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NEUROTRANSMITTERS
&
NEUROENDOCRINOLOGY
BY,
POOJA SAHARAN
M.M.C.O.N, Mullana Ambala
M.Sc Nursing 1st yr.(1915718)
Mental Health Nursing
INTRODUCTION
 Neurotransmitters are chemical messengers that
transmit signals from a neuron to a target cell across
a synapse.
 Target cell may be a neuron or some other kind of cell like
a muscle or gland cell.
 Necessary for rapid communication in synapse.
 Neurotransmitters are packaged into synaptic vesicles -
presynaptic side of a synapse.
Illustration of the major elements in chemical synaptic transmission.
DEFINITION
 Neurotransmitter are the chemicals that
convey information across synaptic cleft to
neighboring target cells.They are stored in
the small vesicles in the axon terminals of the
neuron.
Axon
Vesicles (containing
neurotransmitters)
Synaptic cleft
Receptors
Receiving neuron
Pre synaptic
knob
Post synaptic
knob
A schematic representation of a chemical synapse
PROPERTIES OF
NEUROTRANSMITTERS
1) Synthesized in the presynaptic neuron
2) Localized to vesicles in the presynaptic neuron
3) Released from the presynaptic neuron under
physiological condition
4) Rapidly removed from the synaptic cleft by uptake
or degradation
5) Presence of receptor on the post-synaptic neuron.
6) Binding to the receptor elicits a biological response
Steps in neurotransmitter processing are:
Synthesis: Neurotransmitters are synthesized by the
enzymatic transformation of precursors.
Storage: They are packaged inside synaptic vesicles.
Release: They are released from presynaptic terminal by
exocytosis when calcium enters axon terminal
during an action potential
Diffuse across the synaptic cleft to the
postsynaptic membrane.
Binding: They bind to receptor proteins.
Inactivation: The neurotransmitter is degraded either by
being broken down enzymatically, or reused by
active reuptake.
TYPES OF NEUROTRANSMITTERS
BOTH
Acetylcholine
Nor epinephrine
EXCITATORY
Glutamate
Aspartate
Nitric oxide
INHIBITORY
Glycine
GABA
Serotonin
Dopamine
ON THE BASIS OF SIZE:
SMALL MOLECULE NEUROTRANSMITTER:
It include small molecule neurotransmitter eg.
Acetylcholine, amino acids, biogenic amines
etc.
NEUROPEPTIDES:
It consists of 3-40 amino acids linked by peptide
bonds.
Numerous and widespread in CNS & PNS .They
have both excitatory and inhibitory actions.
Neurotransmitter Location
Possible
Implications for
Mental illness
I. Cholinergics
A. Acetycholine ANS-Sympathetic and parasympathetic
presynaptic nerve terminals;
parasympathetic post-synaptic nerve
terminals.
CNS- Cerebral cortex ,hippocampus
,limbic structures, and basal ganglia.
Functions : Sleep, arousal, pain ,
perception, movement, memory
Increased levels:
Depression
Decreased levels :
Alzheimer’s Disease,
Huntington’s disease,
Parkinson’s
Disease
I. Monoamines
A. Norepinephrine ANS - Sympathetic post-synaptic nerve
terminals.
CNS – Thalamus, hypothalamus ,limbic
system ,hippocampus, cerebellum
,cerebral cortex.
Functions: Mood, cognition ,perception
,locomotion ,cardiovascular functioning
and sleep and arousal.
Decreased levels :
Depression
Increased levels :
Mania, Anxiety
states, Schizophrenia
A. Dopamine Frontal cortex, limbic system ,basal
ganglia, thalamus ,posterior pituitary and
spinal cord.
Functions : Movement and coordination,
emotions ,voluntary judgment ,release of
prolactin.
Decreased Levels :
Parkinson’s disease
and Depression
Increased levels :
Mania and
Schizophrenia
A. Serotonin Hypothalamus ,thalamus, limbic system,
cerebral cortex, cerebellum, spinal cord
Function : Sleep and arousal, libido,
appetite, mood ,aggression ,pain,
perception, coordination, judgement.
Increased levels :
Anxiety states
Decreased levels :
Depression
A. Histamine Hypothalamus
Functions : Wakefulness,pain,sensation
and inflammatory response
Decreased levels -
Depression
I. Amino Acids
A. Gamma-amino-
butyric acid(GABA)
Hypothalamus, hippocampus, cortex,
cerebellum ,basal ganglia, spinal cord,
retina
Functions: Slowdown of body activity
Decreased levels :
Huntington’s disease,
anxiety disorders,
schizophrenia, and
various forms of
epilepsy
B. Glycine Spinal cord and brain stem
Functions : Recurrent inhibition of
motor neurons
Toxic levels :”glycine
encephalopathy”,
decreased levels are
correlated with spastic
motor movements.
C. Glutamate and
Asparate
Pyramidal cells of the cortex,
cerebellum and the primary sensory
afferent systems ,hippocampus.
thalamus, hypothalamus, spinal cord
Functions: Relay of sensory
information and in the regulation of
various motor and spinal reflexes
Increased levels :
Huntington’s disease,
temporal lobe epilepsy,
spinal cerebellar
degeneration.
 NEUROPEPTIDES
Endorphins and Enkephalins
 Hypothalamus, thalamus ,limbic structures
,mid brain and brain stem;
 Enkephalins are also found in the gastro-
intestinal tract
 Functions : Modulation of pain and reduced
peristalsis (enkephalins)
 Modulation of dopamine activity by opoid
neuropeptides may indicate some link to the
symptoms of schizophrenia
 SUBSTANCE P
 Hypothalamus, thalamus ,midbrain, brain
stem, limbic structures ,basal ganglia and
spinal cord ,also found in gastro-intestinal
tract and salivary glands.
 Function: Regulation of pain.
 Increased levels : Depression
 Decreased levels : Huntington’s disease and
Alzheimer’s disease
SOMATOSTATIN
 Cerebral cortex, hippocampus ,thalamus
,basal ganglia, brain stem and spinal cord
 Function
 stimulates release of dopamine ,serotonin
,norepinephrine and acetylcholine, and
inhibits release of norepinephrine, histamine
and glutamate .
 Also acts as a neuromodulator for serotonin
in the hypothalamus
 Increased levels : Huntington’s disease
 Decreased levels : Alzheimer's disease
ALCOHOL& NEUROTRANSMITTERS
 It binds directly to receptors for ACh,
serotonin, GABA and glutamate.
 It enhances the effects of the GABA,
which is an inhibitory neurotransmitter.
 Enhancing an inhibitor make things sluggish.
 The neuron activity is diminished- sedative effects of
alcohol.
 Alcohol inhibits glutamate receptor function.
 This causes discoordination, slurred speech, staggering,
memory disruption, and blackout.
 Alcohol raises dopamine levels.
NICOTINE & NEUROTRANSMITTERS
 Nicotine imitates the action of ACh &
binds to ACh receptor.
 Like acetylcholine, nicotine leads to a burst of
receptor activity.
 Nicotine activates cholinergic neurons in many
different regions throughout your brain
simultaneously.
 This stimulation leads to:
 Increased release of glutamate.
 Stimulation of cholinergic neurons promotes the
release of dopamine. The production of dopamine
causes feelings of reward and pleasure.
DIAGNOSIS OFNEUROTRANSMITTER
IMBALANCE
 Identify the causes
 Identify the symptoms
Symptoms of Neurotransmitter Imbalances or Neurotransmitter
Deficiency
 Diagnostic tests
 Neurotransmitter Testing and Screening using urine samples
Urine test that measures the actual levels of neurotransmitters in
the urine.
 Brain Scans
 Live Studies
 Brain Tissue Assays
DRUGSALTER NEUROTRANSMISSION
 Agonist: A drug that facilitates the effects of a
particular neurotransmitter on the postsynaptic cell.
 Ways that drugs can agonize
 block auto-receptors
 inhibition of reuptake
 inhibition of deactivation
 precursor to neurotransmitter
 stimulate release
 receptor binding etc.
DRUGSALTER NEUROTRANSMISSION
 Antagonist: A drug that opposes or inhibits the
effects of a particular neurotransmitter on the
postsynaptic cell.
 Ways that drugs can antagonize
 prevent synthesis
 prevents storage
 block release
 receptor blocker
 stimulates autoreceptors
 Binds at same site neurotransmitter would.
 Binds at different site.
NURSES’ CONCERN IN
NEUROTRANSMITTER IMBALANCE
 Assessment
 Identify the markers showing adverse effects due to
prolonged use of medications
 Replenishing neurotransmitters
 Diet
 Aminoacid therapy
 Health education
 Rehabilitation
NURSING DIAGNOSIS
 Risk for injury related to accelerated motor activity
 Disturbed thought process related to impaired
judgement associated with manic behaviour
 Self-care deficit (unkempt appearance) related to
hyperactivity
 Impaired verbal communication –flight of ideas
related to accelerated thinking
 Ineffective coping related to elated expressive
mood
 Disturbed thought process –grandiosity related
to elevated mood
 Ineffective coping related to emotional
liability associated with manic behaviour
 Disturbed thought process –related to delusion
of grandeur
RESEARCH STUDIES
 A 1999 study at Duke University and
published in the Archives of Internal Medicine
found that regular exercise was effective in
decreasing symptoms of major depressive
disorder..
 "Journal of Psychiatry & Neuroscience," -
exercise also increases serotonin levels in your
brain, leading to improved mood
 And " exposure to the great outdoors, even on
a cloudy day, can provide enough natural light
to raise your serotonin levels.
NEUROENDOCRINOLOGY
 INTRODUCTION:
Study of the interaction between the nervous
system and the endocrine system and the
effect of various hormones on COGNITIVE,
EMOTIONAL AND BEHAVIOURAL
FUNCTIONING.
PITUITARY GLAND
PHYSIOLOGY OF PITUITARY
GLAND
ANTERIOR PITUITARY OR
ADENOHYPOPHYSIS
Location:
Anterior pituitary, stimulated by growth
hormone releasing hormone.
Target organs:
Bone and tissues
Function:
Growth in children
Protein synthesis in adults
Possible behavioral coorelation to altered
secretion:
ANOREXIA NERVOSA
ANTERIOR PITUITARY OR
ADENOHYPOPHYSIS
Location:
Anterior pituitary, stimulated by thyrotropin
releasing hormone by hypothalamus.
Target organs:
Thyroid gland
Function:
Stimulation of secretion of needed thyroid
hormones.
Possible behavioral correlation to altered
secretion:
Increased level: Insomnia, anxiety
Decreased level: Fatigue and depression
ANTERIOR PITUITARY OR
ADENOHYPOPHYSIS
Location:
Anterior pituitary, stimulated by thyrotropin
releasing hormone by hypothalamus.
Target organs:
Adrenal gland
Function:
Secretion of cortisol, which plays an important role
in response to stress.
Possible behavioral correlation to altered
secretion:
Increased level: Mood disorder and psychosis
Decreased level: Fatigue and depression
ANTERIOR PITUITARY OR
ADENOHYPOPHYSIS
Location:
Anterior pituitary, stimulated by prolactin
releasing hormone from hypothalamus.
Target organs:
Breasts
Function:
Stimulation of milk production.
Possible behavioral correlation to altered
secretion:
Depression, Decreased libido, anxiety,
irritability.
ANTERIOR PITUITARY OR
ADENOHYPOPHYSIS
 Location:
Anterior pituitary, stimulated by gonadotropin
releasing hormone from hypothalamus.
 Target organs:
Ovaries and testes
 Function:
Stimulation of secretion of estrogen, progesterone and
testosterone, role in ovulation and sperm
production.
 Possible behavioral correlation to altered secretion:
Increased level: Aggressiveness and increased sexual
behavior.
Decreased level: Depression and anorexia nervosa
ANTERIOR PITUITARY OR
ADENOHYPOPHYSIS
Location:
Anterior pituitary, release stimulated by onset
of darkness.
Target organs:
Pineal gland
Function:
Stimulation of secretion of Melatonin.
Possible behavioral correlation to altered
secretion:
Increased level: Depression .
POSTERIOR PITUITARY OR
NEUROHYPOPHYSIS
Location:
Posterior pituitary, release stimulated by
dehydration, pain, stress.
Target organs:
Kidney
Function:
Conservation of body water and maintenance
of blood pressure.
Possible behavioral correlation to altered
secretion:
Polydypsia , Modified sleep pattern.
POSTERIOR PITUITARY OR
NEUROHYPOPHYSIS
Location:
Posterior pituitary, release stimulated by
pregnancy, sexual arousal, stress.
Target organs:
Uterus
Breasts
Function:
Contraction of the uterus for the labor and release
of breast milk.
Possible behavioral correlation to altered
secretion:
Stress
THYROID GLAND
PHYSIOLOGY OF THYROID GLAND
T3 ANDT4
Function:
 Breathing
 Heart rate
 Central and peripheral nervous systems
 Body weight
 Muscle strength
 Menstrual cycles
 Body temperature
 Cholesterol levels
Possible behavioral correlation to altered
secretion:
BIPOLAR DISORDER
PANIC DISORDER
CONCLUSION
 The ability of nervous system to orchestrate complex
behaviors, learn and remember depends on
communication between vast no: of neurons.
 Mediated by neurotransmitters.
Many neurological diseases and mental disorders are due
to improper functioning of neurotransmitters.
 Study of the interaction between the nervous system
and the endocrine system and the effect of various
hormones on COGNITIVE, EMOTIONAL AND
BEHAVIOURAL FUNCTIONING.
Research abstract
 Title: Neurotransmitter Switching in
the Adult Brain Regulates Behavior
Authors:Davide Dulcis, Pouya Jamshidi, Stefan
Leutgeb
School of Medicine, University of California.
Dated: 26.april.2013.
 Neurotransmitters have been thought to be fixed
throughout life, but whether sensory stimuli alter
behaviorally relevant transmitter expression in the
mature brain is unknown.We found that populations of
interneurons in the adult rat hypothalamus switched
between dopamine and somatostatin expression in
response to exposure to short- and long-day
photoperiods. Changes in postsynaptic dopamine
receptor expression matched changes in presynaptic
dopamine, whereas somatostatin receptor expression
remained constant. Pharmacological blockade or
ablation of these dopaminergic neurons led to anxious
and depressed behavior, phenocopying performance
after exposure to the long-day photoperiod. Induction of
newly dopaminergic neurons through exposure to the
short-day photoperiod rescued the behavioral
consequences of lesions. Natural stimulation of other
sensory modalities may cause changes in transmitter
expression that regulate different behaviors.
 Expression of the appropriate
neurotransmitters is essential for the function
of neural circuits. Can neurons change their
transmitter phenotype to deal with
alterations in the environment? exposed
adult rats to different photoperiods
mimicking summer and winter daylengths.
Neurotransmitter expression switched
between dopamine and somatostatin in
hypothalamic neurons that regulate release
of corticotropin-releasing factor.Transmitter
switching occurred at the transcriptional level
and was accompanied by changes in
postsynaptic receptors.
REFERENCES
Books:
 Townsend Mary. C, Psychiatric Mental Health Nursing, 8th
edition, published by Jaypee Brothers medical
publishers(2015)
 Snell Richard S, Clinical Neuroanatomy, 7th edition, Published by
wolterskluwer(2010)
Internet:
 http://www.sciencedaily.com/releases/2011/12/1112051659
07.htm
 http://www.columbia.edu/cu/psychology/courses/1010/man
gels/neuro/transmission/transmission.html
 http://www.chemistryexplained.com/NeNu/Neurotransmitt
ers.html#b
Lets do some brain storming…
Q 1. Which hormones are
responsible for milk
production and milk
secretion?
 ANSWER:
MILK PRODUCTION: PROLACTIN
MILK SECRETION: OXYTOCIN
Q.2 IDENTIFY THE MISSING
PARTS.
Q.3 POSSIBLE IMPLICATIONS
FOR MENTAL ILLNESS CAUSED BY
THE ALTERATION IN THE LEVEL
OF SEROTNIN ARE:
Increased Serotonine:
Anxiety
Decreased level: Depression
TRUE OR FALSE???????
HEY I AM EXCITEDTO SAY
THANKYOUTO ALL FOR
ATTENDING OUR
PRESENTATION WITHTHEIR
KIND ATTENTION……AREN’T
YOU?????
Neurotransmitter and neuroendocrinology

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Neurotransmitter and neuroendocrinology

  • 1. NEUROTRANSMITTERS & NEUROENDOCRINOLOGY BY, POOJA SAHARAN M.M.C.O.N, Mullana Ambala M.Sc Nursing 1st yr.(1915718) Mental Health Nursing
  • 2. INTRODUCTION  Neurotransmitters are chemical messengers that transmit signals from a neuron to a target cell across a synapse.  Target cell may be a neuron or some other kind of cell like a muscle or gland cell.  Necessary for rapid communication in synapse.  Neurotransmitters are packaged into synaptic vesicles - presynaptic side of a synapse.
  • 3. Illustration of the major elements in chemical synaptic transmission.
  • 4. DEFINITION  Neurotransmitter are the chemicals that convey information across synaptic cleft to neighboring target cells.They are stored in the small vesicles in the axon terminals of the neuron.
  • 5. Axon Vesicles (containing neurotransmitters) Synaptic cleft Receptors Receiving neuron Pre synaptic knob Post synaptic knob A schematic representation of a chemical synapse
  • 6.
  • 7. PROPERTIES OF NEUROTRANSMITTERS 1) Synthesized in the presynaptic neuron 2) Localized to vesicles in the presynaptic neuron 3) Released from the presynaptic neuron under physiological condition 4) Rapidly removed from the synaptic cleft by uptake or degradation 5) Presence of receptor on the post-synaptic neuron. 6) Binding to the receptor elicits a biological response
  • 8. Steps in neurotransmitter processing are: Synthesis: Neurotransmitters are synthesized by the enzymatic transformation of precursors. Storage: They are packaged inside synaptic vesicles. Release: They are released from presynaptic terminal by exocytosis when calcium enters axon terminal during an action potential Diffuse across the synaptic cleft to the postsynaptic membrane. Binding: They bind to receptor proteins. Inactivation: The neurotransmitter is degraded either by being broken down enzymatically, or reused by active reuptake.
  • 9. TYPES OF NEUROTRANSMITTERS BOTH Acetylcholine Nor epinephrine EXCITATORY Glutamate Aspartate Nitric oxide INHIBITORY Glycine GABA Serotonin Dopamine
  • 10.
  • 11. ON THE BASIS OF SIZE: SMALL MOLECULE NEUROTRANSMITTER: It include small molecule neurotransmitter eg. Acetylcholine, amino acids, biogenic amines etc. NEUROPEPTIDES: It consists of 3-40 amino acids linked by peptide bonds. Numerous and widespread in CNS & PNS .They have both excitatory and inhibitory actions.
  • 12. Neurotransmitter Location Possible Implications for Mental illness I. Cholinergics A. Acetycholine ANS-Sympathetic and parasympathetic presynaptic nerve terminals; parasympathetic post-synaptic nerve terminals. CNS- Cerebral cortex ,hippocampus ,limbic structures, and basal ganglia. Functions : Sleep, arousal, pain , perception, movement, memory Increased levels: Depression Decreased levels : Alzheimer’s Disease, Huntington’s disease, Parkinson’s Disease I. Monoamines A. Norepinephrine ANS - Sympathetic post-synaptic nerve terminals. CNS – Thalamus, hypothalamus ,limbic system ,hippocampus, cerebellum ,cerebral cortex. Functions: Mood, cognition ,perception ,locomotion ,cardiovascular functioning and sleep and arousal. Decreased levels : Depression Increased levels : Mania, Anxiety states, Schizophrenia
  • 13. A. Dopamine Frontal cortex, limbic system ,basal ganglia, thalamus ,posterior pituitary and spinal cord. Functions : Movement and coordination, emotions ,voluntary judgment ,release of prolactin. Decreased Levels : Parkinson’s disease and Depression Increased levels : Mania and Schizophrenia A. Serotonin Hypothalamus ,thalamus, limbic system, cerebral cortex, cerebellum, spinal cord Function : Sleep and arousal, libido, appetite, mood ,aggression ,pain, perception, coordination, judgement. Increased levels : Anxiety states Decreased levels : Depression A. Histamine Hypothalamus Functions : Wakefulness,pain,sensation and inflammatory response Decreased levels - Depression
  • 14. I. Amino Acids A. Gamma-amino- butyric acid(GABA) Hypothalamus, hippocampus, cortex, cerebellum ,basal ganglia, spinal cord, retina Functions: Slowdown of body activity Decreased levels : Huntington’s disease, anxiety disorders, schizophrenia, and various forms of epilepsy B. Glycine Spinal cord and brain stem Functions : Recurrent inhibition of motor neurons Toxic levels :”glycine encephalopathy”, decreased levels are correlated with spastic motor movements. C. Glutamate and Asparate Pyramidal cells of the cortex, cerebellum and the primary sensory afferent systems ,hippocampus. thalamus, hypothalamus, spinal cord Functions: Relay of sensory information and in the regulation of various motor and spinal reflexes Increased levels : Huntington’s disease, temporal lobe epilepsy, spinal cerebellar degeneration.
  • 15.  NEUROPEPTIDES Endorphins and Enkephalins  Hypothalamus, thalamus ,limbic structures ,mid brain and brain stem;  Enkephalins are also found in the gastro- intestinal tract  Functions : Modulation of pain and reduced peristalsis (enkephalins)  Modulation of dopamine activity by opoid neuropeptides may indicate some link to the symptoms of schizophrenia
  • 16.  SUBSTANCE P  Hypothalamus, thalamus ,midbrain, brain stem, limbic structures ,basal ganglia and spinal cord ,also found in gastro-intestinal tract and salivary glands.  Function: Regulation of pain.  Increased levels : Depression  Decreased levels : Huntington’s disease and Alzheimer’s disease
  • 17. SOMATOSTATIN  Cerebral cortex, hippocampus ,thalamus ,basal ganglia, brain stem and spinal cord  Function  stimulates release of dopamine ,serotonin ,norepinephrine and acetylcholine, and inhibits release of norepinephrine, histamine and glutamate .  Also acts as a neuromodulator for serotonin in the hypothalamus  Increased levels : Huntington’s disease  Decreased levels : Alzheimer's disease
  • 18.
  • 19.
  • 20. ALCOHOL& NEUROTRANSMITTERS  It binds directly to receptors for ACh, serotonin, GABA and glutamate.  It enhances the effects of the GABA, which is an inhibitory neurotransmitter.  Enhancing an inhibitor make things sluggish.  The neuron activity is diminished- sedative effects of alcohol.  Alcohol inhibits glutamate receptor function.  This causes discoordination, slurred speech, staggering, memory disruption, and blackout.  Alcohol raises dopamine levels.
  • 21. NICOTINE & NEUROTRANSMITTERS  Nicotine imitates the action of ACh & binds to ACh receptor.  Like acetylcholine, nicotine leads to a burst of receptor activity.  Nicotine activates cholinergic neurons in many different regions throughout your brain simultaneously.  This stimulation leads to:  Increased release of glutamate.  Stimulation of cholinergic neurons promotes the release of dopamine. The production of dopamine causes feelings of reward and pleasure.
  • 22. DIAGNOSIS OFNEUROTRANSMITTER IMBALANCE  Identify the causes  Identify the symptoms Symptoms of Neurotransmitter Imbalances or Neurotransmitter Deficiency  Diagnostic tests  Neurotransmitter Testing and Screening using urine samples Urine test that measures the actual levels of neurotransmitters in the urine.  Brain Scans  Live Studies  Brain Tissue Assays
  • 23. DRUGSALTER NEUROTRANSMISSION  Agonist: A drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell.  Ways that drugs can agonize  block auto-receptors  inhibition of reuptake  inhibition of deactivation  precursor to neurotransmitter  stimulate release  receptor binding etc.
  • 24. DRUGSALTER NEUROTRANSMISSION  Antagonist: A drug that opposes or inhibits the effects of a particular neurotransmitter on the postsynaptic cell.  Ways that drugs can antagonize  prevent synthesis  prevents storage  block release  receptor blocker  stimulates autoreceptors  Binds at same site neurotransmitter would.  Binds at different site.
  • 25. NURSES’ CONCERN IN NEUROTRANSMITTER IMBALANCE  Assessment  Identify the markers showing adverse effects due to prolonged use of medications  Replenishing neurotransmitters  Diet  Aminoacid therapy  Health education  Rehabilitation
  • 26. NURSING DIAGNOSIS  Risk for injury related to accelerated motor activity  Disturbed thought process related to impaired judgement associated with manic behaviour  Self-care deficit (unkempt appearance) related to hyperactivity  Impaired verbal communication –flight of ideas related to accelerated thinking
  • 27.  Ineffective coping related to elated expressive mood  Disturbed thought process –grandiosity related to elevated mood  Ineffective coping related to emotional liability associated with manic behaviour  Disturbed thought process –related to delusion of grandeur
  • 28. RESEARCH STUDIES  A 1999 study at Duke University and published in the Archives of Internal Medicine found that regular exercise was effective in decreasing symptoms of major depressive disorder..  "Journal of Psychiatry & Neuroscience," - exercise also increases serotonin levels in your brain, leading to improved mood  And " exposure to the great outdoors, even on a cloudy day, can provide enough natural light to raise your serotonin levels.
  • 29.
  • 30. NEUROENDOCRINOLOGY  INTRODUCTION: Study of the interaction between the nervous system and the endocrine system and the effect of various hormones on COGNITIVE, EMOTIONAL AND BEHAVIOURAL FUNCTIONING.
  • 34. Location: Anterior pituitary, stimulated by growth hormone releasing hormone. Target organs: Bone and tissues Function: Growth in children Protein synthesis in adults Possible behavioral coorelation to altered secretion: ANOREXIA NERVOSA
  • 36. Location: Anterior pituitary, stimulated by thyrotropin releasing hormone by hypothalamus. Target organs: Thyroid gland Function: Stimulation of secretion of needed thyroid hormones. Possible behavioral correlation to altered secretion: Increased level: Insomnia, anxiety Decreased level: Fatigue and depression
  • 38. Location: Anterior pituitary, stimulated by thyrotropin releasing hormone by hypothalamus. Target organs: Adrenal gland Function: Secretion of cortisol, which plays an important role in response to stress. Possible behavioral correlation to altered secretion: Increased level: Mood disorder and psychosis Decreased level: Fatigue and depression
  • 40. Location: Anterior pituitary, stimulated by prolactin releasing hormone from hypothalamus. Target organs: Breasts Function: Stimulation of milk production. Possible behavioral correlation to altered secretion: Depression, Decreased libido, anxiety, irritability.
  • 42.  Location: Anterior pituitary, stimulated by gonadotropin releasing hormone from hypothalamus.  Target organs: Ovaries and testes  Function: Stimulation of secretion of estrogen, progesterone and testosterone, role in ovulation and sperm production.  Possible behavioral correlation to altered secretion: Increased level: Aggressiveness and increased sexual behavior. Decreased level: Depression and anorexia nervosa
  • 44. Location: Anterior pituitary, release stimulated by onset of darkness. Target organs: Pineal gland Function: Stimulation of secretion of Melatonin. Possible behavioral correlation to altered secretion: Increased level: Depression .
  • 46. Location: Posterior pituitary, release stimulated by dehydration, pain, stress. Target organs: Kidney Function: Conservation of body water and maintenance of blood pressure. Possible behavioral correlation to altered secretion: Polydypsia , Modified sleep pattern.
  • 48. Location: Posterior pituitary, release stimulated by pregnancy, sexual arousal, stress. Target organs: Uterus Breasts Function: Contraction of the uterus for the labor and release of breast milk. Possible behavioral correlation to altered secretion: Stress
  • 51. T3 ANDT4 Function:  Breathing  Heart rate  Central and peripheral nervous systems  Body weight  Muscle strength  Menstrual cycles  Body temperature  Cholesterol levels
  • 52. Possible behavioral correlation to altered secretion: BIPOLAR DISORDER PANIC DISORDER
  • 53. CONCLUSION  The ability of nervous system to orchestrate complex behaviors, learn and remember depends on communication between vast no: of neurons.  Mediated by neurotransmitters. Many neurological diseases and mental disorders are due to improper functioning of neurotransmitters.  Study of the interaction between the nervous system and the endocrine system and the effect of various hormones on COGNITIVE, EMOTIONAL AND BEHAVIOURAL FUNCTIONING.
  • 54. Research abstract  Title: Neurotransmitter Switching in the Adult Brain Regulates Behavior Authors:Davide Dulcis, Pouya Jamshidi, Stefan Leutgeb School of Medicine, University of California. Dated: 26.april.2013.
  • 55.  Neurotransmitters have been thought to be fixed throughout life, but whether sensory stimuli alter behaviorally relevant transmitter expression in the mature brain is unknown.We found that populations of interneurons in the adult rat hypothalamus switched between dopamine and somatostatin expression in response to exposure to short- and long-day photoperiods. Changes in postsynaptic dopamine receptor expression matched changes in presynaptic dopamine, whereas somatostatin receptor expression remained constant. Pharmacological blockade or ablation of these dopaminergic neurons led to anxious and depressed behavior, phenocopying performance after exposure to the long-day photoperiod. Induction of newly dopaminergic neurons through exposure to the short-day photoperiod rescued the behavioral consequences of lesions. Natural stimulation of other sensory modalities may cause changes in transmitter expression that regulate different behaviors.
  • 56.  Expression of the appropriate neurotransmitters is essential for the function of neural circuits. Can neurons change their transmitter phenotype to deal with alterations in the environment? exposed adult rats to different photoperiods mimicking summer and winter daylengths. Neurotransmitter expression switched between dopamine and somatostatin in hypothalamic neurons that regulate release of corticotropin-releasing factor.Transmitter switching occurred at the transcriptional level and was accompanied by changes in postsynaptic receptors.
  • 57. REFERENCES Books:  Townsend Mary. C, Psychiatric Mental Health Nursing, 8th edition, published by Jaypee Brothers medical publishers(2015)  Snell Richard S, Clinical Neuroanatomy, 7th edition, Published by wolterskluwer(2010) Internet:  http://www.sciencedaily.com/releases/2011/12/1112051659 07.htm  http://www.columbia.edu/cu/psychology/courses/1010/man gels/neuro/transmission/transmission.html  http://www.chemistryexplained.com/NeNu/Neurotransmitt ers.html#b
  • 58. Lets do some brain storming…
  • 59. Q 1. Which hormones are responsible for milk production and milk secretion?
  • 60.  ANSWER: MILK PRODUCTION: PROLACTIN MILK SECRETION: OXYTOCIN
  • 61. Q.2 IDENTIFY THE MISSING PARTS.
  • 62.
  • 63. Q.3 POSSIBLE IMPLICATIONS FOR MENTAL ILLNESS CAUSED BY THE ALTERATION IN THE LEVEL OF SEROTNIN ARE: Increased Serotonine: Anxiety Decreased level: Depression TRUE OR FALSE???????
  • 64.
  • 65. HEY I AM EXCITEDTO SAY THANKYOUTO ALL FOR ATTENDING OUR PRESENTATION WITHTHEIR KIND ATTENTION……AREN’T YOU?????