16 nr. 2

GENERAL STUDIES

Adrian V. Rus Relationship between neurotransmitters, behavior, and maltreatment: A review

adopie temporar de un an. Cu toate acestea,

copilul avea reacii extreme n prezena mamei
n timpul vizitelor. Copilul a fost testat pentru
a urmri activitatea neurotransmitorilor la
baz i imediat dup ce a fost vizitat de ctre
mam. O cretere brusc a nivelului mai multor
neurotransmtori dup vizit a indicat un rs*
INTRODUCTION
This review paper examined the following eight
neurotransmitters: dopamine, norepinephrine, epinephrine, serotonin, histamine, phenylethylamine
(PEA), glutamate, and gamma-aminobutyric acid
(GABA). The relationship between behavior and
these neurotransmitters is discussed below. Some of
the neurochemicals listed above are not consistently
defined as neurotransmitters in the literature due to
ambiguity as to whether they affect the central or peripheral nervous system. However, to facilitate reading of this article we will address them all as neurotransmitters.
Neurotransmitters, described as chemical messengers of the nervous system, support the transmission
of signals from one neuron to another and ultimately
allow the signal to be carried throughout all organs
within the body. Neurotransmitters are present in
body fluids such as serum, cerebral spinal fluid (CSF),
saliva, and urine (Ailts, Ailts, & Bull, 2007). Though
present throughout the body, neurotransmitters are
primarily synthesized, stored, and released by specialized neurons within the central nervous system
(CNS). Most of the essential neurotransmitters are
synthesized from amino acids obtained from dietary
intake and therefore neurotransmitter precursors may
pass through the blood-brain barrier (Ailts, Ailts, &
Bull, 2007).
Catecholaminergic neurotransmitters - dopamine, epinephrine and
norepinephrine
The major catecholamines in the nervous system
are biogenic amines and include dopamine, norepinephrine, and epinephrine (Smeets & Gonzlez,

puns de stres dramatic asociat cu vizita. Atunci

cnd mamei i s-a prezentat rezultatul acestor
analize precum i rezultatele pe care le-a obinut
ea n urma parcurgerii Interviului de Ataament
al Adultului (AAI), femeia a mrturisit c utiliza practici parentale abuzive cu copilul (Purvis,
McKenzie, Kellermann, & Cross, 2010).
*

*
2000). Catecholamines are involved in many behaviors including mood regulation, reward-seeking behavior, and modulation of cardiovascular function, as
well as self-regulatory behaviors, cognitive functions,
and memory consolidation. These catecholamines
and their relationship with normal and psychopathological behaviors are discussed below.
Dopamine
Dopamine, which has both excitatory and
inhibitory effects (Carlson, 2007), is involved in
mood regulation and plays a central role in rewardseeking behavior, such as approach, consumption, and
addiction; behavioral activation; and goal-directed
behavior (Baar & Gntekin, 2008; Pessiglione
et al., 2006; Wise, 2004). In particular, dopamine
transmission from the sustantia nigra and ventral
tegmentum to the forebrain structures such as
the nucleus accumbens and neostriatum plays an
important role in mediating the reward value of
food, drink, sex, social reinforcement, drugs of
abuse, and brain stimulation (Berridge & Robinson,
1998). Furthermore, as a principal catecholamine
in the mammalian brain, dopamine also aids in the
modulation of cardiovascular function, catecholamine
release, hormone secretion, vascular tone, renal
function, and gastrointestinal motility (Missale, Nash,
Robinson, Jaber, & Caron, 1998).
Dopamine is involved also in cognitive functions,
in working memory, and intentional and attentional
processes (Herschkowitz, 2000). Disturbances in
the development of the dopaminergic system may
lead to several disorders or abnormalities, including
dyskinesia, dystonia, tics, obsessive-compulsive
disorders, and abnormal eye movements (Herlenius &
Lagererantz, 2001). Dopamine, along with serotonin,

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13

Adrian V. Rus Relationship between neurotransmitters, behavior, and maltreatment: A review 

GABA, glutamate, opioids, and oxytocin, has also

been linked to autism (Penn, 2006). Beard and Conner
(2003) suggested that iron deficiency in early life
relates to alterations in dopamine metabolism, which
may cause problems with perception and motivation;
and therefore, problems with cognitive and behavioral
development as well. Georgieff (2007) noted that
fetal and neonatal iron deficiency can result in low
levels of dopamine. Low levels of dopamine have also
been correlated with attention problems and ADHD
(Volkow et al., 2009; Konrad, Gauggel, & Scurek,
2003). Elevated levels have been linked to cognitive,
attention problems (Herschkowitz, 2000), and posttraumatic stress disorder symptoms in adult females
(Glover et al., 2003).
Moreover, De Bellis et al. (1999a) found higher
levels of urinary dopamine in prepubertal maltreated
children with posttraumatic stress disorder (PTSD).
Specifically, this study compared 18 maltreated
children with PTSD with 24 non-abused children
in a control group. Significantly higher levels of
catecholamines (including dopamine) were found in
the PTSD group than were found in the non-abused
control group. In addition, the levels of urinary
catecolamines and cortisol correlated positively with
intrusive thoughts, avoidance, and hyperarousal.
In another study, De Bellis et al. (1999b) found
that 44 maltreated children and adolescents with
PTSD who were assessed with anatomical magnetic
resonance imaging brain scans had 7% and 8%
smaller intracranial and cerebral volume than the
control group (61 matched controls on age, gender,
handedness, Tanner Stage, race, height, and weight).
In addition, the maltreated, PTSD group showed
increased rates of internalizing and externalizing
disorders consistent with results found in studies
of abused children. Overall, these results may be
explained, according to the authors of that study, as
an effect of chronic maltreatment in children with
PTSD that altered major biological stress systems
(including catecholaminergic neurotransmitters dopamine, epinephrine, and norepinephrine), and had
adverse effects on brain development.
Furthermore, Yehuda, Southwick, Giller, Ma, and
Mason (1992) also found higher levels of dopamine
in Vietnam combat veterans with posttraumatic stress
disorder (PTSD). In this study, authors explained
high levels of dopamine as being a result of increased
sympathetic nervous system activation in people with
14

GENERAL STUDIES

PTSD, and linking severity of PTSD symptom clusters

with the level of sympathetic nervous system arousal.
Norepinephrine
Norepinephrine has both excitatory and inhibitory
effects, however, the behavioral effects of norepinephrine are excitatory (Carlson, 2007). The norepinephrine system is dedicated to self-regulatory functions
such as mediation of the orienting response, selective attention, and possibly vigilance (Solanto, 1998).
Norepinephrine (noradrenaline) is also involved in
sleeping, dreaming, and learning; and because it is
released in the blood vessels, it causes blood vessels
to contract and the heart rate to increase (Baar &
Gntekin, 2008). Beane and Marrocco (2004) proposed that insufficient norepinephrine release may
explain problems in reflexive and voluntary attention.
Viggiano (2008) noted that a decrease in norepinephrine synthesis usually results in hypoactive behavior;
however, a chronic increase may result in hypoactivity
as well. Norepinephrine is also associated with mood
disorders such as manic depression, also known as
bipolar disorder (Baar & Gntekin, 2008); arousal
modulation; and an organisms display of sensitivity
toward the environment, which may result in aggressive responses to novel or threatening environmental
stimuli (Berman & Coccaro, 1998). Rogeness (1991)
found that children with a history of neglect displayed
low levels of urinary norepinephrine.
Furthermore, Yehuda, Southwick, Giller, Ma, and
Mason (1992) showed higher levels of norepinephrine in
Vietnam combat veterans with PTSD than in outpatients
and a normal control group. As in the case of significantly
higher dopamine levels, high levels of norepinephrine
were correlated with increased sympathetic nervous
system activation in people with PTSD.
Animal models show that traumatic stress
activates the locus coeruleus (the nucleus in the
brain that contains catecholamines specifically
norepinephrine) as well as the sympathetic nervous
system leading to the fight-or-flight response.
Consequently, this influences the increase of
catecholamines within the brain, sympathetic nervous
system, and adrenal medulla that affect the increase
in heart rate, blood pressure, alertness and circulation
of epinephrine, norepinephrine, and dopamine.
However, during severe stress the locus coeruleus
stimulates the hypothalamic-pituitary-adrenal axis

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GENERAL STUDIES

Adrian V. Rus Relationship between neurotransmitters, behavior, and maltreatment: A review

(HPA) and corticotropin-releasing hormone (CRH)

is released stimulating adrenocorticotropin (ACTH)
and cortisol release. This cascade of chemical changes
stimulates behavioral activation and intense arousal
expressed in anxiety and hypervigilance (De Bellis, 2002)
The norepinephrine balance is affected not just
by traumatic stress but also by high levels of chronic
physiological stress as shown by Babisch, Fromme,
Beyer, and Ising (2001) on noise exposed subjects.
Specifically, they found that traffic volume as an
indicator of noise exposure was associated with a
higher concentration of noradrenaline in urine.
Epinephrine
Epinephrine (adrenaline) is an excitatory
neurotransmitter (Feldman, Meyer, & Quenzer,
1997) and is considered to have an effect on human
memory consolidation (Cahill, Gorski, & Le, 2003)
and stress (Charmandari, Kino, Souvatzoglou, &
Chrousos, 2003). Delahanty, Nugent, Christopher,
and Walsh (2005) reported that elevated levels of
urinary epinephrine were positively correlated to
levels of post-traumatic stress disorder in children
six weeks after a traumatic event. Krantz, Forsman,
and Lundberg (2004) also found that stress increases
epinephrine levels. They linked epinephrine to
cardiovascular activity and muscle tension. Garde,
Hansen, Persson, Ohlsson, and rbk (2003)
found that arousal, both positive and negative, was
associated with increased concentrations of urinary
adrenaline; thus, both positive and negative emotions
are associated with increased concentrations of
epinephrine. Epinephrine, like dopamine and
norepinephrine, has been linked to ADHD as well
(Konrad, Gauggel, & Schurek, 2003). Furthermore,
Yehuda, Southwick, Giller, Ma, and Mason (1992)
showed higher levels of epinephrine in Vietnam
combat veterans with PTSD than outpatients and a
normal control group.
Catecholamines Conclusion
Higher levels of epinephrine, norepinephrine, and
cortisol in urine may indicate the presence of a state
of acute and chronic stress (Babisch, Fromme, Beyer,
& Ising, 2001). In addition, animal studies showed
altered norepinephrine and epinephrine in plasma as
the result of a chronic intermittent stressor (Marby,

Gold, & McCarty, 1994).

Norepinephrine and dopamine release in the
prefrontal cortex is correlated with a state of arousal
(Arnsten & Pliszka, 2011). Under stress conditions,
high levels of catecholamines (dopamine and
norepinephrine) are released in the prefrontal cortex
(Finlay, Zigmond, & Abercrombie, 1995). In addition,
low levels of arousal are correlated with low levels
of norepinephrine (Foote, Aston-Jones, & Bloom,
1980). The effects of norepinephrine and dopamine
on mood, arousal, and behavior are mediated by
receptors located within the prefrontal cortex that
are sensitive to the neurochemical environment
(Arnsten & Pliszka, 2011). Consequently, release of
catecholamines that is either insufficient or excessive
will lead to impairment of prefrontal cortex function.
Specifically, both norepinephrine and dopamine are
present in low levels during fatigue and boredom
and at moderate levels when an alert state is caused
by relevant stimuli or during non-stressed walking.
Insufficient levels of dopamine are correlated with
unguided attention/responses, distraction, and poor
impulse control (untreated ADHD). Moderate
norepinephrine levels are correlated with guided
attention and responses, and focused, organized
and flexible behaviors (optimally treated ADHD).
Norepinephrine in high levels is correlated with
misguided attention or responses, mental inflexibility
or stimulus bond (excessive dose of stimulants) and,
impairment of prefrontal cortex functioning (Arnsten
& Pliszka, 2011). While the specific cause of ADHD
is unidentified, there is evidence that this disorder
involves dysfunctional modulation of the corticolimbic-striatal circuitry by the catecholamines (in
particular dopamine, and noradrenaline), as well as
serotonin (Dalley, Mar, Economidou, & Robbins,
2008).
Serotonin
Serotonin (5-hydroxytryptamine, 5-HT) has both
excitatory and inhibitory effects (Carlson, 2007)
and may be involved in a wide variety of behaviors
such as appetite; emotion; motor and cognitive
functions; modulation of neuroendocrine function;
and circadian rhythm (Hensler, 2006). Serotonergic
abnormalities have been reported in both autism and
epilepsy (Chugani, 2004); depression and anxiety
disorders (Ressler & Nemeroff, 2000), and ADHD

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Adrian V. Rus Relationship between neurotransmitters, behavior, and maltreatment: A review 

(Hawi et al., 2002). Other researchers have linked

reduced serotonin activity to aggressive behavior
toward others, other peoples property, and towards
oneself (Meyer et al., 2008; Berman & Coccaro,
1998; Meyer et al., 2008; Mitsis et al., 2000; Oades
et al., 2008; Tuinier, Verhoeven, & Van Praag, 1996).
Levels below the optimal range indicate a possibility
of depression (Booij, Van der Does, & Riedel, 2003)
and poor impulse regulation (Kent et al., 2002).
Kaufman et al. (1998) found that childhood abuse can
lead to a serotonin system that operates inefficiently,
leading to cognitive and behavioral problems. One
reason for this may be due to Monoamine oxidase A
(MAO-A), an enzyme that catalyzes the degradation
of dopamine, serotonin, and norepinephrine. Studies
have shown that MAO-A expression is impacted by
environmental factors, such as childhood maltreatment
(Caspi et al., 2002; Foley et al., 2004; Nilsson, 2006;
Nilsson, Sjoberg, Wargelius, & Leppert, 2006). When
MAO-A activity is activated by maltreatment, levels
of dopamine, serotonin, and norephinephrine are also
affected (Oreland, Nilsson, Damberg, & Hallman
2007; Shih & Thompson, 1999).
Histamine
Histamine has both excitatory and inhibitory
effects (Feldman, Meyer, & Quenzer, 1997) and is
involved in various central nervous system functions
such as arousal, anxiety, activation of the sympathetic
nervous system, regulation of sleep-wake cycle,
water retention, and suppression of eating (Brown
et al., 2001). Some researchers consider histamine
to play an important role in regulating energy and
endocrine homeostasis, and synaptic plasticity and
learning as well (Haas & Panula, 2003). Histamine
has also been described as having a modulator role in
immune responses (Hough & Leurs, 2006; Tanaka &
Ichikawa, 2006).
A high concentration of histamine is found in
many foods especially in products of microbiological
fermentation such as aged cheese, sauerkraut,
wine, processed meat, and citrus foods (Bodmer,
Imark & Kneubhl, 1999; Mainz & Novak, 2007;
Ruiz-Capillas, & Jimnez-Colmenero, 2004). The
amount of histamine found in certain foods may be
a contributing factor for high levels of histamine in
children. European legislation permits histamine
levels twice as high as what the U. S. Food and Drug
16

GENERAL STUDIES

Administration allows. Some researchers warn against

histamine toxicity from foods and beverages; thus,
there is a need for health authorities to set safe, legal
limits on biogenic amines such as histamine (RuizCapillas & Jimnez-Colmenero, 2004).
Allergies, mastocytosis, bacterias, or gastrointestinal
bleeding may also cause an excess of histamine (Mainz
& Novak, 2007). Mainz and Novak (2007) reported
that histamine causes smooth muscle cell contraction,
vasodilatation, increased vascular permeability, mucus
secretion, tachycardia, alterations of blood pressure,
and arrhythmias. The histamine system, proposed as
a danger response system, releases more histamine
during extreme conditions such as dehydration,
hypoglycemia, or stress (Brown, Stevens, & Haas,
2001). In animal studies, histamine has been linked
to inducing experimental anxiety, which suggests that
histamine may play an important role in the regulation
of anxiety (Ikarashi & Yuzurihara, 2002).
Histamine has also been linked to Alzheimers
disease and schizophrenia (Fernndez-Novoa &
Cacabelos, 2001) as well as Downs syndrome and
Parkinsons disease (Haas & Panula, 2003). According
to some researchers, histamine also has an effect
on memory processes (Blandina, Efoudebe, Cenni,
Manaioni, & Passani, 2004; Philippu & Prast, 2001).
Histamine has also been associated with anxiety
and sleep problems (Brown et al., 2001; Hough &
Leurs, 2006; Tanaka & Ichikawa, 2006). Adverse
psychological stimulation, such as immobilization
stress or social isolation, results in release of Substance
P in the brain (Ebner, Rupniak, Saria, & Singewald,
2004). Substance P, a neuropeptide, induces histamine
release resulting in inflammation as well as negative
moods, fear, and anxiety (Rosenkranz, 2007).
PEA
Beta-phenylethylamine (PEA) is an excitatory
neurotransmitter that functions like an amphetamine
(Kahane, 2009). Decreased PEA levels have been associated with depression (Nakagawara, 1992;) and
ADHD (Kusaga et al., 2002). Increased levels have
been observed in individuals with anxiety and schizophrenia (see Burchett & Hicks, 2006). There is a very
strong association between Monoamine oxidase B
(MAO-B), an enzyme that catalyzes the degradation of PEA, and adverse psycho-social environments
(e.g., maltreatment) and criminal behavior (Oreland,

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GENERAL STUDIES

Adrian V. Rus Relationship between neurotransmitters, behavior, and maltreatment: A review

2007). In addition, MAO-B is associated with susceptibility to many psychiatric disorders (for a review, see
Volavka, 1999), and plays a role in mood regulation
(Bortolato, Godar, Davarian, Chen, & Shih, 2009);
emotional responses, including exploratory activity,
arousal, and behavioral reinforcement (Sabelli & Javaid, 1995); violent criminality (Asberg, 1997; Belfrage, Lindberg, & Oreland, 1992; Longato-Stadler,
af Klinteberg, Garpenstrand, Oreland, & Hallman,
2002); and suicide (Verkes et al., 1998). In sum, studies have shown that an individuals psycho-social environment influences both MAO activity (which has
a direct effect on PEA levels) and behavioral expression in individuals.
Glutamate
Glutamate is an excitatory neurotransmitter
(Carlson, 2007) and is considered to be the principal
mediator of sensory information, motor coordination,
emotions, and cognition, including memory formation
and memory retrieval (Hassel & Dingledine, 2006).
Glutamate also plays a role in alleviating the neuronal
effects of stress,anxiety,and modulates neuronal activity
throughout the central nervous system ( Johnson et al.,
2005; Niswender, Jones, & Conn, 2005). It has been
implicated in initiation and propagation of seizures
(Holmes, 1995) as well as in the pathophysiology
of mood disorders (Sanacora, Zarate, Krystal, &
Manji, 2008). Glutamate has also been implicated in
depersonalization disorder, which has been associated
with childhood emotional maltreatment and trauma
(Simeon, 2004). Furthermore, an excess of glutamate
has been associated with obsessive-compulsive
disorder (Carlsson, 2000), while a shortage has
been associated with ADHD (Moore et al., 2006)
and depressive symptoms (Tordera et al., 2011).
Glutamate dysfunction has also been associated with
autism (Page et al., 2006; Shinohe et al., 2006) and
schizophrenia (Coyle, 2006). Acute stress alters the
release of glutamate in the brain (Musazzi et al.,
2010) and rearing environments marked by neglect
and isolation are associated with reduced expression
of glutamate in the brain, leading to cognitive deficits
and psychiatric disorders. Glutamate dysfunction
caused by stress is also suspected to play a role in
schizophrenia and addiction (Melendez, Gregory,
Bardo, & Kalivas, 2004). Extremely high glutamate
levels, which lead to cell damage/death, have been

found in children with traumatic brain injury who

have also been victims of child abuse (Ruppel, 2001).
GABA
Gamma-aminobutyric acid (GABA), the major
inhibitory neurotransmitter in the CNS, plays a
trophic role during early brain development, including
neuronal wiring, plasticity of neuronal network,
and neural organization (Herlenius & Lagercrantz,
2001). GABA synthesis reaches peak activity during
the second year of life; thus, at age two, children
should show improvement in integrating information
(Herschkowitz, 2000). Olsen and Betz (2006)
reported a link between altered GABAergic function
and neurological and psychiatric disorders, primarily
related to hyperexcitability, including developmental
malfunctions; mental retardation and epilepsy, sleep
disorders; drug dependence, sensorimotor processing,
and motor coordination. Brambila, Perez, Barale,
Schettini, and Soares (2003) reported low levels
in both depressed and manic patients. Johnston
and Singer (2001) reported low levels of GABA in
cerebral spinal fluid in individuals with seizures.
Moreover, elevated plasma GABA levels have been
found in youngsters with Autistic Disorder, and some
researchers consider GABA to be a biochemical
marker of Autism (Dhossche et al., 2002) as well of
ADHD with conduct disorder (Prosser et al., 1997).
Summary
In summary, maltreatment can affect levels of
the neurotransmitters discussed above. Health and
childcare practitioners should be aware that children
with histories of trauma, neglect, and other forms of
maltreatment often exhibit behavior that is driven by
irregular levels of neurotransmitters that stem from
maltreatment (Purvis, McKenzie, Cross, Kellermann,
& Huisman, 2011). Urinary assays to assess specific
levels of each neurotransmitter to determine whether
they are within optimal ranges may be helpful in
planning appropriate therapies and interventions
(e.g., behavioral or psychological interventions,
supplements, or medication) and also in assessing the
efficacy of interventions.
In a recent study, significant reduction in
maladaptive behaviors was observed for at-risk
children when serotonin and Gaba were increased

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17

Adrian V. Rus Relationship between neurotransmitters, behavior, and maltreatment: A review 

with natural supplements (Cross, Kellermann,

McKenzie, Purvis, Hill, & Huisman, 2011).
Furthermore, NT testing has been used to detect
child abuse. In one case study, a mother was seeking
reinstatement of full custody of her child who had
been in foster care for one year. However, the child
demonstrated extreme reactions to her mothers
presence during visitation sessions. The child was
tested for neurotransmitter activity at baseline and
immediately after visitation by the mother. A spike in
the levels of several neurotransmitters after visitation
indicated a dramatic stress response associated with
the visitation. When the mother was presented with
these neurotransmitter results as well as her results on
the Adult Attachment Interview (AAI), she confessed
to using abusive parenting practices with the child
(Purvis, McKenzie, Kellermann, & Cross, 2010).
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