Take a look at Professor Randolph Nesse's website on this topic. Dopamine is only incidentally involved in reward pathways but is implicated to some extent in Bipolar. However transmitters are not the "Cause" but more a partial mechanism of depressive disorders.

To me Depression is attitude of mind . During our life action , we may have to pass certain phase for which we may not have experience or in certain cases for action of life we may not have received our anticipated result. In such cases we may required  to pass so many time unwanted problems.

With this it is very likely that such working environment if we are lucky with our Will Power & Faith ,our mind takes a negative reshaped of our thinking action . With the result we become more sensitive ,nervous & also undergone depression.

It is only with our controlling mind with a determination & will power by thinking the practice of working environment & habit of our life, we may certainly with the passage of said experience we can reduce depression .

This is my personal opinion 

Depression is a word;a social construction so it can be almost anything to anyone , which is why it is so difficult to consider scientifically . Having said that various systems have attempted to characterise it/them. My view is that negative feelings get lumped together as depression and this can include behaviours and vegetative biological changes. Because depression is a mood and a symptom as well as a diagnosis and can also be seen as a defense as well the field is so heterogeneous that  what one person means or one researcher delineates is not necessarily what another researcher uses. The only thing they all have in common is the word"depression". Consequently research into the phenomenon is hampered by uncontrolled variability in classification and severity. Nevertheless it is or the various types of low mood etc are valid as a target for some relief and assistance. I personally like Randolph Nesse's classification that I added above.

1.Regulation mechanism normal, low mood useful in this instance

2.Regulation mechanism normal, low mood useless in this instance

3.Regulation mechanism threshold abnormal, low mood excessive or deficient

4.Regulation mechanism fundamentally abnormal, depression arises without precipitant

5.Depression arises from mechanisms unrelated to those that regulate mood

The main issue  for me as a clinician is over how to define and delineate disorders , illnesses or conditions, and  whether they can be given a scientific or objective definition, or whether normative and subjective elements are inseparable and essential to our concept of mental conditions.  

I suspect you could argue that there are as many individual sub-types  (Of for instance depression) as there are people in the world but although  that is perhaps useful in some forms of psychotherapy, it is unhelpful in research and pharmacotherapy. 

Paul SJS

Frt those interested!

NICE recommendations for psychotherapy in depression: Of limited clinical utility

D. McQueen,1 P.St. John Smith2

PSYCHIATRIKI 26 (3), 2015 NICE RECOMMENDATIONS FOR PSYCHOTHERAPY IN DEPRESSION: OF LIMITED CLINICAL UTILITY 189

The National Institute for Health and Clinical Excellence (NICE) provides national guidance on promoting good health and preventing and treating ill health. It aspires to be based on the best  available evidence and involve all stakeholders in a transparent and collaborative manner. Once published, health professionals (and employing organisations) are expected to take NICE guidance fully into account when deciding treatments The guidance on depression is aimed at clinicians, managers and commissioners. It makes recommendations on assessment, pharmacotherapy, psychosocial interventions, relapse prevention and service delivery.

The full updated guideline on depression (707 pages)3 starts by describing depression as a broad, heterogeneous condition, influenced by diverse biological, psychological and social factors, and concludes that current diagnostic systems do not capture this complexity. However, having established these facts the guideline oversimplifies in key areas. Firstly it treats depression as a unitary diagnosis. Secondly it takes different psychotherapies at face value as representing distinct wel lcharacterised interventions rather than the complex interventions that they are. Thirdly it treats patients as homogenous, without comorbidity, personality traits or preferences that moderate their responses to treatment. Fourthly it only considers short-term studies in what is a chronic relapsing disorder.

Fifthly it excludes effectiveness studies, because of diagnostic heterogeneity or not being from randomised controlled trials (RCTs). In addition to these oversimplifications NICE actually misrepresents the results of its systematic review and erroneously implies that it has demonstrated that cognitive behavioural therapy (CBT) and interpersonal therapy (IPT) are superior treatments, whereas it has actually showed a lack of difference.

Finally NICE recommends replacing clinical assessment and personalised treatment with an untested service delivery model. Clinicians will be only too aware that “pure depression“ if it exists at all rarely comes to the attention of psychiatrists working in the National Health Service, where comorbidity of all kinds and clinical heterogeneity are the norm. Epidemiological data suggest that NICE’s model of depression separate from mixed neurotic conditions does not exist, the depressive syndrome overlaps with other common neurotic conditions. Depressive symptoms occur in most mental and many physical disorders. Just consider the core depressive syndromes; depressive adjustment reactions, dysthymia and melancholia:  Adjustment disorder may be criticized for vagueness and medicalising problems of living. Dysthymia is defined by mild symptoms, but sufferers spend more time depressed, have more admissions, more self-harm, higher rates of personality disorder, and it is more resistant to brief psychotherapy.  Depressive episodes have worse prognoses when co-occurring with dysthymia.

Furthermore depression has diverse aetiologies: Depressions arising from feelings of loss and activation of the attachment system (anaclitic depression) are associated with tearfulness, somatic complaints, parasuicide and care seeking. Depressions associated with failure, and activation of the social rank system (introjective depression) lead to fatigue, pessimism, guilt, inability to seek help and serious suicide attempts. Anaclitic and introjective depressions appear to have differential responses to psychotherapy. Some depressive behaviour can be seen as adaptive: After loss of an attachment figure, depression inhibits searching and proposal for an unproven service delivery model together seriously undermine the validity of the guidance.

From a psychological perspective depression is maintained by rumination. While our more proximate work on treating depression with metacognitive therapy and discontinuation of rumination leads me to believe that rumination is not adaptive, it may be of interest to consider work on the evolutionary benefits of rumination by Paul Andrews et al.

In our recent studies of depression we have not subcategorised depression. While I am sympathetic to the heterogenous category view of depression, I also find that in lack of knowledge of how to subcategorise effectively it is possible to provide effective treatment to the broad category.

The following chapter may be of specific interest to the current discussion. The volume may also be of general interest.

Chapter Depression: Is Rumination Really Adaptive?

New chapter, maybe of interest:

Chapter Depression